Cutis

Humans possess the ability to recognize and distinguish a large range of odors that can be utilized in a wide range of applications. For example, sommeliers can classify more than 88 smells specific to the roughly 800 volatile organic compounds (VOCs) in wine. Thorough physical examination is essential in dermatology, and although sight and touch play the most important diagnostic roles, the sense of smell often is overlooked. Dermatologists are rigorously trained on the many visual aspects of skin disease and have a plethora of terms to describe these features while there is minimal characterization of odors. Research on odors and the role of olfaction in dermatologic practice is limited.^1,2 We conducted a literature review of PubMed and Google Scholar for peer-reviewed articles discussing the role of odors in dermatologic diseases. Keywords included odor + dermatology, smell + dermatology, cutaneous odor, odor + diagnosis, and disease odor. Relevant studies were identified by screening their abstracts, followed by a full-text review. A total of 38 articles written in English that presented information on the odor associated with dermatologic diseases were included. Articles that were unrelated to the topic or written in a language other than English were excluded.

Common Skin Odors

The human body emits odorants—small VOCs—in various forms (skin/sweat, breath, urine, reproductive fluids). Human odor originates from the oxidation and bacterial metabolism of sweat and sebum on the skin.³ While many odors are physiologic and not cause for concern, others can signal underlying dermatologic pathologies.⁴ Odor-producing conditions can be categorized broadly into infectious diseases, disorders of keratinization and acantholysis, metabolic disorders, and organ dysfunction (Table). Infectious causes include bacterial infections and chronic wounds, which commonly emit characteristic offensive odors. For example, coryneform infections produce methanethiol, causing a cheesy odor of putrid fruit, and pseudomonal pyoderma infections emit a grape juice–like or mousy odor.

Bacterial and Fungal Infections

Bacterial and fungal infections often have distinct smells. Coryneform infections emit an odor of sweaty feet, pseudomonal infections emit a grape juice–like or mousy odor, and trichomycosis infections (caused by Corynebacterium tenuis) present with malodor.⁵ Pseudomonas can infect pyoderma gangrenosum lesions, producing a characteristic malodor.⁵ These smells can be clues for infectious etiology and guide further workup.

Pitted keratolysis, a malodorous pitted rash characterized by infection of the stratum corneum by Kytococcus sedentarius, Dermatophilus congolensis, or Corynebacterium species, is associated with a rotten smell. Its pungent odor, clinical location, and characteristic appearance often are enough to make a diagnosis. The amount of bacteria maintained in the stratum corneum is correlated with the extent of the lesion. Controlling excessive moisture in footwear, aluminum chloride, and topical microbial agents work together to eliminate the skin eruption.⁶ 

Hidradenitis suppurativa, a chronic inflammatory disease of apocrine gland–containing skin, can manifest with abscesses, draining sinuses, and nodules that produce a foul-smelling, purulent discharge. The disease can be debilitating, largely impacting patients’ quality of life, making early diagnosis and treatment critical.^7,8 Therapy is dependent on disease severity and includes topical antibiotics, systemic therapies, and biologics.⁸ 

Patients with atopic dermatitis often experience bacterial superinfection with Staphylococcus aureus. A case report described a patient who developed a fishy odor in this setting that resolved with antibiotic treatment, implicating S aureus in the etiology of the smell.⁹ 

A seminal fluid odor has been reported in cases of Pasteurella wound infection. In such cases, Pasteurella multocida subspecies septica was identified in the wounds caused by a dog scratch and a cat bite. The seminal fluid–like odor was apparent hours after the inciting incident and resolved after treatment with antibiotics.¹⁰ 

Fungal infections frequently emit musty or moldy odors. Tinea pedis (athlete’s foot) is the most prevalent cutaneous fungal infection. The presence of tinea pedis is associated with an intense foul-smelling odor, itching, fissuring, scaling, or maceration of the interdigital regions. The rash and odor resolve with use of topical antifungal agents.^11,12 Seborrheic dermatitis, a prevalent and chronic dermatosis, is characterized by yellow greasy scaling on an erythematous base. In severe cases, a greasy crust with an offensive odor can cover the entire scalp.¹³ The specific cause of this odor is unclear, but it is thought that sebum production and the immunological response to specific Malassezia yeast species may play a role.¹⁴

Genetic and Metabolic Disorders

An array of disorders of keratinization and acantholysis can manifest with distinctive smells that dermatologists frequently encounter. For example, Darier disease, characterized by keratotic papules progressing to crusted plaques, has a signature foul-smelling odor associated with cutaneous bacterial colonization.¹⁵ Similarly, Hailey-Hailey disease, an autosomal-dominant disorder with crusted erosions in skinfold areas, produces a distinct foul smell.¹⁶ Disorders such as pemphigus vulgaris and pemphigus foliaceus emit a peculiar fishy odor that can be helpful in making a diagnosis.¹⁷ Additionally, bullous ichthyosiform erythroderma, keratitis-ichthyosis-deafness syndrome, mal de Meleda, and Papillon-Lefèvre syndrome are all associated with malodor.⁵

Certain metabolic disorders can manifest and present initially with identifiable odors. Trimethylaminuria is a psychologically disabling disease known for its rotting fishy smell due to high amounts of trimethylamine appearing in affected individuals’ sweat, urine, and breath. Previously considered to be very rare, Messenger et al¹⁸ reported the disorder is likely underdiagnosed in those with idiopathic malodor production. Detection and treatment can greatly improve patient quality of life.

Phenylketonuria is an autosomal-recessive inborn error of phenylalanine metabolism that produces a musty body and urine odor as well as other neurologic and dermatologic symptoms.^19,20 Patients can present with eczematous rashes, fair skin, and blue eyes. Phenylacetic acid produces the characteristic odor in the bodily fluids, and the disease is treated with a phenylalanine-free diet.²¹ 

Maple syrup urine disease is a disorder of the oxidative decarboxylation of valine, leucine, and isoleucine (branched-chain amino acids) characterized by urine that smells sweet, resembling maple syrup, in afflicted individuals. The odor also can be present in other bodily secretions, such as sweat. Patients present early in infancy with poor feeding and vomiting as well as neurologic symptoms, eventually leading to intellectual disability. These individuals must avoid the branched-chain amino acids in their diets.²¹ 

Other metabolic storage disorders linked with specific odors are methionine adenosyltransferase deficiency (boiled cabbage), hypermethioninemia (fishy, boiled cabbage), isovaleric acidemia (sweaty feet), methionine malabsorption syndrome (pungent malodor), and dimethylglycine dehydrogenase deficiency (fishy).^5,21,22

In diabetic ketoacidosis, a life-threatening complication of diabetes, the excess of ketone bodies produced causes patients to have a distinct fruity breath and urine odor, as well as fatigue, polyuria, polydipsia, nausea, and vomiting.²² Although patients with type 1 diabetes typically comprise the cohort of patients presenting with diabetic ketoacidosis, patients with type 2 diabetes can exhibit cutaneous manifestations such as infection, xerosis, and inflammatory skin diseases.^23,24 

Organ Dysfunction

A peculiar body odor can be a sign of organ dysfunction. Renal dysfunction may present with both an odor and dermatologic manifestations. Patients with end-stage renal disease can have an ammonialike uremic breath odor as the result of excessive nitrogenous waste products and increased concentrations of urea in their saliva.^4,22 These patients also can exhibit pruritus, xerosis, pigmentation changes, nail changes, other dermatoses, and rarely uremic frost with white urate crystals present on the skin.^25,26 

Liver failure has been associated with an ammonialike musty breath odor termed fetor hepaticus. Shimamoto et al²⁷ reported notably higher levels of breath ammonia levels in patients with hepatic encephalopathy, indicating that excess ammonia is responsible for the odor. Fetor hepaticus has unique characteristics that can permit a diagnosis of liver disease, though it has been reported in cases in which a liver injury could not be identified.²⁸ 

Aging patients typically have a distinctive smell. Haze et al²⁹ analyzed the body odor of patients aged 26 to 75 years and discovered the compound 2-nonenal—an unsaturated aldehyde with a smell described as greasy and grassy—was found only in patients older than 40 years. The researchers’ analysis of skin-surface lipids also revealed that the presence of ω7 unsaturated fatty acids and lipid peroxides increased with age. They concluded that 2-nonenal is generated from the oxidative degradation of ω7 unsaturated fatty acids by lipid peroxides, suggesting that 2-nonenal may be a cause of the odor of old age.²⁹

Cutaneous Malignancies 

Research shows that the profiles of the body’s continuously released VOCs change in the presence of malignancy. Some studies suggest that melanoma may have a unique odor. Willis et al³⁰ reported that after a 13-month training period, a dog was able to correctly identify melanoma and distinguish it from basal cell carcinoma, benign nevi, and healthy skin based on olfaction alone. Additional cases have been reported in which dogs have been able to identify melanoma based on smell, suggesting that canine olfactory detection of melanoma could possibly aid in the diagnosis of skin cancer, which warrants further investigation.^31,32 There is limited evidence on the specific odors of other cutaneous malignancies, such as basal cell carcinoma and squamous cell carcinoma. 

Bacterial superinfection of cutaneous malignancy can secrete pungent odors. An offensive rotting odor has been associated with necrotic malignant ulcers of the vagina. This malodor likely is a result of the formation of putrescine, cadaverine, short-chain fatty acids (isovaleric and butyric acids) and sulfur-containing compounds by bacteria.³³ Recognition of similar smells may aid in management of these infections.

Diagnostic Techniques

Evaluating human skin odor is challenging, as the components of VOCs are complicated and typically found at trace levels. Studies indicate that gas chromatography–mass spectrometry is the most effective way to analyze human odor. This method separates, quantifies, and analyzes VOCs from samples containing odors.³⁴ Gas chromatography–mass spectrometry, however, has limitations, as the time for analysis is lengthy, the equipment is large, and the process is expensive.³ Research supports the usefulness and validity of quantitative gas chromatography–olfactometry to detect odorants and evaluate odor activity of VOCs in various samples.³⁵ With this technique, human assessors act in place of more conventional detectors, such as mass spectrometers. This method has been used to evaluate odorants in human urine with the goal of increasing understanding of metabolization and excretion processes.³⁶ However, gas chromatography–olfactometry typically is used in the analysis of food and drink, and future research should be aimed at applying this method to medicine. 

Zheng et al³ proposed a wearable electronic nose as a tool to identify human odor to emulate the odor recognition of a canine’s nose. They developed a sensor array based on the composites of carbon nanotubes and polymers able to examine and identify odors in the air. Study participants wore the electronic nose on the arm with the sensory array facing the armpits while they walked on a treadmill. Although many issues regarding odor measurement were not addressed in this study, the research suggests further studies are warranted to improve analysis of odor.³

Clinical Cases

Patient 1—Arseculeratne et al³⁷ described a 41-year-old man who presented with a fishy odor that others had noticed since the age of 13 years but that the patient could not smell himself. Based on his presentation, he was worked up for trimethylaminuria and found to have elevated levels of urinary trimethylamine (TMA) with a raised TMA/TMA-oxidase ratio. These findings were consistent with a diagnosis of primary trimethylaminuria, and the patient was referred to a dietician for counseling on foods that contain low amounts of choline and lecithin. Initially his urinary TMA level fell but then rose again, indicating possible relaxation of his diet. He then took a 10-day course of metronidazole, which helped reduce some of the malodor. The authors reported that the most impactful therapy for the patient was being able to discuss the disorder with his friends and family members.³⁷ This case highlighted the importance of confirming the diagnosis and early initiation of dietary and pharmacologic interventions in patients with trimethylaminuria. In patients reporting a persistent fishy body odor, trimethylaminuria should be on the differential.

Patient 2—In 1999, Schissel et al⁶ described a 20-year-old active-duty soldier who presented to the dermatology department with smelly trench foot and tinea pedis. The soldier reported having this malodorous pitted rash for more than 10 years. He also reported occasional interdigital burning and itching and noted no improvement despite using various topical antifungals. Physical examination revealed an “overpowering pungent odor” when the patient removed his shoes. He had many tender, white, and wet plaques with scalloped borders coalescing into shallow pits on the plantar surface of the feet and great toes. Potassium hydroxide preparation of the great toe plaques and interdigital web spaces were positive for fungal elements, and bacterial cultures isolated moderate coagulase-negative staphylococcal and Corynebacterium species. Additionally, fungal cultures identified Acremonium species. The patient was started on clotrimazole cream twice daily, clindamycin solution twice daily, and topical ammonium chloride nightly. Two weeks later, the patient reported resolution of symptoms, including the malodor.⁶ In pitted keratolysis, warm and wet environments within boots or shoes allow for the growth of bacteria and fungi. The extent of the lesions is related to the amount of bacteria within the stratum corneum. The diagnosis often is made based on odor, location, and appearance of the rash alone. The most common organisms implicated as causal agents in the condition are Kytococcus sedentarius, Dermatophilus congolensis, and species of Corynebacterium and Actinomyces. It is thought that these organisms release proteolytic enzymes that degrade the horny layer, releasing a mixture of thiols, thioesters, and sulfides, which cause the pungent odor. Familiarity with the characteristic odor aids in prompt diagnosis and treatment, which will ultimately heal the skin eruption. 

Patient 3—Srivastava et al³² described a 43-year-old woman who presented with a nevus on the back since childhood. She noticed that it had changed and grown over the past few years and reported that her dog would often sniff the lesion and try to scratch and bite the lesion. This reaction from her dog led the patient to seek out evaluation from a dermatologist. The patient had no personal history of skin cancer, bad sunburns, tanning bed use, or use of immunosuppressants. She reported that her father had a history of basal cell carcinoma. Physical examination revealed a 1.2×1.5-cm brown patch with an ulcerated nodule located on the lower aspect of the lesion. The patient underwent a wide local excision and sentinel lymph node biopsy with pathology showing a 4-mm-thick melanoma with positive lymph nodes. She then underwent a right axillary lymphadenectomy and was diagnosed with stage IIIB malignant melanoma. Following the surgery, the patient’s dog would sniff the back and calmly rest his head in her lap. She has not had a recurrence and credits her dog for saving her life.³² Canine olfaction may play a role in detecting skin cancers, as evidenced by this case. Patients and dermatologists should pay attention to the behavior of dogs toward skin lesions. Harnessing this sense into a method to noninvasively screen for melanoma in humans should be further investigated.

Patient 4—Matthews et al³⁸ described a 32-year-old woman who presented to an emergency eye clinic with a white “lump” on the left upper eyelid of 6 months’ duration. Physical examination revealed 3 nodular and cystic lesions oozing a thick yellow-white discharge. Cultures were taken, and the patient was started on chloramphenicol ointment once daily to the skin. At follow-up, the lesions had not changed, and the cultures were negative. The patient reported an intermittent malodorous discharge and noted multiple similar lesions on her body. Excisional biopsy demonstrated histologic findings including dyskeratosis, papillomatosis, and suprabasal acantholysis associated with focal underlying chronic inflammatory infiltrate. She was referred to a dermatologist and was diagnosed with Darier disease. She was started on clobetasone butyrate when necessary and adapalene nocte. Understanding the smell associated with Darier disease in conjunction with the cutaneous findings may aid in earlier diagnosis, improving outcomes for affected patients.³⁸ 

Conclusion

The sense of smell may be an overlooked diagnostic tool that dermatologists innately possess. Odors detected when examining patients should be considered, as these odors may help guide a diagnosis. Early diagnosis and treatment are important in many dermatologic diseases, so it is imperative to consider all diagnostic clues. Although physician olfaction may aid in diagnosis, its utility remains challenging, as there is a lack of consensus and terminology regarding odor in disease. A limitation of training to identify disease-specific odors is the requirement of engaging in often unpleasant odors. Methods to objectively measure odor are expensive and still in the early stages of development. Further research and exploration of olfactory-based diagnostic techniques is warranted to potentially improve dermatologic diagnosis. 

Humans possess the ability to recognize and distinguish a large range of odors that can be utilized in a wide range of applications. For example, sommeliers can classify more than 88 smells specific to the roughly 800 volatile organic compounds (VOCs) in wine. Thorough physical examination is essential in dermatology, and although sight and touch play the most important diagnostic roles, the sense of smell often is overlooked. Dermatologists are rigorously trained on the many visual aspects of skin disease and have a plethora of terms to describe these features while there is minimal characterization of odors. Research on odors and the role of olfaction in dermatologic practice is limited.^1,2 We conducted a literature review of PubMed and Google Scholar for peer-reviewed articles discussing the role of odors in dermatologic diseases. Keywords included odor + dermatology, smell + dermatology, cutaneous odor, odor + diagnosis, and disease odor. Relevant studies were identified by screening their abstracts, followed by a full-text review. A total of 38 articles written in English that presented information on the odor associated with dermatologic diseases were included. Articles that were unrelated to the topic or written in a language other than English were excluded.

Common Skin Odors

The human body emits odorants—small VOCs—in various forms (skin/sweat, breath, urine, reproductive fluids). Human odor originates from the oxidation and bacterial metabolism of sweat and sebum on the skin.³ While many odors are physiologic and not cause for concern, others can signal underlying dermatologic pathologies.⁴ Odor-producing conditions can be categorized broadly into infectious diseases, disorders of keratinization and acantholysis, metabolic disorders, and organ dysfunction (Table). Infectious causes include bacterial infections and chronic wounds, which commonly emit characteristic offensive odors. For example, coryneform infections produce methanethiol, causing a cheesy odor of putrid fruit, and pseudomonal pyoderma infections emit a grape juice–like or mousy odor.

Bacterial and Fungal Infections

Bacterial and fungal infections often have distinct smells. Coryneform infections emit an odor of sweaty feet, pseudomonal infections emit a grape juice–like or mousy odor, and trichomycosis infections (caused by Corynebacterium tenuis) present with malodor.⁵ Pseudomonas can infect pyoderma gangrenosum lesions, producing a characteristic malodor.⁵ These smells can be clues for infectious etiology and guide further workup.

Pitted keratolysis, a malodorous pitted rash characterized by infection of the stratum corneum by Kytococcus sedentarius, Dermatophilus congolensis, or Corynebacterium species, is associated with a rotten smell. Its pungent odor, clinical location, and characteristic appearance often are enough to make a diagnosis. The amount of bacteria maintained in the stratum corneum is correlated with the extent of the lesion. Controlling excessive moisture in footwear, aluminum chloride, and topical microbial agents work together to eliminate the skin eruption.⁶ 

Hidradenitis suppurativa, a chronic inflammatory disease of apocrine gland–containing skin, can manifest with abscesses, draining sinuses, and nodules that produce a foul-smelling, purulent discharge. The disease can be debilitating, largely impacting patients’ quality of life, making early diagnosis and treatment critical.^7,8 Therapy is dependent on disease severity and includes topical antibiotics, systemic therapies, and biologics.⁸ 

Patients with atopic dermatitis often experience bacterial superinfection with Staphylococcus aureus. A case report described a patient who developed a fishy odor in this setting that resolved with antibiotic treatment, implicating S aureus in the etiology of the smell.⁹ 

A seminal fluid odor has been reported in cases of Pasteurella wound infection. In such cases, Pasteurella multocida subspecies septica was identified in the wounds caused by a dog scratch and a cat bite. The seminal fluid–like odor was apparent hours after the inciting incident and resolved after treatment with antibiotics.¹⁰ 

Fungal infections frequently emit musty or moldy odors. Tinea pedis (athlete’s foot) is the most prevalent cutaneous fungal infection. The presence of tinea pedis is associated with an intense foul-smelling odor, itching, fissuring, scaling, or maceration of the interdigital regions. The rash and odor resolve with use of topical antifungal agents.^11,12 Seborrheic dermatitis, a prevalent and chronic dermatosis, is characterized by yellow greasy scaling on an erythematous base. In severe cases, a greasy crust with an offensive odor can cover the entire scalp.¹³ The specific cause of this odor is unclear, but it is thought that sebum production and the immunological response to specific Malassezia yeast species may play a role.¹⁴

Genetic and Metabolic Disorders

An array of disorders of keratinization and acantholysis can manifest with distinctive smells that dermatologists frequently encounter. For example, Darier disease, characterized by keratotic papules progressing to crusted plaques, has a signature foul-smelling odor associated with cutaneous bacterial colonization.¹⁵ Similarly, Hailey-Hailey disease, an autosomal-dominant disorder with crusted erosions in skinfold areas, produces a distinct foul smell.¹⁶ Disorders such as pemphigus vulgaris and pemphigus foliaceus emit a peculiar fishy odor that can be helpful in making a diagnosis.¹⁷ Additionally, bullous ichthyosiform erythroderma, keratitis-ichthyosis-deafness syndrome, mal de Meleda, and Papillon-Lefèvre syndrome are all associated with malodor.⁵

Certain metabolic disorders can manifest and present initially with identifiable odors. Trimethylaminuria is a psychologically disabling disease known for its rotting fishy smell due to high amounts of trimethylamine appearing in affected individuals’ sweat, urine, and breath. Previously considered to be very rare, Messenger et al¹⁸ reported the disorder is likely underdiagnosed in those with idiopathic malodor production. Detection and treatment can greatly improve patient quality of life.

Phenylketonuria is an autosomal-recessive inborn error of phenylalanine metabolism that produces a musty body and urine odor as well as other neurologic and dermatologic symptoms.^19,20 Patients can present with eczematous rashes, fair skin, and blue eyes. Phenylacetic acid produces the characteristic odor in the bodily fluids, and the disease is treated with a phenylalanine-free diet.²¹ 

Maple syrup urine disease is a disorder of the oxidative decarboxylation of valine, leucine, and isoleucine (branched-chain amino acids) characterized by urine that smells sweet, resembling maple syrup, in afflicted individuals. The odor also can be present in other bodily secretions, such as sweat. Patients present early in infancy with poor feeding and vomiting as well as neurologic symptoms, eventually leading to intellectual disability. These individuals must avoid the branched-chain amino acids in their diets.²¹ 

Other metabolic storage disorders linked with specific odors are methionine adenosyltransferase deficiency (boiled cabbage), hypermethioninemia (fishy, boiled cabbage), isovaleric acidemia (sweaty feet), methionine malabsorption syndrome (pungent malodor), and dimethylglycine dehydrogenase deficiency (fishy).^5,21,22

In diabetic ketoacidosis, a life-threatening complication of diabetes, the excess of ketone bodies produced causes patients to have a distinct fruity breath and urine odor, as well as fatigue, polyuria, polydipsia, nausea, and vomiting.²² Although patients with type 1 diabetes typically comprise the cohort of patients presenting with diabetic ketoacidosis, patients with type 2 diabetes can exhibit cutaneous manifestations such as infection, xerosis, and inflammatory skin diseases.^23,24 

Organ Dysfunction

A peculiar body odor can be a sign of organ dysfunction. Renal dysfunction may present with both an odor and dermatologic manifestations. Patients with end-stage renal disease can have an ammonialike uremic breath odor as the result of excessive nitrogenous waste products and increased concentrations of urea in their saliva.^4,22 These patients also can exhibit pruritus, xerosis, pigmentation changes, nail changes, other dermatoses, and rarely uremic frost with white urate crystals present on the skin.^25,26 

Liver failure has been associated with an ammonialike musty breath odor termed fetor hepaticus. Shimamoto et al²⁷ reported notably higher levels of breath ammonia levels in patients with hepatic encephalopathy, indicating that excess ammonia is responsible for the odor. Fetor hepaticus has unique characteristics that can permit a diagnosis of liver disease, though it has been reported in cases in which a liver injury could not be identified.²⁸ 

Aging patients typically have a distinctive smell. Haze et al²⁹ analyzed the body odor of patients aged 26 to 75 years and discovered the compound 2-nonenal—an unsaturated aldehyde with a smell described as greasy and grassy—was found only in patients older than 40 years. The researchers’ analysis of skin-surface lipids also revealed that the presence of ω7 unsaturated fatty acids and lipid peroxides increased with age. They concluded that 2-nonenal is generated from the oxidative degradation of ω7 unsaturated fatty acids by lipid peroxides, suggesting that 2-nonenal may be a cause of the odor of old age.²⁹

Cutaneous Malignancies 

Research shows that the profiles of the body’s continuously released VOCs change in the presence of malignancy. Some studies suggest that melanoma may have a unique odor. Willis et al³⁰ reported that after a 13-month training period, a dog was able to correctly identify melanoma and distinguish it from basal cell carcinoma, benign nevi, and healthy skin based on olfaction alone. Additional cases have been reported in which dogs have been able to identify melanoma based on smell, suggesting that canine olfactory detection of melanoma could possibly aid in the diagnosis of skin cancer, which warrants further investigation.^31,32 There is limited evidence on the specific odors of other cutaneous malignancies, such as basal cell carcinoma and squamous cell carcinoma. 

Bacterial superinfection of cutaneous malignancy can secrete pungent odors. An offensive rotting odor has been associated with necrotic malignant ulcers of the vagina. This malodor likely is a result of the formation of putrescine, cadaverine, short-chain fatty acids (isovaleric and butyric acids) and sulfur-containing compounds by bacteria.³³ Recognition of similar smells may aid in management of these infections.

Diagnostic Techniques

Evaluating human skin odor is challenging, as the components of VOCs are complicated and typically found at trace levels. Studies indicate that gas chromatography–mass spectrometry is the most effective way to analyze human odor. This method separates, quantifies, and analyzes VOCs from samples containing odors.³⁴ Gas chromatography–mass spectrometry, however, has limitations, as the time for analysis is lengthy, the equipment is large, and the process is expensive.³ Research supports the usefulness and validity of quantitative gas chromatography–olfactometry to detect odorants and evaluate odor activity of VOCs in various samples.³⁵ With this technique, human assessors act in place of more conventional detectors, such as mass spectrometers. This method has been used to evaluate odorants in human urine with the goal of increasing understanding of metabolization and excretion processes.³⁶ However, gas chromatography–olfactometry typically is used in the analysis of food and drink, and future research should be aimed at applying this method to medicine. 

Zheng et al³ proposed a wearable electronic nose as a tool to identify human odor to emulate the odor recognition of a canine’s nose. They developed a sensor array based on the composites of carbon nanotubes and polymers able to examine and identify odors in the air. Study participants wore the electronic nose on the arm with the sensory array facing the armpits while they walked on a treadmill. Although many issues regarding odor measurement were not addressed in this study, the research suggests further studies are warranted to improve analysis of odor.³

Clinical Cases

Patient 1—Arseculeratne et al³⁷ described a 41-year-old man who presented with a fishy odor that others had noticed since the age of 13 years but that the patient could not smell himself. Based on his presentation, he was worked up for trimethylaminuria and found to have elevated levels of urinary trimethylamine (TMA) with a raised TMA/TMA-oxidase ratio. These findings were consistent with a diagnosis of primary trimethylaminuria, and the patient was referred to a dietician for counseling on foods that contain low amounts of choline and lecithin. Initially his urinary TMA level fell but then rose again, indicating possible relaxation of his diet. He then took a 10-day course of metronidazole, which helped reduce some of the malodor. The authors reported that the most impactful therapy for the patient was being able to discuss the disorder with his friends and family members.³⁷ This case highlighted the importance of confirming the diagnosis and early initiation of dietary and pharmacologic interventions in patients with trimethylaminuria. In patients reporting a persistent fishy body odor, trimethylaminuria should be on the differential.

Patient 2—In 1999, Schissel et al⁶ described a 20-year-old active-duty soldier who presented to the dermatology department with smelly trench foot and tinea pedis. The soldier reported having this malodorous pitted rash for more than 10 years. He also reported occasional interdigital burning and itching and noted no improvement despite using various topical antifungals. Physical examination revealed an “overpowering pungent odor” when the patient removed his shoes. He had many tender, white, and wet plaques with scalloped borders coalescing into shallow pits on the plantar surface of the feet and great toes. Potassium hydroxide preparation of the great toe plaques and interdigital web spaces were positive for fungal elements, and bacterial cultures isolated moderate coagulase-negative staphylococcal and Corynebacterium species. Additionally, fungal cultures identified Acremonium species. The patient was started on clotrimazole cream twice daily, clindamycin solution twice daily, and topical ammonium chloride nightly. Two weeks later, the patient reported resolution of symptoms, including the malodor.⁶ In pitted keratolysis, warm and wet environments within boots or shoes allow for the growth of bacteria and fungi. The extent of the lesions is related to the amount of bacteria within the stratum corneum. The diagnosis often is made based on odor, location, and appearance of the rash alone. The most common organisms implicated as causal agents in the condition are Kytococcus sedentarius, Dermatophilus congolensis, and species of Corynebacterium and Actinomyces. It is thought that these organisms release proteolytic enzymes that degrade the horny layer, releasing a mixture of thiols, thioesters, and sulfides, which cause the pungent odor. Familiarity with the characteristic odor aids in prompt diagnosis and treatment, which will ultimately heal the skin eruption. 

Patient 3—Srivastava et al³² described a 43-year-old woman who presented with a nevus on the back since childhood. She noticed that it had changed and grown over the past few years and reported that her dog would often sniff the lesion and try to scratch and bite the lesion. This reaction from her dog led the patient to seek out evaluation from a dermatologist. The patient had no personal history of skin cancer, bad sunburns, tanning bed use, or use of immunosuppressants. She reported that her father had a history of basal cell carcinoma. Physical examination revealed a 1.2×1.5-cm brown patch with an ulcerated nodule located on the lower aspect of the lesion. The patient underwent a wide local excision and sentinel lymph node biopsy with pathology showing a 4-mm-thick melanoma with positive lymph nodes. She then underwent a right axillary lymphadenectomy and was diagnosed with stage IIIB malignant melanoma. Following the surgery, the patient’s dog would sniff the back and calmly rest his head in her lap. She has not had a recurrence and credits her dog for saving her life.³² Canine olfaction may play a role in detecting skin cancers, as evidenced by this case. Patients and dermatologists should pay attention to the behavior of dogs toward skin lesions. Harnessing this sense into a method to noninvasively screen for melanoma in humans should be further investigated.

Patient 4—Matthews et al³⁸ described a 32-year-old woman who presented to an emergency eye clinic with a white “lump” on the left upper eyelid of 6 months’ duration. Physical examination revealed 3 nodular and cystic lesions oozing a thick yellow-white discharge. Cultures were taken, and the patient was started on chloramphenicol ointment once daily to the skin. At follow-up, the lesions had not changed, and the cultures were negative. The patient reported an intermittent malodorous discharge and noted multiple similar lesions on her body. Excisional biopsy demonstrated histologic findings including dyskeratosis, papillomatosis, and suprabasal acantholysis associated with focal underlying chronic inflammatory infiltrate. She was referred to a dermatologist and was diagnosed with Darier disease. She was started on clobetasone butyrate when necessary and adapalene nocte. Understanding the smell associated with Darier disease in conjunction with the cutaneous findings may aid in earlier diagnosis, improving outcomes for affected patients.³⁸ 

Conclusion

The sense of smell may be an overlooked diagnostic tool that dermatologists innately possess. Odors detected when examining patients should be considered, as these odors may help guide a diagnosis. Early diagnosis and treatment are important in many dermatologic diseases, so it is imperative to consider all diagnostic clues. Although physician olfaction may aid in diagnosis, its utility remains challenging, as there is a lack of consensus and terminology regarding odor in disease. A limitation of training to identify disease-specific odors is the requirement of engaging in often unpleasant odors. Methods to objectively measure odor are expensive and still in the early stages of development. Further research and exploration of olfactory-based diagnostic techniques is warranted to potentially improve dermatologic diagnosis. 

Humans possess the ability to recognize and distinguish a large range of odors that can be utilized in a wide range of applications. For example, sommeliers can classify more than 88 smells specific to the roughly 800 volatile organic compounds (VOCs) in wine. Thorough physical examination is essential in dermatology, and although sight and touch play the most important diagnostic roles, the sense of smell often is overlooked. Dermatologists are rigorously trained on the many visual aspects of skin disease and have a plethora of terms to describe these features while there is minimal characterization of odors. Research on odors and the role of olfaction in dermatologic practice is limited.^1,2 We conducted a literature review of PubMed and Google Scholar for peer-reviewed articles discussing the role of odors in dermatologic diseases. Keywords included odor + dermatology, smell + dermatology, cutaneous odor, odor + diagnosis, and disease odor. Relevant studies were identified by screening their abstracts, followed by a full-text review. A total of 38 articles written in English that presented information on the odor associated with dermatologic diseases were included. Articles that were unrelated to the topic or written in a language other than English were excluded.

Common Skin Odors

The human body emits odorants—small VOCs—in various forms (skin/sweat, breath, urine, reproductive fluids). Human odor originates from the oxidation and bacterial metabolism of sweat and sebum on the skin.³ While many odors are physiologic and not cause for concern, others can signal underlying dermatologic pathologies.⁴ Odor-producing conditions can be categorized broadly into infectious diseases, disorders of keratinization and acantholysis, metabolic disorders, and organ dysfunction (Table). Infectious causes include bacterial infections and chronic wounds, which commonly emit characteristic offensive odors. For example, coryneform infections produce methanethiol, causing a cheesy odor of putrid fruit, and pseudomonal pyoderma infections emit a grape juice–like or mousy odor.

Bacterial and Fungal Infections

Bacterial and fungal infections often have distinct smells. Coryneform infections emit an odor of sweaty feet, pseudomonal infections emit a grape juice–like or mousy odor, and trichomycosis infections (caused by Corynebacterium tenuis) present with malodor.⁵ Pseudomonas can infect pyoderma gangrenosum lesions, producing a characteristic malodor.⁵ These smells can be clues for infectious etiology and guide further workup.

Pitted keratolysis, a malodorous pitted rash characterized by infection of the stratum corneum by Kytococcus sedentarius, Dermatophilus congolensis, or Corynebacterium species, is associated with a rotten smell. Its pungent odor, clinical location, and characteristic appearance often are enough to make a diagnosis. The amount of bacteria maintained in the stratum corneum is correlated with the extent of the lesion. Controlling excessive moisture in footwear, aluminum chloride, and topical microbial agents work together to eliminate the skin eruption.⁶ 

Hidradenitis suppurativa, a chronic inflammatory disease of apocrine gland–containing skin, can manifest with abscesses, draining sinuses, and nodules that produce a foul-smelling, purulent discharge. The disease can be debilitating, largely impacting patients’ quality of life, making early diagnosis and treatment critical.^7,8 Therapy is dependent on disease severity and includes topical antibiotics, systemic therapies, and biologics.⁸ 

Patients with atopic dermatitis often experience bacterial superinfection with Staphylococcus aureus. A case report described a patient who developed a fishy odor in this setting that resolved with antibiotic treatment, implicating S aureus in the etiology of the smell.⁹ 

A seminal fluid odor has been reported in cases of Pasteurella wound infection. In such cases, Pasteurella multocida subspecies septica was identified in the wounds caused by a dog scratch and a cat bite. The seminal fluid–like odor was apparent hours after the inciting incident and resolved after treatment with antibiotics.¹⁰ 

Fungal infections frequently emit musty or moldy odors. Tinea pedis (athlete’s foot) is the most prevalent cutaneous fungal infection. The presence of tinea pedis is associated with an intense foul-smelling odor, itching, fissuring, scaling, or maceration of the interdigital regions. The rash and odor resolve with use of topical antifungal agents.^11,12 Seborrheic dermatitis, a prevalent and chronic dermatosis, is characterized by yellow greasy scaling on an erythematous base. In severe cases, a greasy crust with an offensive odor can cover the entire scalp.¹³ The specific cause of this odor is unclear, but it is thought that sebum production and the immunological response to specific Malassezia yeast species may play a role.¹⁴

Genetic and Metabolic Disorders

An array of disorders of keratinization and acantholysis can manifest with distinctive smells that dermatologists frequently encounter. For example, Darier disease, characterized by keratotic papules progressing to crusted plaques, has a signature foul-smelling odor associated with cutaneous bacterial colonization.¹⁵ Similarly, Hailey-Hailey disease, an autosomal-dominant disorder with crusted erosions in skinfold areas, produces a distinct foul smell.¹⁶ Disorders such as pemphigus vulgaris and pemphigus foliaceus emit a peculiar fishy odor that can be helpful in making a diagnosis.¹⁷ Additionally, bullous ichthyosiform erythroderma, keratitis-ichthyosis-deafness syndrome, mal de Meleda, and Papillon-Lefèvre syndrome are all associated with malodor.⁵

Certain metabolic disorders can manifest and present initially with identifiable odors. Trimethylaminuria is a psychologically disabling disease known for its rotting fishy smell due to high amounts of trimethylamine appearing in affected individuals’ sweat, urine, and breath. Previously considered to be very rare, Messenger et al¹⁸ reported the disorder is likely underdiagnosed in those with idiopathic malodor production. Detection and treatment can greatly improve patient quality of life.

Phenylketonuria is an autosomal-recessive inborn error of phenylalanine metabolism that produces a musty body and urine odor as well as other neurologic and dermatologic symptoms.^19,20 Patients can present with eczematous rashes, fair skin, and blue eyes. Phenylacetic acid produces the characteristic odor in the bodily fluids, and the disease is treated with a phenylalanine-free diet.²¹ 

Maple syrup urine disease is a disorder of the oxidative decarboxylation of valine, leucine, and isoleucine (branched-chain amino acids) characterized by urine that smells sweet, resembling maple syrup, in afflicted individuals. The odor also can be present in other bodily secretions, such as sweat. Patients present early in infancy with poor feeding and vomiting as well as neurologic symptoms, eventually leading to intellectual disability. These individuals must avoid the branched-chain amino acids in their diets.²¹ 

Other metabolic storage disorders linked with specific odors are methionine adenosyltransferase deficiency (boiled cabbage), hypermethioninemia (fishy, boiled cabbage), isovaleric acidemia (sweaty feet), methionine malabsorption syndrome (pungent malodor), and dimethylglycine dehydrogenase deficiency (fishy).^5,21,22

In diabetic ketoacidosis, a life-threatening complication of diabetes, the excess of ketone bodies produced causes patients to have a distinct fruity breath and urine odor, as well as fatigue, polyuria, polydipsia, nausea, and vomiting.²² Although patients with type 1 diabetes typically comprise the cohort of patients presenting with diabetic ketoacidosis, patients with type 2 diabetes can exhibit cutaneous manifestations such as infection, xerosis, and inflammatory skin diseases.^23,24 

Organ Dysfunction

A peculiar body odor can be a sign of organ dysfunction. Renal dysfunction may present with both an odor and dermatologic manifestations. Patients with end-stage renal disease can have an ammonialike uremic breath odor as the result of excessive nitrogenous waste products and increased concentrations of urea in their saliva.^4,22 These patients also can exhibit pruritus, xerosis, pigmentation changes, nail changes, other dermatoses, and rarely uremic frost with white urate crystals present on the skin.^25,26 

Liver failure has been associated with an ammonialike musty breath odor termed fetor hepaticus. Shimamoto et al²⁷ reported notably higher levels of breath ammonia levels in patients with hepatic encephalopathy, indicating that excess ammonia is responsible for the odor. Fetor hepaticus has unique characteristics that can permit a diagnosis of liver disease, though it has been reported in cases in which a liver injury could not be identified.²⁸ 

Aging patients typically have a distinctive smell. Haze et al²⁹ analyzed the body odor of patients aged 26 to 75 years and discovered the compound 2-nonenal—an unsaturated aldehyde with a smell described as greasy and grassy—was found only in patients older than 40 years. The researchers’ analysis of skin-surface lipids also revealed that the presence of ω7 unsaturated fatty acids and lipid peroxides increased with age. They concluded that 2-nonenal is generated from the oxidative degradation of ω7 unsaturated fatty acids by lipid peroxides, suggesting that 2-nonenal may be a cause of the odor of old age.²⁹

Cutaneous Malignancies 

Research shows that the profiles of the body’s continuously released VOCs change in the presence of malignancy. Some studies suggest that melanoma may have a unique odor. Willis et al³⁰ reported that after a 13-month training period, a dog was able to correctly identify melanoma and distinguish it from basal cell carcinoma, benign nevi, and healthy skin based on olfaction alone. Additional cases have been reported in which dogs have been able to identify melanoma based on smell, suggesting that canine olfactory detection of melanoma could possibly aid in the diagnosis of skin cancer, which warrants further investigation.^31,32 There is limited evidence on the specific odors of other cutaneous malignancies, such as basal cell carcinoma and squamous cell carcinoma. 

Bacterial superinfection of cutaneous malignancy can secrete pungent odors. An offensive rotting odor has been associated with necrotic malignant ulcers of the vagina. This malodor likely is a result of the formation of putrescine, cadaverine, short-chain fatty acids (isovaleric and butyric acids) and sulfur-containing compounds by bacteria.³³ Recognition of similar smells may aid in management of these infections.

Diagnostic Techniques

Evaluating human skin odor is challenging, as the components of VOCs are complicated and typically found at trace levels. Studies indicate that gas chromatography–mass spectrometry is the most effective way to analyze human odor. This method separates, quantifies, and analyzes VOCs from samples containing odors.³⁴ Gas chromatography–mass spectrometry, however, has limitations, as the time for analysis is lengthy, the equipment is large, and the process is expensive.³ Research supports the usefulness and validity of quantitative gas chromatography–olfactometry to detect odorants and evaluate odor activity of VOCs in various samples.³⁵ With this technique, human assessors act in place of more conventional detectors, such as mass spectrometers. This method has been used to evaluate odorants in human urine with the goal of increasing understanding of metabolization and excretion processes.³⁶ However, gas chromatography–olfactometry typically is used in the analysis of food and drink, and future research should be aimed at applying this method to medicine. 

Zheng et al³ proposed a wearable electronic nose as a tool to identify human odor to emulate the odor recognition of a canine’s nose. They developed a sensor array based on the composites of carbon nanotubes and polymers able to examine and identify odors in the air. Study participants wore the electronic nose on the arm with the sensory array facing the armpits while they walked on a treadmill. Although many issues regarding odor measurement were not addressed in this study, the research suggests further studies are warranted to improve analysis of odor.³

Clinical Cases

Patient 1—Arseculeratne et al³⁷ described a 41-year-old man who presented with a fishy odor that others had noticed since the age of 13 years but that the patient could not smell himself. Based on his presentation, he was worked up for trimethylaminuria and found to have elevated levels of urinary trimethylamine (TMA) with a raised TMA/TMA-oxidase ratio. These findings were consistent with a diagnosis of primary trimethylaminuria, and the patient was referred to a dietician for counseling on foods that contain low amounts of choline and lecithin. Initially his urinary TMA level fell but then rose again, indicating possible relaxation of his diet. He then took a 10-day course of metronidazole, which helped reduce some of the malodor. The authors reported that the most impactful therapy for the patient was being able to discuss the disorder with his friends and family members.³⁷ This case highlighted the importance of confirming the diagnosis and early initiation of dietary and pharmacologic interventions in patients with trimethylaminuria. In patients reporting a persistent fishy body odor, trimethylaminuria should be on the differential.

Patient 2—In 1999, Schissel et al⁶ described a 20-year-old active-duty soldier who presented to the dermatology department with smelly trench foot and tinea pedis. The soldier reported having this malodorous pitted rash for more than 10 years. He also reported occasional interdigital burning and itching and noted no improvement despite using various topical antifungals. Physical examination revealed an “overpowering pungent odor” when the patient removed his shoes. He had many tender, white, and wet plaques with scalloped borders coalescing into shallow pits on the plantar surface of the feet and great toes. Potassium hydroxide preparation of the great toe plaques and interdigital web spaces were positive for fungal elements, and bacterial cultures isolated moderate coagulase-negative staphylococcal and Corynebacterium species. Additionally, fungal cultures identified Acremonium species. The patient was started on clotrimazole cream twice daily, clindamycin solution twice daily, and topical ammonium chloride nightly. Two weeks later, the patient reported resolution of symptoms, including the malodor.⁶ In pitted keratolysis, warm and wet environments within boots or shoes allow for the growth of bacteria and fungi. The extent of the lesions is related to the amount of bacteria within the stratum corneum. The diagnosis often is made based on odor, location, and appearance of the rash alone. The most common organisms implicated as causal agents in the condition are Kytococcus sedentarius, Dermatophilus congolensis, and species of Corynebacterium and Actinomyces. It is thought that these organisms release proteolytic enzymes that degrade the horny layer, releasing a mixture of thiols, thioesters, and sulfides, which cause the pungent odor. Familiarity with the characteristic odor aids in prompt diagnosis and treatment, which will ultimately heal the skin eruption. 

Patient 3—Srivastava et al³² described a 43-year-old woman who presented with a nevus on the back since childhood. She noticed that it had changed and grown over the past few years and reported that her dog would often sniff the lesion and try to scratch and bite the lesion. This reaction from her dog led the patient to seek out evaluation from a dermatologist. The patient had no personal history of skin cancer, bad sunburns, tanning bed use, or use of immunosuppressants. She reported that her father had a history of basal cell carcinoma. Physical examination revealed a 1.2×1.5-cm brown patch with an ulcerated nodule located on the lower aspect of the lesion. The patient underwent a wide local excision and sentinel lymph node biopsy with pathology showing a 4-mm-thick melanoma with positive lymph nodes. She then underwent a right axillary lymphadenectomy and was diagnosed with stage IIIB malignant melanoma. Following the surgery, the patient’s dog would sniff the back and calmly rest his head in her lap. She has not had a recurrence and credits her dog for saving her life.³² Canine olfaction may play a role in detecting skin cancers, as evidenced by this case. Patients and dermatologists should pay attention to the behavior of dogs toward skin lesions. Harnessing this sense into a method to noninvasively screen for melanoma in humans should be further investigated.

Patient 4—Matthews et al³⁸ described a 32-year-old woman who presented to an emergency eye clinic with a white “lump” on the left upper eyelid of 6 months’ duration. Physical examination revealed 3 nodular and cystic lesions oozing a thick yellow-white discharge. Cultures were taken, and the patient was started on chloramphenicol ointment once daily to the skin. At follow-up, the lesions had not changed, and the cultures were negative. The patient reported an intermittent malodorous discharge and noted multiple similar lesions on her body. Excisional biopsy demonstrated histologic findings including dyskeratosis, papillomatosis, and suprabasal acantholysis associated with focal underlying chronic inflammatory infiltrate. She was referred to a dermatologist and was diagnosed with Darier disease. She was started on clobetasone butyrate when necessary and adapalene nocte. Understanding the smell associated with Darier disease in conjunction with the cutaneous findings may aid in earlier diagnosis, improving outcomes for affected patients.³⁸ 

Conclusion

The sense of smell may be an overlooked diagnostic tool that dermatologists innately possess. Odors detected when examining patients should be considered, as these odors may help guide a diagnosis. Early diagnosis and treatment are important in many dermatologic diseases, so it is imperative to consider all diagnostic clues. Although physician olfaction may aid in diagnosis, its utility remains challenging, as there is a lack of consensus and terminology regarding odor in disease. A limitation of training to identify disease-specific odors is the requirement of engaging in often unpleasant odors. Methods to objectively measure odor are expensive and still in the early stages of development. Further research and exploration of olfactory-based diagnostic techniques is warranted to potentially improve dermatologic diagnosis. 

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

THE DIAGNOSIS: Impetigo Herpetiformis

Histopathology revealed epidermal acanthosis and spongiosis with overlying parakeratosis associated with subcorneal and intracorneal neutrophils, papillary dermal edema, and dermal mixed inflammation with neutrophils and eosinophils. Both direct immunofluorescence and periodic acid–Schiff studies were negative. Blood and pustule cultures were sterile and the skin flora were normal. Based on these findings, a diagnosis of impetigo herpetiformis (IH) was made. The condition improved with systemic and topical steroids, supportive care, and an intravenous infusion of infliximab 5 mg/kg. At 3 weeks’ follow-up, the patient demonstrated near-complete resolution and later delivered successfully at 40 weeks’ gestation without complications.

Impetigo herpetiformis, also known as pustular psoriasis of pregnancy, is an exceedingly rare gestational dermatosis that typically manifests in the third trimester and can be life-threatening for both the mother and fetus. The term was first used in 1872 to describe 5 pregnant women with extensive acute pustular eruptions, all in unstable condition; 4 (80%)of the cases resulted in maternal death, and all resulted in fetal death.¹ Impetigo herpetiformis is characterized by pruritic and painful erythematous patches studded at the periphery with subcorneal pustules. Eruptions usually occur in the flexural areas and spread centrifugally, with extension of the lesions peripherally as the center erodes and crusts. Sparing of the face, palms, and soles is expected, and mucosal involvement is rare. Generalized involvement and exfoliation may occur in extreme cases.² While IH typically manifests during the third trimester, it may occur any time throughout pregnancy or immediately postpartum.³ A few cases have been reported in the puerperium.² Common symptoms include fever, chills, malaise, anorexia, nausea, vomiting, diarrhea, and arthralgias. Less common complications include hypoalbuminemia and severe hypocalcemia leading to tetany, seizures, and delirium.^2,3 While maternal mortality is uncommon, fetal mortality often is a more pressing risk and is attributed to placental insufficiency.^3,4 For this reason, early delivery commonly is considered in severe cases.

Whether IH is a separate entity or a variant of pustular psoriasis remains heavily debated. Although the histopathology of IH is identical to pustular psoriasis, the lack of a personal and family history of psoriasis, symptom resolution with delivery, and possible recurrence during successive pregnancies help differentiate IH from generalized pustular psoriasis.^2,5 Earlier onset, diffuse involvement, faster progression, and recurrence in subsequent pregnancies all have been linked to a worse prognosis.⁴

The differential diagnosis for IH includes acute generalized exanthematous pustulosis, pemphigoid gestationis, dermatitis herpetiformis, and subcorneal pustular dermatosis. Acute generalized exanthematous pustulosis is an uncommon severe cutaneous drug reaction characterized by the sudden onset of numerous sterile pustules on erythematous skin within 48 hours of exposure. The most common offending medications include pristinamycin and beta-lactam antibiotics. A high fever, neutrophilic leukocytosis, and hypocalcemia often accompany acute generalized exanthematous pustulosis.⁶ Prompt diagnosis and withdrawal of the offending drug as well as supportive care and symptomatic treatment are crucial for disease management, as systemic symptoms and even organ involvement may occur.⁶

Pemphigoid gestationis, also known as gestational pemphigoid or herpes gestationis, is a rare autoimmune blistering disorder that primarily affects pregnant women. It typically manifests in the second or third trimester or shortly after delivery. Clinically, it manifests as an intensely pruritic polymorphic eruption of urticarial papules and plaques accompanied by vesicles and bullae and often is distributed on the abdomen and extends to other body regions. Although the exact etiology is unknown, pemphigoid gestationis is caused by autoantibodies targeting the BP180 and BP230 hemidesmosomal proteins.⁷ Treatment usually involves systemic corticosteroids and may require additional immunosuppressive therapy. In most cases, patients see resolution within 6 months of delivery.⁷

Dermatitis herpetiformis is a chronic autoimmune blistering skin disorder characterized by intensely pruritic, grouped vesicles and papules, often distributed symmetrically on extensor surfaces such as the elbows, knees, buttocks, and back. It is closely associated with celiac disease and is triggered by gluten ingestion in genetically predisposed individuals with human leukocyte antigen DQ2 and DQ8 haplotypes. Dermatitis herpetiformis is caused by deposition of IgA antibodies that target tissue transglutaminase 3 at the dermal papillae, leading to inflammation and blister formation. ⁸ Treatment typically involves a gluten-free diet and medications such as dapsone to alleviate symptoms and prevent recurrence.

Subcorneal pustular dermatosis, also known as Sneddon-Wilkinson disease, is a rare chronic relapsing pustular dermatosis characterized by sterile superficial pustules arranged in annular or circinate patterns on erythematous plaques. It predominantly affects middleaged women and often is associated with underlying conditions such as IgA gammopathy or monoclonal gammopathy of undetermined significance. The pathogenesis remains unclear, but immune dysregulation is thought to play a role. Some authors still question whether subcorneal pustular dermatosis is a distinct entity from pustular psoriasis.^4,5,12 Dapsone is the preferred first-line treatment, with adjunct therapies including topical or systemic corticosteroids, other immunosuppressive agents, tumor necrosis factor inhibitors, and UV light therapy.⁹

Definitive management of IH is achieved through early delivery; however, systemic corticosteroids often are used in varying doses to control the disease and to extend the pregnancy period closer to term or until delivery is considered viable. Additional therapies that can be considered include infliximab, cyclosporine, and topical corticosteroids, in conjunction with fluid and electrolyte maintenance.^2,4,10 If symptoms persist despite supportive care and pharmacologic intervention, induction of labor or termination of pregnancy may be indicated. In nonbreastfeeding postpartum mothers with persistent disease, therapies commonly used in generalized pustular psoriasis may be given.¹¹

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

Fluoroscopy is an imaging technique that allows for real-time visualization of internal structures in the body using continuous radiography beams. More than 1 million fluoroscopy-guided procedures are performed annually in the United States.¹ Utilization of these procedures continues to increase, and so does the probability of related complications, as prolonged exposure to ionizing radiation can cause skin injuries.² Fortunately, the incidence of radiation-induced skin injuries compared with the total number of fluoroscopic procedures performed remains small,² although one study suggested the incidence may be as high as 8.9% in at-risk populations.³

Radiation dermatitis is well recognized in dermatology as a complication of oncologic management; however, radiation dermatitis as a complication of fluoroscopic procedures is underrecognized.⁴ Fluoroscopy-induced radiation dermatitis can be categorized as acute, subacute, or chronic.⁵ Common fluoroscopic procedures that have been associated with fluoroscopy-induced radiation dermatitis include interventional cardiac procedures, neurovascular procedures, transjugular intrahepatic portosystemic shunt procedures, and endovascular abdominal aortic aneurysm repairs.^6,7

Patients with fluoroscopy-induced radiation dermatitis, particularly fluoroscopy-induced chronic radiation dermatitis (FICRD), can present to dermatology up to several years after the initial fluoroscopy procedure with no awareness of the association between the procedure and their skin findings. This presents a diagnostic challenge, and FICRD often is overlooked.^5,8-10

We conducted a literature search of PubMed articles indexed for MEDLINE using the search terms ­fluoroscopy and dermatitis. In this reappraisal, we will provide a comprehensive overview of fluoroscopy-induced ­radiation dermatitis with an emphasis on FICRD, covering its clinical manifestations, pathophysiology, risk factors, ­differential diagnosis, histology, and management. The aim of this review is to highlight the salient features and mimickers of FICRD and inform readers how to approach suspected cases, leading to accurate diagnosis and ­effective management.

Pathophysiology 

Fluoroscopy-induced radiation dermatitis is the result of dose-dependent radiation-induced tissue damage. As the peak skin dosage (PSD) of radiation increases over the course of a procedure or multiple procedures, the severity of skin injury predictably increases. During fluoroscopic procedures, the standard irradiation dosage ranges from 0.02 Gy/min to 0.05 Gy/min.¹¹ Transient skin changes may start to be seen around 2 Gy of cumulative exposure. Fluoroscopic procedures typically range in duration from 60 to 120 minutes; however, complex cases may exceed that. Additionally, multiple procedures performed within shorter intervals can result in greater PSD accumulation. Shorter intervals between procedures do not allow enough time for damage repair from the previous ­procedure and can result in further severe damage when the skin is re-exposed to radiation.² The American College of Radiology recommends medical follow-up after 10 Gy of cumulative exposure, while cumulative exposure above 15 Gy within a 6- to 12-month period is defined as a sentinel event, according to The Joint Commission.^12-14

Depending on the patient’s total radiation dosage during one or more procedures, the result of the tissue damage manifests differently at varying times: early skin changes are categorized as fluoroscopy-induced acute radiation dermatitis, and late skin changes are categorized as FICRD (Table 1).

Clinical Manifestations

Acute radiation dermatitis from fluoroscopic procedures manifests within hours to days up to 90 days following radiation exposure and can be characterized by erythema with blistering, desquamation, epilation, pigmentation changes, and even necrosis if the accumulated dosage exceeds 15 Gy.¹⁵ Chronic radiation dermatitis (which as related to fluoroscopic procedures is termed FICRD) has a longer onset of weeks to years and is clinically characterized by telangiectasias, permanent erythema, dermal atrophy, or ulcerations. Clinically, subacute radiation dermatitis shares features of both acute and chronic radiation dermatitis; therefore, it is differentiated based on its histologic features.^5,16

Although fluoroscopy-induced acute radiation dermatitis (Table 1) may precede FICRD, acute manifestations of fluoroscopy-related dermatitis can be subtle and often manifest in areas not easily visualized. Because referrals to dermatologists for full-skin examinations after fluoroscopy procedures are not standard, patients may not be aware of the association between these procedures and the development of skin lesions. Nonetheless, some patients may report a history of skin changes such as redness days or weeks after a fluoroscopic procedure with accompanying pain and pruritus limited to the fluoroscopy-exposed region, which tend to self-resolve.¹⁷ The risk for FICRD is thought to increase if a history of fluoroscopy-induced acute radiation dermatitis is present.¹⁸

The location of the skin findings correlates to the area exposed to prolonged radiation during the procedure(s). The most common areas include the scapular and subscapular regions, the right lateral trunk inferior to the axilla, the mid back, and the right anterolateral chest.^16,19,20 These regions are associated with more complex (eg, cardiac) procedures that have been reported to lead to prolonged radiation exposure. The skin findings in FICRD are described as geometric, corresponding to the squarish or rectangular radiography beam that is directed at the patient. Additionally, radiography beams spread outward as they travel in space; therefore, skin injuries are common at the region more distal to the path of origination of the beam.^21-23 Subsequently, a geometric, dyspigmented, indurated or atrophic plaque with telangiectasias and erosions or ulcerations with progressive worsening is a common manifestation of FICRD.^5,16,23 Patients also commonly present with pruritus or severe pain associated with the lesion.^24,25  

Dermatologic Manifestations of FICRD

Skin responses seen weeks to years after a fluoroscopic procedure and typically after cumulative radiation exposure of 10 Gy or greater are categorized as FICRD (Table 2). These changes also can be clinically graded based on the Radiation Therapy Oncology Group classification of radiation dermatitis (Tables 3 and 4).²⁶ Chronic changes in the skin largely result from remodeling of the vasculature and the subcutaneous tissue over time. Unlike acute changes, chronic changes typically persist and continue to worsen.²⁷

Telangiectasias—Anywhere from months to 1 year after exposure to 10 Gy of radiation, proliferation of atypical superficial vessels in the dermis can be seen, typically manifesting as telangiectasias on physical examination. Telangiectasias can increase with time and can even exhibit a dose-dependent relationship to the radiation exposure.²⁸

Atrophy—Atrophic-appearing skin after radiation exposure is the result of direct injury to both the epidermis and fibroblasts in the dermis. The destruction of keratinocytes leads to a thin epidermis, and destruction of dermal fibroblasts causes insufficient collagen production.²⁹ Clinically, this process manifests as an atrophic plaque that can be seen 12 weeks to 1 year after the procedure. 

Fibrosis—Approximately 1 year after the exposure, the initial damage can lead to disruption of molecular pathways, causing fibrosis. Transforming growth factor (TGF) β1 is the main factor involved.²⁹ Damage to the endothelial cells results in increased TGF-β1 levels, which causes increased stimulation of remaining atypical fibroblasts and thus increased irregular collagen deposition.³⁰ Further adding to this knowledge, Wei et al³¹ recently proposed that damage to the epidermal keratinocytes leads to disruption of yes-associated protein 1, which is a protective factor released from keratinocytes that regulates the dermal fibroblasts. However, extensive damage to the keratinocytes can lead to lower yes-associated protein 1 levels and its downstream activity, leading to increased levels of TGF-β1 and fibroblast activity.³¹ Clinically, this fibrotic stage is seen as indurated plaques in patients. 

Necrosis—There are 2 forms of necrosis that can be seen. Ischemic dermal necrosis typically occurs in the acute phase after 10 weeks and approximately 18 Gy of cumulative exposure. It results from substantial skin damage, including microvascular damage and reduction in dermal capillaries, leading to ischemia of the tissue.² Late dermal necrosis is the process seen in the chronic stage of FICRD and radiation dermatitis not related to ­fluoroscopy. It results from the inability of the fibrotic dermis to vascularly support the epidermis above it.² It can be seen anywhere from 1 to 4 years after the procedure. This stage clinically manifests as worsening ulcerations with major pain and increased risk for secondary infections.¹⁶ 

Dyspigmentation—Dyspigmentation at the site of the radiation exposure can be seen acutely and chronically. Dosage above 15 to 18 Gy can lead to destruction of melanocytes, which can cause hypopigmentation in exposed areas. However, melanocytes are relatively resistant to radiation; therefore, dosages below the threshold of destruction of 15 to 18 Gy can cause melanocytic hyperactivity leading to hyperpigmentation.³² Hence, pigmentary changes can vary greatly. Classically, a central area of hypopigmentation with surrounding hyperpigmentation is seen.

Histology 

Histologic appearance of radiation dermatitis varies depending on its stage. Acute radiation dermatitis primarily demonstrates superficial dermal edema, damage to the basal cell layer, small vessel dilation with thrombi, and hemorrhage along with a sparse inflammatory cell infiltrate.³³ Histology typically is the only way to characterize subacute radiation dermatitis.⁵ Lichenoid tissue reaction is its characteristic feature. Mononuclear cells are found adjected to necrotic keratinocytes along with prominent vacuolization of the basal cell layer.³³

The key histologic features of chronic radiation dermatitis include epidermal atrophy, hyperkeratosis, telangiectasias, loss of adnexal structures, and dermal fibrosis along with sparse atypical stellate fibroblasts.³⁴ However, clinical context of fluoroscopic exposure is required for the dermatopathologist to differentiate chronic radiation dermatitis from its histologic differential of morphea and lichen sclerosus. In a cross-sectional study, only 1 of 6 cases (16.7%) was correctly diagnosed as chronic radiation dermatitis in the absence of correlating clinical history.³⁵ 

Risk Factors for FICRD 

Since the diagnosis of FICRD can be a clinical challenge, understanding the risk factors can be helpful. The general likelihood of developing FICRD is related to the duration, frequency, interval, intensity, and area of radiation exposure. Procedures exceeding the normal duration of 60 to 120 minutes have been well documented as a substantial risk factor for radiation dermatitis and FICRD.^36-38 The risk tends to be higher in longer procedures because they result in more radiation exposure and higher accumulated PSD. Obesity (ie, body mass index >26) is the major risk factor that has been associated with longer procedure times, as higher radiation dosages are necessary to penetrate the body of a larger patient and a larger skin surface area is exposed.^37-39

Other risk factors associated with FICRD relate to how prone a patient is to radiation-induced DNA damage. Older patients are at higher risk due to lower intrinsic ability of the tissue to repair itself.¹¹ Patients with a history of connective tissue diseases—particularly lupus, scleroderma, and mixed connective tissue disease—are at an increased risk.⁴⁰ Furthermore, patients with genetic disorders that impair DNA repair are more susceptible to radiation-induced DNA damage; therefore, patients with ataxia-telangiectasia, xeroderma pigmentosum, Fanconi anemia, and hereditary nevoid basal cell carcinoma are at higher risk for FICRD.³⁹ Similarly, medications that can affect DNA repair also have been shown to be risk factors. These medications include chemotherapeutic agents such as actinomycin D, cyclophosphamide, doxorubicin, methotrexate, and 5-fluorouracil.^2,39 Diabetes, hyperthyroidism, and tobacco use also have been shown to increase a patient’s risk for FICRD.³⁹ It also is reasonable to believe that patients with defects in fibroblasts or with elastin or collagen disorders (eg, Ehlers-Danlos syndrome) would be at higher risk, but there are no known studies highlighting the association in the literature.

Differential Diagnosis of FICRD 

Acute allergic or irritant contact dermatitis manifests with a localized area of erythematous skin accompanied by pruritus.⁴¹ Patients with FICRD can present with a localized area of erythema and hyperpigmentation with minimal atrophy. The lesion may accompany substantial pruritus, which can favor the more common diagnosis of contact dermatitis.^35,42,43

Fixed-drug eruption manifests as a well-defined, hyperpigmented plaque in a fixed location that occurs upon ingestion of a drug.⁴⁴ Fluoroscopy-induced chronic radiation dermatitis lesions are well demarcated and geometrically shaped and therefore can mimic lesions seen in fixed-drug eruptions.⁴⁵ Additionally, the patient population undergoing fluoroscopic procedures tends to have major comorbidities requiring multiple medications.⁴

Decubitus ulcers are a result of vascular compromise to an area of skin due to constant pressure and are most commonly seen in the sacral region of patients with ­obesity.⁴⁶ Ulcerated FICRD lesions can manifest on the lower midback. These lesions can be seen after endovascular repair of abdominal aortic aneurysm or prostatic artery embolization.^20,21 The location of these lesions can mimic decubitus ulcers if fluoroscopic history is unknown. As mentioned, obesity also increases the risk for FICRD. 

Morphea can manifest as a localized area of induration and hyperpigmentation of the skin.⁴⁷ When FICRD has progressed to dermal fibrosis, patients can present with indurated plaques without ulcerations, which can be hard to differentiate from morphea.^16,48 However, the presence of ulcerations or hyperkeratosis can differentiate morphea from FICRD.¹⁶

Ultimately, it is the location of FICRD lesions that remains the biggest diagnostic clue. Any suspicious lesion present on the scapular or subscapular areas, anterolateral chest, and/or mid back should prompt an investigation into recent or remote history of fluoroscopic procedures. 

Management of FICRD

Diagnosis of FICRD should be made clinically based on the history and physical examination whenever possible, since a biopsy is not recommended.³⁵ Wound healing in FICRD is delayed, and biopsies can lead to ulcerations or secondary infections.¹⁷ Therefore, it is important to remain suspicious for FICRD. Management of FICRD should correspond to the clinical findings outlined by a recent Delphi consensus survey.⁴⁹ Regardless, the core of FICRD management framework should always include good hygiene, maintenance of skin hydration to improve epithelialization, and sufficient photoprotection.^49,50

Among the first signs of FICRD are telangiectasias. Although asymptomatic, their appearance can be distressing for patients. Pulsed dye laser therapy is a first-line option that has been studied and has shown clinical efficacy for treatment of telangiectasias and vascular changes in patients with FICRD.^49,51

If patients develop fibrotic changes, treatment options are limited. Fibrosis is hard to reverse, and the management approach is limited to symptomatic relief. Mechanical and deep-friction massages have been shown to be effective at reducing skin induration in patients.⁵² Fractional ablative lasers also may be utilized for skin contractures, especially if range of motion is affected.^53,54 Although it comes with its own challenges, autologous fat grafting has shown promise in reducing postradiation fibrosis and inducing angiogenesis in tissue.⁵⁵ Oral pentoxifylline also has shown mild efficacy, as it may be able to suppress TGF-β1 levels.⁵³ However, prevention of fibrotic changes may be the most important. Wei et al³¹ suggested that low-dose oral prednisolone at 5 mg twice daily for 3 weeks might be an option to prevent the progression of skin changes and even reverse fibrosis to an extent; however, further evidence regarding its efficacy still is necessary. Additionally, no evidence was identified to support the use of topical corticosteroids for fibrotic changes seen in FICRD.⁵⁶

Patients with FICRD or even acute radiation dermatitis after fluoroscopy tend to develop superficial ulcerations from minor traumas. Good wound hygiene, antiseptic care, and absorbent dressings, such as hydrogel and hydrocolloid, may be sufficient for treating these wounds, as seen in the Figure.^42,48 However, once patients develop refractory ulcerations or necrosis, treatment options are then limited to surgical removal with a flap or graft.^5,33,42,45
 

Risk for basal cell carcinomas and squamous cell carcinomas is higher in patients with radiation exposure; however, the exact risk from fluoroscopic procedures is unknown. One study demonstrated an increased risk of 6.9% in development of skin cancer after a median radiation exposure of 15.5 Gy and a mean latency period of 38.3 years,⁵⁷ and in another retrospective study, the risk was higher in Fitzpatrick skin types I and II.⁵⁸ Unlike the development of radiodermatitis itself, which shows a dose-dependent response, development of skin cancers follows a stochastic pattern (not dose dependent).⁵⁹ Therefore, it is important to identify these high-risk patients and establish follow-up.

Conclusion

Fluoroscopy-induced chronic radiation dermatitis can be a diagnostic challenge, as skin changes may not be readily associated with the procedure by patients. Therefore, any lesion with a geometric shape and accompanying chronic radiation dermatitis features located on the scapular or subscapular areas, anterolateral chest, and midback should prompt an investigation into history of fluoroscopic procedures. Treatment of chronic skin changes in FICRD depends on the clinical manifestations. Good hygiene, skin hydration, and sufficient photoprotection are crucial. Finally, long-term monitoring with skin examinations is important to assess for the development of skin cancers in the treated area.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.

THE DIAGNOSIS: Idiopathic Facial Aseptic Granuloma

Histopathology showed a ruptured follicle, perifollicular granulomatous inflammation, and admixed multinucleated giant cells in the superficial dermis. The deeper tissue exhibited edema, histiocytic/granulomatous inflammation forming ill-defined loose granulomas, and a single neutrophilic microabscess (Figure). Stains for periodic acid-Schiff with diastase and acid-fast bacillus were negative for microorganisms. The clinical examination and pathology findings supported a diagnosis of idiopathic facial aseptic granuloma (IFAG).

First reported in 1999, IFAG was described using the French term pyodermite froide du visage, which translates to “cold pyoderma of the face”; however, it was renamed to represent its granulomatous characteristics and noninfectious etiology.¹ The pathogenesis of IFAG is unknown, but the leading hypothesis is that it may be a type of childhood granulomatous rosacea, given its association with relapsing chalazions, papulopustular eruptions on the face, and facial flushing.² Other hypotheses are that IFAG is idiopathic or a granulomatous response to an insect bite, minor trauma, or embryologic remnant.³

A rare condition arising in early childhood, IFAG manifests as a single or multiple, painless, erythematous or violaceous nodule(s) on the face, most often on the cheeks or eyelids.⁴ A thorough history and clinical examination often suffice for diagnosis. Dermoscopy may reveal white perifollicular halos and follicular plugs on an erythematous base with linear vessels.⁴ If diagnostic tests are performed, there are notable characteristic findings: ultrasonography often shows a well-circumscribed, hypoechoic, ovoid dermal lesion without calcifications. Bacterial, fungal, and mycobacterial cultures commonly are negative.⁴ On biopsy, histopathology may reveal granulomatous inflammation in the superficial and deep dermis, multinucleated giant cells, and surrounding lymphocytic, neutrophilic, and eosinophilic infiltration with no calcium deposits.^3,5,6 Histopathology findings for IFAG and rosacea lesions are similar; both may demonstrate folliculitis, perifollicular granulomas, and admixed lymphohistiocytic inflammation.⁷

Differentiating IFAG from other dermatologic lesions can be challenging, as the differential includes benign neoplasms (eg, dermoid cyst, chalazion, pilomatricoma, xanthoma, xanthogranuloma²) and infectious etiologies such as bacterial pyoderma and mycobacterial, fungal, and parasitic infections (eg, cutaneous leishmaniasis). Pilomatricomas, although often seen on the face or extremities in young girls, more often are well circumscribed and located in the dermis. Ultrasonography of a pilomatricoma classically shows variable foci of calcification. Xanthoma and xanthogranuloma also were considered in our case since the lesion was subtly yellowish on examination. Similar to IFAG, these conditions may manifest as single or multiple lesions. Abnormalities in the patient’s blood lipid panel or family history may be needed to diagnose xanthoma. Biopsy of a juvenile xanthogranuloma would exhibit a dense dermal nodular proliferation of histiocytic cells with a smaller number of admixed lymphocytes, neutrophils, and eosinophils, in contrast to the multiple smaller loose epithelioid granulomas seen in IFAG. Additional diagnoses in the differential for IFAG include pyogenic granuloma, Spitz nevus, nodulocystic infantile acne, granulomatous rosacea, and hemangioma.^1,3,9 In particular, granulomatous rosacea is challenging to differentiate from IFAG given the overlapping clinical findings. Multiple lesions, the presence of papules and pustules, and associated rosacea symptoms such as flushing suggest a diagnosis of granulomatous rosacea over IFAG.²

The prognosis for IFAG is excellent; most lesions self-resolve without treatment or procedural intervention within 1 year without scarring or relapse.³ Topical and oral antibiotic treatments such as metronidazole 0.75% gel or cream, oral erythromycin, oral clarithromycin, and doxycycline (in patients older than 8 years) have been used to treat IFAG with variable clinic responses.^2,3,6,8 Persistent IFAG has been treated with surgical excision.³ Our patient was treated with a combination of gentamicin ointment 0.3% and tacrolimus ointment 0.3% and experienced approximately 50% improvement in the first month of treatment.

THE DIAGNOSIS: Rhabdomyomatous Mesenchymal Hamartoma

Histopathologic examination of the excised tissue revealed haphazardly arranged bundles of mature striated muscle within the dermis and subcutaneous tissue admixed with adipose tissue, adnexal structures, blood vessels, and nerves. The presence of the lesion since birth, midline clinical presentation, and histologic findings were consistent with a diagnosis of rhabdomyomatous mesenchymal hamartoma (RMH).

Also referred to as striated muscle hamartoma, RMH is a rare benign lesion thought to have embryonic origin due to its midline presentation.¹ The etiology of RMH is unknown but is hypothesized to be due to abnormal migration or growth of embryonic mesenchymal tissue. Rhabdomyomatous mesenchymal hamartoma typically manifests in infancy or early childhood as a solitary midline papule on the head or neck, although there have been rare reports of development in adulthood.^2-4 Lesions often are polypoid or exophytic but may manifest as smooth papules or subcutaneous nodules.² Although benign, RMH may be associated with other congenital abnormalities and conditions, such as Delleman syndrome, which is caused by a sporadic genetic abnormality and results in defects of the eye, central nervous system, and skin.⁵ Treatment for RMH is not needed, but surgical excision for cosmetic purposes can be performed with low risk for recurrence. Histologically, RMH demonstrates a normal epidermis overlying disorganized bundles of skeletal muscle accompanied by varying amounts of other mature dermal and subcutaneous tissues including nerves, blood vessels, adipose tissue, and other adnexal structures.^2,6 Myoglobin and desmin are positive within the skeletal muscle bundles.⁷

Fibrous hamartoma of infancy (FHI) often manifests as a movable, ill-defined nodule within the subcutaneous tissue. While also occurring in young children—typically within the first 2 years of life—FHI primarily is found on the upper arms, back, and axillae, in contrast to FHI.⁸ The classic histopathologic presentation of FHI consists of a triphasic morphology consisting of undifferentiated mesenchymal cells and dense fibroblastic/myofibroblastic tissue with mature adipose tissue woven throughout in islands (Figure 1).⁹ Skeletal muscle is not a component of this tumor.

Neurofibromas also may manifest clinically as papules or nodules and arise from the peripheral nerve sheath. There are 3 major subtypes of neurofibromas—localized, diffuse, and plexiform—with the last being strongly associated with neurofibromatosis type 1.¹⁰ The plexiform type has a rare risk for malignant transformation. The typical histopathologic finding of a localized cutaneous neurofibroma is a dermal proliferation of spindle cells with wavy nuclei within a variably myxoid stroma (Figure 2).¹¹ Interspersed mast cells also can be seen. A plexiform neurofibroma typically involves multiple nerve fascicles and comprises multinodular or tortuous bundles of cytologically bland spindle cells. Compared to RMH, skeletal muscle is not a component of this tumor.

Nevus lipomatosus superficialis is a benign hamartoma that can manifest as a pedunculated or exophytic papule. The lesions may be solitary or multiple and, unlike RMH, are most common on the buttocks, upper thighs, and trunk.¹² The histopathologic features of nevus lipomatosus superficialis include clusters of mature adipose tissue in the superficial dermis admixed with collagen fibers and variably increased vasculature (Figure 3).¹³ Nevus lipomatosus superficialis does not contain skeletal muscle within the tumor in comparison to RMH.

It is important to distinguish rhabdomyosarcoma (RMS) from RMH, as it is associated with increased mortality and morbidity. Rhabdomyosarcoma is the most common soft-tissue sarcoma in children and is derived from mesenchyme with variable degrees of skeletal muscle differentiation.¹⁴ Due to its mesenchymal origin, these tumors can manifest in a variety of places but most commonly on the head and neck and in the genital region.¹⁵ The most common subtype is embryonal rhabdomyosarcoma. Histologically, embryonal RMS shows a moderately cellular tumor composed of sheets of spindle-shaped or round cells with scant or eosinophilic cytoplasm (Figure 4). The absence of genetic translocation in the paired box-forkhead box protein 01 (PAX-FOXO1) gene helps distinguish it from solid alveolar RMS, the second most common and more aggressive subtype.¹² Positive immunohistochemical staining for desmin, myoblast determination protein 1 (MyoD1), and myogenin supports myogenic differentiation.¹⁴

THE DIAGNOSIS: Rhabdomyomatous Mesenchymal Hamartoma

Histopathologic examination of the excised tissue revealed haphazardly arranged bundles of mature striated muscle within the dermis and subcutaneous tissue admixed with adipose tissue, adnexal structures, blood vessels, and nerves. The presence of the lesion since birth, midline clinical presentation, and histologic findings were consistent with a diagnosis of rhabdomyomatous mesenchymal hamartoma (RMH).

Also referred to as striated muscle hamartoma, RMH is a rare benign lesion thought to have embryonic origin due to its midline presentation.¹ The etiology of RMH is unknown but is hypothesized to be due to abnormal migration or growth of embryonic mesenchymal tissue. Rhabdomyomatous mesenchymal hamartoma typically manifests in infancy or early childhood as a solitary midline papule on the head or neck, although there have been rare reports of development in adulthood.^2-4 Lesions often are polypoid or exophytic but may manifest as smooth papules or subcutaneous nodules.² Although benign, RMH may be associated with other congenital abnormalities and conditions, such as Delleman syndrome, which is caused by a sporadic genetic abnormality and results in defects of the eye, central nervous system, and skin.⁵ Treatment for RMH is not needed, but surgical excision for cosmetic purposes can be performed with low risk for recurrence. Histologically, RMH demonstrates a normal epidermis overlying disorganized bundles of skeletal muscle accompanied by varying amounts of other mature dermal and subcutaneous tissues including nerves, blood vessels, adipose tissue, and other adnexal structures.^2,6 Myoglobin and desmin are positive within the skeletal muscle bundles.⁷

Fibrous hamartoma of infancy (FHI) often manifests as a movable, ill-defined nodule within the subcutaneous tissue. While also occurring in young children—typically within the first 2 years of life—FHI primarily is found on the upper arms, back, and axillae, in contrast to FHI.⁸ The classic histopathologic presentation of FHI consists of a triphasic morphology consisting of undifferentiated mesenchymal cells and dense fibroblastic/myofibroblastic tissue with mature adipose tissue woven throughout in islands (Figure 1).⁹ Skeletal muscle is not a component of this tumor.

Neurofibromas also may manifest clinically as papules or nodules and arise from the peripheral nerve sheath. There are 3 major subtypes of neurofibromas—localized, diffuse, and plexiform—with the last being strongly associated with neurofibromatosis type 1.¹⁰ The plexiform type has a rare risk for malignant transformation. The typical histopathologic finding of a localized cutaneous neurofibroma is a dermal proliferation of spindle cells with wavy nuclei within a variably myxoid stroma (Figure 2).¹¹ Interspersed mast cells also can be seen. A plexiform neurofibroma typically involves multiple nerve fascicles and comprises multinodular or tortuous bundles of cytologically bland spindle cells. Compared to RMH, skeletal muscle is not a component of this tumor.

Nevus lipomatosus superficialis is a benign hamartoma that can manifest as a pedunculated or exophytic papule. The lesions may be solitary or multiple and, unlike RMH, are most common on the buttocks, upper thighs, and trunk.¹² The histopathologic features of nevus lipomatosus superficialis include clusters of mature adipose tissue in the superficial dermis admixed with collagen fibers and variably increased vasculature (Figure 3).¹³ Nevus lipomatosus superficialis does not contain skeletal muscle within the tumor in comparison to RMH.

It is important to distinguish rhabdomyosarcoma (RMS) from RMH, as it is associated with increased mortality and morbidity. Rhabdomyosarcoma is the most common soft-tissue sarcoma in children and is derived from mesenchyme with variable degrees of skeletal muscle differentiation.¹⁴ Due to its mesenchymal origin, these tumors can manifest in a variety of places but most commonly on the head and neck and in the genital region.¹⁵ The most common subtype is embryonal rhabdomyosarcoma. Histologically, embryonal RMS shows a moderately cellular tumor composed of sheets of spindle-shaped or round cells with scant or eosinophilic cytoplasm (Figure 4). The absence of genetic translocation in the paired box-forkhead box protein 01 (PAX-FOXO1) gene helps distinguish it from solid alveolar RMS, the second most common and more aggressive subtype.¹² Positive immunohistochemical staining for desmin, myoblast determination protein 1 (MyoD1), and myogenin supports myogenic differentiation.¹⁴

THE DIAGNOSIS: Rhabdomyomatous Mesenchymal Hamartoma

Histopathologic examination of the excised tissue revealed haphazardly arranged bundles of mature striated muscle within the dermis and subcutaneous tissue admixed with adipose tissue, adnexal structures, blood vessels, and nerves. The presence of the lesion since birth, midline clinical presentation, and histologic findings were consistent with a diagnosis of rhabdomyomatous mesenchymal hamartoma (RMH).

Also referred to as striated muscle hamartoma, RMH is a rare benign lesion thought to have embryonic origin due to its midline presentation.¹ The etiology of RMH is unknown but is hypothesized to be due to abnormal migration or growth of embryonic mesenchymal tissue. Rhabdomyomatous mesenchymal hamartoma typically manifests in infancy or early childhood as a solitary midline papule on the head or neck, although there have been rare reports of development in adulthood.^2-4 Lesions often are polypoid or exophytic but may manifest as smooth papules or subcutaneous nodules.² Although benign, RMH may be associated with other congenital abnormalities and conditions, such as Delleman syndrome, which is caused by a sporadic genetic abnormality and results in defects of the eye, central nervous system, and skin.⁵ Treatment for RMH is not needed, but surgical excision for cosmetic purposes can be performed with low risk for recurrence. Histologically, RMH demonstrates a normal epidermis overlying disorganized bundles of skeletal muscle accompanied by varying amounts of other mature dermal and subcutaneous tissues including nerves, blood vessels, adipose tissue, and other adnexal structures.^2,6 Myoglobin and desmin are positive within the skeletal muscle bundles.⁷

Fibrous hamartoma of infancy (FHI) often manifests as a movable, ill-defined nodule within the subcutaneous tissue. While also occurring in young children—typically within the first 2 years of life—FHI primarily is found on the upper arms, back, and axillae, in contrast to FHI.⁸ The classic histopathologic presentation of FHI consists of a triphasic morphology consisting of undifferentiated mesenchymal cells and dense fibroblastic/myofibroblastic tissue with mature adipose tissue woven throughout in islands (Figure 1).⁹ Skeletal muscle is not a component of this tumor.

Neurofibromas also may manifest clinically as papules or nodules and arise from the peripheral nerve sheath. There are 3 major subtypes of neurofibromas—localized, diffuse, and plexiform—with the last being strongly associated with neurofibromatosis type 1.¹⁰ The plexiform type has a rare risk for malignant transformation. The typical histopathologic finding of a localized cutaneous neurofibroma is a dermal proliferation of spindle cells with wavy nuclei within a variably myxoid stroma (Figure 2).¹¹ Interspersed mast cells also can be seen. A plexiform neurofibroma typically involves multiple nerve fascicles and comprises multinodular or tortuous bundles of cytologically bland spindle cells. Compared to RMH, skeletal muscle is not a component of this tumor.

Nevus lipomatosus superficialis is a benign hamartoma that can manifest as a pedunculated or exophytic papule. The lesions may be solitary or multiple and, unlike RMH, are most common on the buttocks, upper thighs, and trunk.¹² The histopathologic features of nevus lipomatosus superficialis include clusters of mature adipose tissue in the superficial dermis admixed with collagen fibers and variably increased vasculature (Figure 3).¹³ Nevus lipomatosus superficialis does not contain skeletal muscle within the tumor in comparison to RMH.

It is important to distinguish rhabdomyosarcoma (RMS) from RMH, as it is associated with increased mortality and morbidity. Rhabdomyosarcoma is the most common soft-tissue sarcoma in children and is derived from mesenchyme with variable degrees of skeletal muscle differentiation.¹⁴ Due to its mesenchymal origin, these tumors can manifest in a variety of places but most commonly on the head and neck and in the genital region.¹⁵ The most common subtype is embryonal rhabdomyosarcoma. Histologically, embryonal RMS shows a moderately cellular tumor composed of sheets of spindle-shaped or round cells with scant or eosinophilic cytoplasm (Figure 4). The absence of genetic translocation in the paired box-forkhead box protein 01 (PAX-FOXO1) gene helps distinguish it from solid alveolar RMS, the second most common and more aggressive subtype.¹² Positive immunohistochemical staining for desmin, myoblast determination protein 1 (MyoD1), and myogenin supports myogenic differentiation.¹⁴

Cosmetic laser procedures as well as energy-based fat reduction and body-contouring devices are increasingly popular among individuals with skin of color (SOC). Innovations in cosmetic devices and procedures tailored for SOC have allowed for the optimization of outcomes in this patient population. In this article, SOC is defined as darker skin types, including Fitzpatrick skin types (FSTs) IV to VI and ethnic backgrounds such as LatinX, African American, Southeast Asian, Native American, Pacific Islander, Middle Eastern, Asian, and African. Indications for laser treatment include dermatosis papulosa nigrans (DPN), acne scars, skin rejuvenation, and hyperpigmentation. There currently are 6 procedures for nonsurgical fat reduction that are approved by the US Food and Drug Administration (FDA): high-frequency focused ultrasound, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring (Supplementary Table S1).¹

In this review, our initial focus is cosmetic laser ­procedures, encompassing FDA-cleared indications along with the associated risks and benefits in SOC populations. Subsequently, we delve into the realms of energy-based fat reduction and body contouring, offering a comprehensive overview of these noninvasive therapies and addressing considerations for efficacy and safety in these patients.

Dermatosis Papulosa Nigra

In patients with SOC, scissor excision, curettage, or electrodesiccation are the mainstay treatments for removal of DPN (Figure 1). Curettage and electrodesiccation can cause temporary postinflammatory hyperpigmentation (PIH) in these populations, while cryotherapy is not a preferred method in patients with SOC due to the possibility of cryotherapy-induced depigmentation. In a 14-patient split-face study comparing the 532-nm potassium titanyl phosphate (KTP) laser vs electrodesiccation in FSTs IV to VI, the KTP-treated side showed an improvement rate of 96%, while the electrodesiccation side showed an improvement rate of 79%. There was a statistically significant favorable experience for KTP with regard to pain tolerability (P=.002).² Complete resolution of lesions may be seen after 3 to 4 sessions at 4-week intervals. Additionally, the 1064-nm Nd:YAG laser was assessed for treatment of DPN in 2 patients, with 70% to 90% of lesions resolved after a single treatment with no complications.³

Most dermatologists still rely on curettage and electrodesiccation instead of laser therapy to remove DPNs in patients with SOC. The use of the Nd:YAG laser is promising yet expensive for the provider both to purchase and maintain. Electrodesiccation has been used by dermatology practices for decades and can be used without permanent discoloration. To minimize the risk for PIH, we recommend application of a healing ointment such as petroleum jelly or aloe vera gel to the treated lesions as well as lightening agents for PIH and daily use of sunscreen. Overall, providers do not need to purchase an expensive laser device for DPN removal.

Acne Scars

The invention of fractional technology in the early 2000s and its favorable safety profile have changed how dermatologists treat scarring in patients with SOC.^4,5 In fact, nonablative fractional (NAF) resurfacing is a preferred treatment modality for management of acne scars in patients with SOC.⁶ In one study of the 1550-nm erbium-doped fiber laser for treatment of acne scars (3 treatments at intervals of 2-3 weeks) in 10 Japanese patients, clinical improvement was seen in all patients and no severe adverse effects were reported.⁷ In another study, 27 Korean patients with FSTs IV and V were treated with an NAF resurfacing device for acne scars. Excellent results were reported in 30% (8/27) of patients, substantial improvement in 59% (16/27), and moderate improvement in 11% (3/27).⁸ To evaluate outcomes in patients treated with NAF resurfacing, a retrospective review of 961 treatments showed a hyperpigmentation rate of 11.6% in those with FST IV and 33% in FST V.⁹

In one study of the short-pulsed nonablative Nd:YAG laser, 9 patients with FSTs I to V and 2 patients with FSTs IV to V underwent 8 treatments at 2-week intervals. Three blinded observers found a 29% improvement in the Global Acne Scar Severity score, while 89% (8/9) of patients self-reported subjective improvement in their acne scars.¹⁰

The 755-nm picosecond laser and diffractive lens array also have been shown to reduce the appearance of acne scars in patients with SOC, as shown via serial photography in a retrospective study of 56 patients with FSTs IV to VI. Transient hyperpigmentation, erythema, and edema were reported.¹¹

Nonablative laser therapy is preferred for skin rejuvenation in patients with SOC due to a reduced risk for postprocedural hyperpigmentation.¹¹ Ablative resurfacing (eg, CO₂ laser) poses major risks for postprocedural hyperpigmentation, hypopigmentation, and scar formation and therefore should be avoided in these populations.^12,13 A study involving 30 Asian patients (FSTs III-IV) demonstrated that the 1550-nm fractional laser was well tolerated, though higher treatment densities and fluences may lead to temporary adverse effects such as increased redness, swelling, and pain (P<.01).¹⁴ Furthermore, greater density was shown to cause higher levels of redness, hyperpigmentation, and swelling in comparison to higher fluence settings. Of note, patient satisfaction was markedly higher in patients who underwent treatment with higher fluence settings but not in patients with higher densities (P<.05). Postprocedural hyperpigmentation was noted in 6.7% (2/30) of patients studied.¹⁴ In another study, 8 patients with FSTs II to V were treated with either the 1064-nm long-pulsed Nd:YAG laser or the grid fractional monopolar radiofrequency laser.¹⁵ All participants experienced a significant decrease in mean wrinkle count using the Lemperle wrinkle assessment (P<.05). A significant decrease in mean wrinkle assessment score from 3.5 to 3.17 in clinical assessment and a decrease from 3.165 to 2.33 for photographic assessment was noted in patients treated with the grid laser (P<.05). A similar decrease in mean wrinkle assessment score was observed in the Nd:YAG group, with a mean decrease of 3.665 to 2.83 after 2 months for clinical assessment and 3.5 to 2.67 for photographic assessment. Among all patients in the study, 68% (6/8) experienced erythema, 25% (2/8) had a burning sensation, and 25% (2/8) experienced urticaria immediately postprocedure.¹⁵

Nonablative fractional resurfacing is preferred for the management of acne scars in patients with SOC. Adverse effects such as hyperpigmentation typically are transient, and the risk may be minimized with strict photoprotective practices following the procedure. Furthermore, avoidance of topicals containing exfoliants or α-hydroxy acids applied to the treated area following the procedure also may mitigate the risk for postprocedural hyperpigmentation.¹⁶ If hyperpigmentation does occur, use of topical melanogenesis inhibitors such as hydroquinone, kojic acid, or azelaic acid has shown some utility in practice.

Skin Rejuvenation

Nonablative fractional lasers (NAFLs) continue to be popular for treatment of photoaging. One study including 10 Asian patients (FSTs III-V) assessed the 1440-nm diode-based fractional laser for facial rejuvenation.¹⁷ After 4 sessions at 2-week intervals, 80% (8/10) of patients reported decreased skin roughness after both the second and third treatments, while 90% (9/10) had improved texture 1 month after the final procedure. Adverse effects included moderate facial edema and one case of transient hyperpigmentation.¹⁷ Another study reported a significant reduction in pore score (P<.002), with patients noting an overall improvement in skin appearance with minimal erythema, dryness, and flaking following 6 sessions at 2-week intervals using the 1440-nm diode-based fractional laser.¹⁸

The 1550-nm diode fractional laser significantly improved skin pigmentation (P<.001) and texture (P<.001) in 10 patients with FSTs II to IV following 5 sessions at 2- to 3-week intervals, with self-resolving erythema and edema posttreatment (Supplementary Table S2).¹⁹ Overall, NAFLs for the treatment of photoaging are effective with minimal adverse effects (eg, facial edema), which can be reduced with application of cold compression to the face and elevation of the head following treatment as well as the use of additional pillows during overnight sleep.

Laser Treatment for Hyperpigmentation Disorders

Melasma—The FDA recently approved fractional photothermolysis for the treatment of melasma; however, due to the risk for hyperpigmentation given its pathogenesis linked to hyperactive melanocytes, this laser is not considered a first-line therapy for melasma.²⁰ In a split-face, randomized study, 22 patients with FSTs III to V who were diagnosed with either dermal or mixed-type melasma were treated with a low-fluence Q-switched Nd:YAG laser combined with hydroquinone 2% vs hydroquinone 2% alone (Supplementary Table S3).²¹ Each patient was treated weekly for 5 consecutive weeks. The laser-treated side was found to reach an average of 92.5% improvement compared with 19.7% on the hydroquinone-only side. Three of the 22 (13.6%) patients developed mottled hypopigmentation after 5 laser treatments, and 8 (36.4%) developed confetti-type hypopigmentation. Four (18.2%) patients developed rebound hyperpigmentation, and all 22 patients experienced recurrence of melasma by 12 weeks posttreatment.²¹

First-line treatment for melasma involves the application of topical lightening agents such as hydroquinone, azelaic acid, kojic acid, retinoids, or mild topical steroids. Combining laser technology with topical medications can enhance treatment outcomes, particularly yielding positive results for patients with persistent pigmentation concerns. Notably, utilization of 650-microsecond technology with the 1064-nm Nd:YAG laser is considered superior in clinical practice, especially for patients with FSTs IV through VI.

Postinflammatory Hyperpigmentation—A retrospective evaluation of 61 patients with FSTs IV to VI with PIH treated with a 1927-nm NAFL showed a mean improvement of 43.24%, as assessed by 2 dermatologists.²² Additionally, the Nd:YAG 1064-nm 650-microsecond pulse duration laser is an emerging treatment that delivers high and low fluences between 4 J/cm² and 255 J/cm² within a single 650-microsecond pulse duration.²³ The short-pulse duration avoids overheating the skin, mitigating procedural discomfort and the risk for adverse effects commonly seen with the previous generation of low-pulsed lasers. In addition to PIH, this laser has been successfully used to treat pseudofolliculitis barbae.²⁴

Solar Lentigos—In a split-face study treating solar lentigos in Asian patients, 4 treatments with a low-pulsed KTP 532-nm laser were administered with and without a second treatment with a low-pulsed 1064-nm Nd:YAG laser.²⁵ Scoring of a modified pigment severity index and measurement of the melanin index showed that skin treated with the low-pulsed 532-nm laser alone and in combination with the low-pulsed 1064-nm Nd:YAG laser resulted in improvement at 3 months’ follow-up. However, there was no difference between the 2 sides of the face, leading the researchers to conclude that the low-pulsed 532-nm laser appears to be safe and effective for treatment of solar lentigos in Asian patients and does not require the addition of the low-pulsed 1064-nm laser.²⁵  

To avoid hyperpigmentation in patients with SOC, strict photoprotection to the treated areas should be advised. Proper cooling of the laser-treated area is required to minimize PIH, as cooling decreases tissue damage and excessive thermal injury. Test spots should be considered prior to initiation of the full laser treatment. Hydroquinone in a 4% concentration applied daily for 2 weeks preprocedure commonly is employed to reduce the risk for postprocedural hyperpigmentation in clinical practice.^26,27

Skin Tightening and Body Contouring

In general, skin-tightening and body-contouring devices are among the most sought-after procedures. Studies performed in patients with SOC are limited. Herein, we provide background on why these devices are favorable for patients with SOC and our experiences in using them. A summary of these devices can be found in Supplementary Table S4.

Radiofrequency Skin Tightening—Radiofrequency devices are utilized for skin tightening as well as mild fat reduction; they commonly are used on the abdomen, thighs, buttocks, and face.²⁸ People with SOC are more responsive to radiofrequency skin-tightening therapy due to higher baseline collagen content and dermal thickness, more sebaceous activity and skin elasticity, and more melanin content which offers protective thermal buffering.^29,30 As the radiofrequency device emits heat, penetrating deep into the dermis, it generates collagen remodeling and synthesis within 4 to 6 months posttreatment.

Nonsurgical Fat Reduction

Procedures for nonsurgical fat reduction are favorable due to minimal recovery time, manageable cost, and an in-office procedure setting. As noted previously, there are 6 FDA-indicated interventions for nonsurgical fat reduction: ultrasonography, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring.³¹

Ultrasonography—Ultrasound devices designed for body contouring are used for skin tightening and mild fat reduction through the use of acoustic energy.³² These devices can be divided into 2 categories: high frequency and low frequency, with the high-frequency devices being the most popular. High-frequency ultrasound energy produces heat at target sites, which induces necrosis of adipocytes and stimulates collagen remodeling within the tissue matrix.³³ Tissue temperatures above 56°C stimulate adipocyte necrosis while sparing nearby nerves and vessels.²⁸ Because of the short duration of the procedure, the risk for epidermal damage is minimal. Contrary to high-frequency ultrasonography, focus-pulsed ultrasonography employs low-frequency waves to induce the mechanical disruption of adipocytes, which is generally better tolerated due to its nonthermal mechanism. The latter may be advantageous in patients with SOC due to a reduced risk for thermal injury to the epidermis. Multiple treatments often are needed at 3- to 4-week intervals, resulting in gradual improvement observed over 2 to 6 months. One study of microfocused ultrasonography in 25 Asian patients for treatment of face and neck laxity reported that skin laxity was improved or much improved in 84% (21/25) of patients following treatment.³⁴ Adverse effects were reported as mild and transient, resolving within 90 days.³⁴ Ultrasound devices also were shown to improve wrinkles, texture, and overall appearance of the skin in a 71-year-old African American woman 4 months following treatment (Figure 2). These photographs highlight the clinical utility of a microfocused ultrasound skin-tightening treatment in African American patients.

Cryolipolysis—Cryolipolysis is a noninvasive body contouring procedure that employs controlled cooling to induce subcutaneous panniculitis. Through cold-induced apoptosis of adipocytes, this procedure selectively reduces adipose tissue in localized areas such as the flank, abdomen, thighs, buttocks, back, submental area, and upper arms. The temperature used in cryolipolysis is approximately –10°C.³⁵ The lethal temperature for melanocytes is –4 °C, below which melanocyte apoptosis may be induced, resulting in depigmentation. Given the prolonged contact of the skin with a cryolipolysis device for up to 60 minutes during a body-contouring procedure, there is a risk for resultant depigmentation in darker skin types. Controlled studies are needed to fully evaluate the safety and efficacy of cryolipolysis in patients with SOC. One retrospective study of cryolipolysis applied to the abdomen and upper arm of 4122 Asian patients reported a significant (P<.05) reduction in the circumference of the abdomen and the upper-arm areas. No long-term adverse effects were reported.³⁶

Laser Lipolysis—The 1060-nm diode laser for body contouring selectively destroys adipose tissue, resulting in body contouring via thermally induced inflammation. Hyperthermic exposure for 15 minutes selectively elevates adipocyte temperature between 42°C to 47°C, which triggers apoptosis and the eventual clearance of destroyed cells from the interstitial space.³⁷ The selectivity of the 1060-nm wavelength coupled with the device’s contact cooling system preserves the overlying skin and adnexa during the procedure,³⁷ which would minimize epidermal damage that may induce dyspigmentation in patients with SOC. No notable adverse effects or dyspigmentation have been reported using this device.

Injection Lipolysis—Deoxycholic acid is an injectable adipocytolytic for the reduction of submental fat. It nonselectively lyses muscle and other adjacent nonfatty tissue. One study of 50 Indian patients demonstrated a substantial reduction of submental fat in 90% (45/50).³⁸ For each treatment, 5 mL of 30 mg/mL deoxycholic acid was injected. Serial sessions were conducted at 2-month intervals, and most (64% [32/50]) patients required 3 sessions to see a treatment effect. Adverse effects included transient swelling, lumpiness, and tenderness. A phase 2a investigation of the novel injectable small-molecule drug CBL-514 in 43 Asian and White participants found a significant improvement in the reduction in abdominal fat volume (P<.00001) and thickness (P<.0001) relative to baseline at higher doses (unit dose, 2.0 mg/cm² and 1.6 mg/cm²).³⁹ In addition to the adverse effects mentioned previously, pruritus, repeated urticaria, body rash, and fever also were reported.³⁹  

Radiofrequency Lipolysis—Radiofrequency is used for adipolysis through heat-induced apoptosis. To achieve this effect, adipose tissue must sustain a temperature of 42 °C to 45 °C for at least 15 minutes.⁴⁰ In one study, 4 treatments performed at 7-day intervals resulted in a statistically significant reduction in circumference to the treated areas of the inner and outer thighs without any reported adverse effects (P<0.001).⁴¹ Of note, there was 1 cm of distance between the applicator and the skin. The absence of direct contact with the skin is likely to reduce the risk for postprocedural complications in patients with SOC.

Magnetic Resonance Contouring—Magnetic resonance contouring with high-intensity focused electromagnetic technology is an emerging treatment modality for noninvasive body contouring. One distinguishing characteristic from other currently available noninvasive fat-­reduction therapies is that magnetic resonance may improve strength, tone, and muscle thickness.⁴² This modality is FDA approved for contouring of the buttocks and abdomen and employs electromagnetic energy to stimulate approximately 20,000 muscle contractions within a time frame of 30 minutes. Though the mechanisms causing benefits to muscular and adipose tissue have not been elucidated, current findings suggest that the contractions stimulate substantial lipolysis of adipocytes, resulting in the release of large amounts of free fatty acids that cause damage to nearby adipose tissue.⁴³ Multiple treatments are required over time to maintain effect. No major adverse effects have been reported. The likely mechanism of action of magnetic resonance contouring does not appear to pose an increased risk to patients with SOC.

Final Thoughts

One of the major roadblocks in distilling indications along with associated risks and benefits for nonsurgical cosmetic practices for patients with SOC is a void in the primary literature involving these populations. Clinical experience serves to address this deficit in combination with a thorough review of the literature. The 1064-nm Nd:YAG laser has shown clinical utility in the treatment of DPN, melanoma, and acne scars, but it poses financial constraints to the provider in comparison to modalities used for many years. Notably, NAF resurfacing is preferred for the management of acne scars in patients with SOC and continues to gain popularity for the treatment of photoaging. Regarding skin-tightening and body-contouring devices, studies performed in patients with SOC are limited and affected by factors such as small sample sizes, underrepresentation of FSTs IV through VI, short follow-up durations, and a lack of standardized outcome measures. Additionally, few studies assess pigmentary adverse effects or stratify results by skin type, which is critical given the higher risk for PIH in SOC. Ultrasound devices showed clinical utility in improvement of skin laxity, texture, and overall improvement. Patients with SOC respond well to skin-tightening devices due to the increased collagen synthesis. Regarding emerging devices for reduction of adipocytes, deoxycholic acid when injected showed notable improvement in fat reduction but also had adverse effects. As additional studies on cosmetic procedures in SOC emerge, an expansion of treatment options could be offered to this demographic group with confidence, provided proper treatment and follow-up protocols are in place.

Cosmetic laser procedures as well as energy-based fat reduction and body-contouring devices are increasingly popular among individuals with skin of color (SOC). Innovations in cosmetic devices and procedures tailored for SOC have allowed for the optimization of outcomes in this patient population. In this article, SOC is defined as darker skin types, including Fitzpatrick skin types (FSTs) IV to VI and ethnic backgrounds such as LatinX, African American, Southeast Asian, Native American, Pacific Islander, Middle Eastern, Asian, and African. Indications for laser treatment include dermatosis papulosa nigrans (DPN), acne scars, skin rejuvenation, and hyperpigmentation. There currently are 6 procedures for nonsurgical fat reduction that are approved by the US Food and Drug Administration (FDA): high-frequency focused ultrasound, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring (Supplementary Table S1).¹

In this review, our initial focus is cosmetic laser ­procedures, encompassing FDA-cleared indications along with the associated risks and benefits in SOC populations. Subsequently, we delve into the realms of energy-based fat reduction and body contouring, offering a comprehensive overview of these noninvasive therapies and addressing considerations for efficacy and safety in these patients.

Dermatosis Papulosa Nigra

In patients with SOC, scissor excision, curettage, or electrodesiccation are the mainstay treatments for removal of DPN (Figure 1). Curettage and electrodesiccation can cause temporary postinflammatory hyperpigmentation (PIH) in these populations, while cryotherapy is not a preferred method in patients with SOC due to the possibility of cryotherapy-induced depigmentation. In a 14-patient split-face study comparing the 532-nm potassium titanyl phosphate (KTP) laser vs electrodesiccation in FSTs IV to VI, the KTP-treated side showed an improvement rate of 96%, while the electrodesiccation side showed an improvement rate of 79%. There was a statistically significant favorable experience for KTP with regard to pain tolerability (P=.002).² Complete resolution of lesions may be seen after 3 to 4 sessions at 4-week intervals. Additionally, the 1064-nm Nd:YAG laser was assessed for treatment of DPN in 2 patients, with 70% to 90% of lesions resolved after a single treatment with no complications.³

Most dermatologists still rely on curettage and electrodesiccation instead of laser therapy to remove DPNs in patients with SOC. The use of the Nd:YAG laser is promising yet expensive for the provider both to purchase and maintain. Electrodesiccation has been used by dermatology practices for decades and can be used without permanent discoloration. To minimize the risk for PIH, we recommend application of a healing ointment such as petroleum jelly or aloe vera gel to the treated lesions as well as lightening agents for PIH and daily use of sunscreen. Overall, providers do not need to purchase an expensive laser device for DPN removal.

Acne Scars

The invention of fractional technology in the early 2000s and its favorable safety profile have changed how dermatologists treat scarring in patients with SOC.^4,5 In fact, nonablative fractional (NAF) resurfacing is a preferred treatment modality for management of acne scars in patients with SOC.⁶ In one study of the 1550-nm erbium-doped fiber laser for treatment of acne scars (3 treatments at intervals of 2-3 weeks) in 10 Japanese patients, clinical improvement was seen in all patients and no severe adverse effects were reported.⁷ In another study, 27 Korean patients with FSTs IV and V were treated with an NAF resurfacing device for acne scars. Excellent results were reported in 30% (8/27) of patients, substantial improvement in 59% (16/27), and moderate improvement in 11% (3/27).⁸ To evaluate outcomes in patients treated with NAF resurfacing, a retrospective review of 961 treatments showed a hyperpigmentation rate of 11.6% in those with FST IV and 33% in FST V.⁹

In one study of the short-pulsed nonablative Nd:YAG laser, 9 patients with FSTs I to V and 2 patients with FSTs IV to V underwent 8 treatments at 2-week intervals. Three blinded observers found a 29% improvement in the Global Acne Scar Severity score, while 89% (8/9) of patients self-reported subjective improvement in their acne scars.¹⁰

The 755-nm picosecond laser and diffractive lens array also have been shown to reduce the appearance of acne scars in patients with SOC, as shown via serial photography in a retrospective study of 56 patients with FSTs IV to VI. Transient hyperpigmentation, erythema, and edema were reported.¹¹

Nonablative laser therapy is preferred for skin rejuvenation in patients with SOC due to a reduced risk for postprocedural hyperpigmentation.¹¹ Ablative resurfacing (eg, CO₂ laser) poses major risks for postprocedural hyperpigmentation, hypopigmentation, and scar formation and therefore should be avoided in these populations.^12,13 A study involving 30 Asian patients (FSTs III-IV) demonstrated that the 1550-nm fractional laser was well tolerated, though higher treatment densities and fluences may lead to temporary adverse effects such as increased redness, swelling, and pain (P<.01).¹⁴ Furthermore, greater density was shown to cause higher levels of redness, hyperpigmentation, and swelling in comparison to higher fluence settings. Of note, patient satisfaction was markedly higher in patients who underwent treatment with higher fluence settings but not in patients with higher densities (P<.05). Postprocedural hyperpigmentation was noted in 6.7% (2/30) of patients studied.¹⁴ In another study, 8 patients with FSTs II to V were treated with either the 1064-nm long-pulsed Nd:YAG laser or the grid fractional monopolar radiofrequency laser.¹⁵ All participants experienced a significant decrease in mean wrinkle count using the Lemperle wrinkle assessment (P<.05). A significant decrease in mean wrinkle assessment score from 3.5 to 3.17 in clinical assessment and a decrease from 3.165 to 2.33 for photographic assessment was noted in patients treated with the grid laser (P<.05). A similar decrease in mean wrinkle assessment score was observed in the Nd:YAG group, with a mean decrease of 3.665 to 2.83 after 2 months for clinical assessment and 3.5 to 2.67 for photographic assessment. Among all patients in the study, 68% (6/8) experienced erythema, 25% (2/8) had a burning sensation, and 25% (2/8) experienced urticaria immediately postprocedure.¹⁵

Nonablative fractional resurfacing is preferred for the management of acne scars in patients with SOC. Adverse effects such as hyperpigmentation typically are transient, and the risk may be minimized with strict photoprotective practices following the procedure. Furthermore, avoidance of topicals containing exfoliants or α-hydroxy acids applied to the treated area following the procedure also may mitigate the risk for postprocedural hyperpigmentation.¹⁶ If hyperpigmentation does occur, use of topical melanogenesis inhibitors such as hydroquinone, kojic acid, or azelaic acid has shown some utility in practice.

Skin Rejuvenation

Nonablative fractional lasers (NAFLs) continue to be popular for treatment of photoaging. One study including 10 Asian patients (FSTs III-V) assessed the 1440-nm diode-based fractional laser for facial rejuvenation.¹⁷ After 4 sessions at 2-week intervals, 80% (8/10) of patients reported decreased skin roughness after both the second and third treatments, while 90% (9/10) had improved texture 1 month after the final procedure. Adverse effects included moderate facial edema and one case of transient hyperpigmentation.¹⁷ Another study reported a significant reduction in pore score (P<.002), with patients noting an overall improvement in skin appearance with minimal erythema, dryness, and flaking following 6 sessions at 2-week intervals using the 1440-nm diode-based fractional laser.¹⁸

The 1550-nm diode fractional laser significantly improved skin pigmentation (P<.001) and texture (P<.001) in 10 patients with FSTs II to IV following 5 sessions at 2- to 3-week intervals, with self-resolving erythema and edema posttreatment (Supplementary Table S2).¹⁹ Overall, NAFLs for the treatment of photoaging are effective with minimal adverse effects (eg, facial edema), which can be reduced with application of cold compression to the face and elevation of the head following treatment as well as the use of additional pillows during overnight sleep.

Laser Treatment for Hyperpigmentation Disorders

Melasma—The FDA recently approved fractional photothermolysis for the treatment of melasma; however, due to the risk for hyperpigmentation given its pathogenesis linked to hyperactive melanocytes, this laser is not considered a first-line therapy for melasma.²⁰ In a split-face, randomized study, 22 patients with FSTs III to V who were diagnosed with either dermal or mixed-type melasma were treated with a low-fluence Q-switched Nd:YAG laser combined with hydroquinone 2% vs hydroquinone 2% alone (Supplementary Table S3).²¹ Each patient was treated weekly for 5 consecutive weeks. The laser-treated side was found to reach an average of 92.5% improvement compared with 19.7% on the hydroquinone-only side. Three of the 22 (13.6%) patients developed mottled hypopigmentation after 5 laser treatments, and 8 (36.4%) developed confetti-type hypopigmentation. Four (18.2%) patients developed rebound hyperpigmentation, and all 22 patients experienced recurrence of melasma by 12 weeks posttreatment.²¹

First-line treatment for melasma involves the application of topical lightening agents such as hydroquinone, azelaic acid, kojic acid, retinoids, or mild topical steroids. Combining laser technology with topical medications can enhance treatment outcomes, particularly yielding positive results for patients with persistent pigmentation concerns. Notably, utilization of 650-microsecond technology with the 1064-nm Nd:YAG laser is considered superior in clinical practice, especially for patients with FSTs IV through VI.

Postinflammatory Hyperpigmentation—A retrospective evaluation of 61 patients with FSTs IV to VI with PIH treated with a 1927-nm NAFL showed a mean improvement of 43.24%, as assessed by 2 dermatologists.²² Additionally, the Nd:YAG 1064-nm 650-microsecond pulse duration laser is an emerging treatment that delivers high and low fluences between 4 J/cm² and 255 J/cm² within a single 650-microsecond pulse duration.²³ The short-pulse duration avoids overheating the skin, mitigating procedural discomfort and the risk for adverse effects commonly seen with the previous generation of low-pulsed lasers. In addition to PIH, this laser has been successfully used to treat pseudofolliculitis barbae.²⁴

Solar Lentigos—In a split-face study treating solar lentigos in Asian patients, 4 treatments with a low-pulsed KTP 532-nm laser were administered with and without a second treatment with a low-pulsed 1064-nm Nd:YAG laser.²⁵ Scoring of a modified pigment severity index and measurement of the melanin index showed that skin treated with the low-pulsed 532-nm laser alone and in combination with the low-pulsed 1064-nm Nd:YAG laser resulted in improvement at 3 months’ follow-up. However, there was no difference between the 2 sides of the face, leading the researchers to conclude that the low-pulsed 532-nm laser appears to be safe and effective for treatment of solar lentigos in Asian patients and does not require the addition of the low-pulsed 1064-nm laser.²⁵  

To avoid hyperpigmentation in patients with SOC, strict photoprotection to the treated areas should be advised. Proper cooling of the laser-treated area is required to minimize PIH, as cooling decreases tissue damage and excessive thermal injury. Test spots should be considered prior to initiation of the full laser treatment. Hydroquinone in a 4% concentration applied daily for 2 weeks preprocedure commonly is employed to reduce the risk for postprocedural hyperpigmentation in clinical practice.^26,27

Skin Tightening and Body Contouring

In general, skin-tightening and body-contouring devices are among the most sought-after procedures. Studies performed in patients with SOC are limited. Herein, we provide background on why these devices are favorable for patients with SOC and our experiences in using them. A summary of these devices can be found in Supplementary Table S4.

Radiofrequency Skin Tightening—Radiofrequency devices are utilized for skin tightening as well as mild fat reduction; they commonly are used on the abdomen, thighs, buttocks, and face.²⁸ People with SOC are more responsive to radiofrequency skin-tightening therapy due to higher baseline collagen content and dermal thickness, more sebaceous activity and skin elasticity, and more melanin content which offers protective thermal buffering.^29,30 As the radiofrequency device emits heat, penetrating deep into the dermis, it generates collagen remodeling and synthesis within 4 to 6 months posttreatment.

Nonsurgical Fat Reduction

Procedures for nonsurgical fat reduction are favorable due to minimal recovery time, manageable cost, and an in-office procedure setting. As noted previously, there are 6 FDA-indicated interventions for nonsurgical fat reduction: ultrasonography, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring.³¹

Ultrasonography—Ultrasound devices designed for body contouring are used for skin tightening and mild fat reduction through the use of acoustic energy.³² These devices can be divided into 2 categories: high frequency and low frequency, with the high-frequency devices being the most popular. High-frequency ultrasound energy produces heat at target sites, which induces necrosis of adipocytes and stimulates collagen remodeling within the tissue matrix.³³ Tissue temperatures above 56°C stimulate adipocyte necrosis while sparing nearby nerves and vessels.²⁸ Because of the short duration of the procedure, the risk for epidermal damage is minimal. Contrary to high-frequency ultrasonography, focus-pulsed ultrasonography employs low-frequency waves to induce the mechanical disruption of adipocytes, which is generally better tolerated due to its nonthermal mechanism. The latter may be advantageous in patients with SOC due to a reduced risk for thermal injury to the epidermis. Multiple treatments often are needed at 3- to 4-week intervals, resulting in gradual improvement observed over 2 to 6 months. One study of microfocused ultrasonography in 25 Asian patients for treatment of face and neck laxity reported that skin laxity was improved or much improved in 84% (21/25) of patients following treatment.³⁴ Adverse effects were reported as mild and transient, resolving within 90 days.³⁴ Ultrasound devices also were shown to improve wrinkles, texture, and overall appearance of the skin in a 71-year-old African American woman 4 months following treatment (Figure 2). These photographs highlight the clinical utility of a microfocused ultrasound skin-tightening treatment in African American patients.

Cryolipolysis—Cryolipolysis is a noninvasive body contouring procedure that employs controlled cooling to induce subcutaneous panniculitis. Through cold-induced apoptosis of adipocytes, this procedure selectively reduces adipose tissue in localized areas such as the flank, abdomen, thighs, buttocks, back, submental area, and upper arms. The temperature used in cryolipolysis is approximately –10°C.³⁵ The lethal temperature for melanocytes is –4 °C, below which melanocyte apoptosis may be induced, resulting in depigmentation. Given the prolonged contact of the skin with a cryolipolysis device for up to 60 minutes during a body-contouring procedure, there is a risk for resultant depigmentation in darker skin types. Controlled studies are needed to fully evaluate the safety and efficacy of cryolipolysis in patients with SOC. One retrospective study of cryolipolysis applied to the abdomen and upper arm of 4122 Asian patients reported a significant (P<.05) reduction in the circumference of the abdomen and the upper-arm areas. No long-term adverse effects were reported.³⁶

Laser Lipolysis—The 1060-nm diode laser for body contouring selectively destroys adipose tissue, resulting in body contouring via thermally induced inflammation. Hyperthermic exposure for 15 minutes selectively elevates adipocyte temperature between 42°C to 47°C, which triggers apoptosis and the eventual clearance of destroyed cells from the interstitial space.³⁷ The selectivity of the 1060-nm wavelength coupled with the device’s contact cooling system preserves the overlying skin and adnexa during the procedure,³⁷ which would minimize epidermal damage that may induce dyspigmentation in patients with SOC. No notable adverse effects or dyspigmentation have been reported using this device.

Injection Lipolysis—Deoxycholic acid is an injectable adipocytolytic for the reduction of submental fat. It nonselectively lyses muscle and other adjacent nonfatty tissue. One study of 50 Indian patients demonstrated a substantial reduction of submental fat in 90% (45/50).³⁸ For each treatment, 5 mL of 30 mg/mL deoxycholic acid was injected. Serial sessions were conducted at 2-month intervals, and most (64% [32/50]) patients required 3 sessions to see a treatment effect. Adverse effects included transient swelling, lumpiness, and tenderness. A phase 2a investigation of the novel injectable small-molecule drug CBL-514 in 43 Asian and White participants found a significant improvement in the reduction in abdominal fat volume (P<.00001) and thickness (P<.0001) relative to baseline at higher doses (unit dose, 2.0 mg/cm² and 1.6 mg/cm²).³⁹ In addition to the adverse effects mentioned previously, pruritus, repeated urticaria, body rash, and fever also were reported.³⁹  

Radiofrequency Lipolysis—Radiofrequency is used for adipolysis through heat-induced apoptosis. To achieve this effect, adipose tissue must sustain a temperature of 42 °C to 45 °C for at least 15 minutes.⁴⁰ In one study, 4 treatments performed at 7-day intervals resulted in a statistically significant reduction in circumference to the treated areas of the inner and outer thighs without any reported adverse effects (P<0.001).⁴¹ Of note, there was 1 cm of distance between the applicator and the skin. The absence of direct contact with the skin is likely to reduce the risk for postprocedural complications in patients with SOC.

Magnetic Resonance Contouring—Magnetic resonance contouring with high-intensity focused electromagnetic technology is an emerging treatment modality for noninvasive body contouring. One distinguishing characteristic from other currently available noninvasive fat-­reduction therapies is that magnetic resonance may improve strength, tone, and muscle thickness.⁴² This modality is FDA approved for contouring of the buttocks and abdomen and employs electromagnetic energy to stimulate approximately 20,000 muscle contractions within a time frame of 30 minutes. Though the mechanisms causing benefits to muscular and adipose tissue have not been elucidated, current findings suggest that the contractions stimulate substantial lipolysis of adipocytes, resulting in the release of large amounts of free fatty acids that cause damage to nearby adipose tissue.⁴³ Multiple treatments are required over time to maintain effect. No major adverse effects have been reported. The likely mechanism of action of magnetic resonance contouring does not appear to pose an increased risk to patients with SOC.

Final Thoughts

One of the major roadblocks in distilling indications along with associated risks and benefits for nonsurgical cosmetic practices for patients with SOC is a void in the primary literature involving these populations. Clinical experience serves to address this deficit in combination with a thorough review of the literature. The 1064-nm Nd:YAG laser has shown clinical utility in the treatment of DPN, melanoma, and acne scars, but it poses financial constraints to the provider in comparison to modalities used for many years. Notably, NAF resurfacing is preferred for the management of acne scars in patients with SOC and continues to gain popularity for the treatment of photoaging. Regarding skin-tightening and body-contouring devices, studies performed in patients with SOC are limited and affected by factors such as small sample sizes, underrepresentation of FSTs IV through VI, short follow-up durations, and a lack of standardized outcome measures. Additionally, few studies assess pigmentary adverse effects or stratify results by skin type, which is critical given the higher risk for PIH in SOC. Ultrasound devices showed clinical utility in improvement of skin laxity, texture, and overall improvement. Patients with SOC respond well to skin-tightening devices due to the increased collagen synthesis. Regarding emerging devices for reduction of adipocytes, deoxycholic acid when injected showed notable improvement in fat reduction but also had adverse effects. As additional studies on cosmetic procedures in SOC emerge, an expansion of treatment options could be offered to this demographic group with confidence, provided proper treatment and follow-up protocols are in place.

Cosmetic laser procedures as well as energy-based fat reduction and body-contouring devices are increasingly popular among individuals with skin of color (SOC). Innovations in cosmetic devices and procedures tailored for SOC have allowed for the optimization of outcomes in this patient population. In this article, SOC is defined as darker skin types, including Fitzpatrick skin types (FSTs) IV to VI and ethnic backgrounds such as LatinX, African American, Southeast Asian, Native American, Pacific Islander, Middle Eastern, Asian, and African. Indications for laser treatment include dermatosis papulosa nigrans (DPN), acne scars, skin rejuvenation, and hyperpigmentation. There currently are 6 procedures for nonsurgical fat reduction that are approved by the US Food and Drug Administration (FDA): high-frequency focused ultrasound, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring (Supplementary Table S1).¹

In this review, our initial focus is cosmetic laser ­procedures, encompassing FDA-cleared indications along with the associated risks and benefits in SOC populations. Subsequently, we delve into the realms of energy-based fat reduction and body contouring, offering a comprehensive overview of these noninvasive therapies and addressing considerations for efficacy and safety in these patients.

Dermatosis Papulosa Nigra

In patients with SOC, scissor excision, curettage, or electrodesiccation are the mainstay treatments for removal of DPN (Figure 1). Curettage and electrodesiccation can cause temporary postinflammatory hyperpigmentation (PIH) in these populations, while cryotherapy is not a preferred method in patients with SOC due to the possibility of cryotherapy-induced depigmentation. In a 14-patient split-face study comparing the 532-nm potassium titanyl phosphate (KTP) laser vs electrodesiccation in FSTs IV to VI, the KTP-treated side showed an improvement rate of 96%, while the electrodesiccation side showed an improvement rate of 79%. There was a statistically significant favorable experience for KTP with regard to pain tolerability (P=.002).² Complete resolution of lesions may be seen after 3 to 4 sessions at 4-week intervals. Additionally, the 1064-nm Nd:YAG laser was assessed for treatment of DPN in 2 patients, with 70% to 90% of lesions resolved after a single treatment with no complications.³

Most dermatologists still rely on curettage and electrodesiccation instead of laser therapy to remove DPNs in patients with SOC. The use of the Nd:YAG laser is promising yet expensive for the provider both to purchase and maintain. Electrodesiccation has been used by dermatology practices for decades and can be used without permanent discoloration. To minimize the risk for PIH, we recommend application of a healing ointment such as petroleum jelly or aloe vera gel to the treated lesions as well as lightening agents for PIH and daily use of sunscreen. Overall, providers do not need to purchase an expensive laser device for DPN removal.

Acne Scars

The invention of fractional technology in the early 2000s and its favorable safety profile have changed how dermatologists treat scarring in patients with SOC.^4,5 In fact, nonablative fractional (NAF) resurfacing is a preferred treatment modality for management of acne scars in patients with SOC.⁶ In one study of the 1550-nm erbium-doped fiber laser for treatment of acne scars (3 treatments at intervals of 2-3 weeks) in 10 Japanese patients, clinical improvement was seen in all patients and no severe adverse effects were reported.⁷ In another study, 27 Korean patients with FSTs IV and V were treated with an NAF resurfacing device for acne scars. Excellent results were reported in 30% (8/27) of patients, substantial improvement in 59% (16/27), and moderate improvement in 11% (3/27).⁸ To evaluate outcomes in patients treated with NAF resurfacing, a retrospective review of 961 treatments showed a hyperpigmentation rate of 11.6% in those with FST IV and 33% in FST V.⁹

In one study of the short-pulsed nonablative Nd:YAG laser, 9 patients with FSTs I to V and 2 patients with FSTs IV to V underwent 8 treatments at 2-week intervals. Three blinded observers found a 29% improvement in the Global Acne Scar Severity score, while 89% (8/9) of patients self-reported subjective improvement in their acne scars.¹⁰

The 755-nm picosecond laser and diffractive lens array also have been shown to reduce the appearance of acne scars in patients with SOC, as shown via serial photography in a retrospective study of 56 patients with FSTs IV to VI. Transient hyperpigmentation, erythema, and edema were reported.¹¹

Nonablative laser therapy is preferred for skin rejuvenation in patients with SOC due to a reduced risk for postprocedural hyperpigmentation.¹¹ Ablative resurfacing (eg, CO₂ laser) poses major risks for postprocedural hyperpigmentation, hypopigmentation, and scar formation and therefore should be avoided in these populations.^12,13 A study involving 30 Asian patients (FSTs III-IV) demonstrated that the 1550-nm fractional laser was well tolerated, though higher treatment densities and fluences may lead to temporary adverse effects such as increased redness, swelling, and pain (P<.01).¹⁴ Furthermore, greater density was shown to cause higher levels of redness, hyperpigmentation, and swelling in comparison to higher fluence settings. Of note, patient satisfaction was markedly higher in patients who underwent treatment with higher fluence settings but not in patients with higher densities (P<.05). Postprocedural hyperpigmentation was noted in 6.7% (2/30) of patients studied.¹⁴ In another study, 8 patients with FSTs II to V were treated with either the 1064-nm long-pulsed Nd:YAG laser or the grid fractional monopolar radiofrequency laser.¹⁵ All participants experienced a significant decrease in mean wrinkle count using the Lemperle wrinkle assessment (P<.05). A significant decrease in mean wrinkle assessment score from 3.5 to 3.17 in clinical assessment and a decrease from 3.165 to 2.33 for photographic assessment was noted in patients treated with the grid laser (P<.05). A similar decrease in mean wrinkle assessment score was observed in the Nd:YAG group, with a mean decrease of 3.665 to 2.83 after 2 months for clinical assessment and 3.5 to 2.67 for photographic assessment. Among all patients in the study, 68% (6/8) experienced erythema, 25% (2/8) had a burning sensation, and 25% (2/8) experienced urticaria immediately postprocedure.¹⁵

Nonablative fractional resurfacing is preferred for the management of acne scars in patients with SOC. Adverse effects such as hyperpigmentation typically are transient, and the risk may be minimized with strict photoprotective practices following the procedure. Furthermore, avoidance of topicals containing exfoliants or α-hydroxy acids applied to the treated area following the procedure also may mitigate the risk for postprocedural hyperpigmentation.¹⁶ If hyperpigmentation does occur, use of topical melanogenesis inhibitors such as hydroquinone, kojic acid, or azelaic acid has shown some utility in practice.

Skin Rejuvenation

Nonablative fractional lasers (NAFLs) continue to be popular for treatment of photoaging. One study including 10 Asian patients (FSTs III-V) assessed the 1440-nm diode-based fractional laser for facial rejuvenation.¹⁷ After 4 sessions at 2-week intervals, 80% (8/10) of patients reported decreased skin roughness after both the second and third treatments, while 90% (9/10) had improved texture 1 month after the final procedure. Adverse effects included moderate facial edema and one case of transient hyperpigmentation.¹⁷ Another study reported a significant reduction in pore score (P<.002), with patients noting an overall improvement in skin appearance with minimal erythema, dryness, and flaking following 6 sessions at 2-week intervals using the 1440-nm diode-based fractional laser.¹⁸

The 1550-nm diode fractional laser significantly improved skin pigmentation (P<.001) and texture (P<.001) in 10 patients with FSTs II to IV following 5 sessions at 2- to 3-week intervals, with self-resolving erythema and edema posttreatment (Supplementary Table S2).¹⁹ Overall, NAFLs for the treatment of photoaging are effective with minimal adverse effects (eg, facial edema), which can be reduced with application of cold compression to the face and elevation of the head following treatment as well as the use of additional pillows during overnight sleep.

Laser Treatment for Hyperpigmentation Disorders

Melasma—The FDA recently approved fractional photothermolysis for the treatment of melasma; however, due to the risk for hyperpigmentation given its pathogenesis linked to hyperactive melanocytes, this laser is not considered a first-line therapy for melasma.²⁰ In a split-face, randomized study, 22 patients with FSTs III to V who were diagnosed with either dermal or mixed-type melasma were treated with a low-fluence Q-switched Nd:YAG laser combined with hydroquinone 2% vs hydroquinone 2% alone (Supplementary Table S3).²¹ Each patient was treated weekly for 5 consecutive weeks. The laser-treated side was found to reach an average of 92.5% improvement compared with 19.7% on the hydroquinone-only side. Three of the 22 (13.6%) patients developed mottled hypopigmentation after 5 laser treatments, and 8 (36.4%) developed confetti-type hypopigmentation. Four (18.2%) patients developed rebound hyperpigmentation, and all 22 patients experienced recurrence of melasma by 12 weeks posttreatment.²¹

First-line treatment for melasma involves the application of topical lightening agents such as hydroquinone, azelaic acid, kojic acid, retinoids, or mild topical steroids. Combining laser technology with topical medications can enhance treatment outcomes, particularly yielding positive results for patients with persistent pigmentation concerns. Notably, utilization of 650-microsecond technology with the 1064-nm Nd:YAG laser is considered superior in clinical practice, especially for patients with FSTs IV through VI.

Postinflammatory Hyperpigmentation—A retrospective evaluation of 61 patients with FSTs IV to VI with PIH treated with a 1927-nm NAFL showed a mean improvement of 43.24%, as assessed by 2 dermatologists.²² Additionally, the Nd:YAG 1064-nm 650-microsecond pulse duration laser is an emerging treatment that delivers high and low fluences between 4 J/cm² and 255 J/cm² within a single 650-microsecond pulse duration.²³ The short-pulse duration avoids overheating the skin, mitigating procedural discomfort and the risk for adverse effects commonly seen with the previous generation of low-pulsed lasers. In addition to PIH, this laser has been successfully used to treat pseudofolliculitis barbae.²⁴

Solar Lentigos—In a split-face study treating solar lentigos in Asian patients, 4 treatments with a low-pulsed KTP 532-nm laser were administered with and without a second treatment with a low-pulsed 1064-nm Nd:YAG laser.²⁵ Scoring of a modified pigment severity index and measurement of the melanin index showed that skin treated with the low-pulsed 532-nm laser alone and in combination with the low-pulsed 1064-nm Nd:YAG laser resulted in improvement at 3 months’ follow-up. However, there was no difference between the 2 sides of the face, leading the researchers to conclude that the low-pulsed 532-nm laser appears to be safe and effective for treatment of solar lentigos in Asian patients and does not require the addition of the low-pulsed 1064-nm laser.²⁵  

To avoid hyperpigmentation in patients with SOC, strict photoprotection to the treated areas should be advised. Proper cooling of the laser-treated area is required to minimize PIH, as cooling decreases tissue damage and excessive thermal injury. Test spots should be considered prior to initiation of the full laser treatment. Hydroquinone in a 4% concentration applied daily for 2 weeks preprocedure commonly is employed to reduce the risk for postprocedural hyperpigmentation in clinical practice.^26,27

Skin Tightening and Body Contouring

In general, skin-tightening and body-contouring devices are among the most sought-after procedures. Studies performed in patients with SOC are limited. Herein, we provide background on why these devices are favorable for patients with SOC and our experiences in using them. A summary of these devices can be found in Supplementary Table S4.

Radiofrequency Skin Tightening—Radiofrequency devices are utilized for skin tightening as well as mild fat reduction; they commonly are used on the abdomen, thighs, buttocks, and face.²⁸ People with SOC are more responsive to radiofrequency skin-tightening therapy due to higher baseline collagen content and dermal thickness, more sebaceous activity and skin elasticity, and more melanin content which offers protective thermal buffering.^29,30 As the radiofrequency device emits heat, penetrating deep into the dermis, it generates collagen remodeling and synthesis within 4 to 6 months posttreatment.

Nonsurgical Fat Reduction

Procedures for nonsurgical fat reduction are favorable due to minimal recovery time, manageable cost, and an in-office procedure setting. As noted previously, there are 6 FDA-indicated interventions for nonsurgical fat reduction: ultrasonography, cryolipolysis, laser lipolysis, injection lipolysis, radiofrequency lipolysis, and magnetic resonance contouring.³¹

Ultrasonography—Ultrasound devices designed for body contouring are used for skin tightening and mild fat reduction through the use of acoustic energy.³² These devices can be divided into 2 categories: high frequency and low frequency, with the high-frequency devices being the most popular. High-frequency ultrasound energy produces heat at target sites, which induces necrosis of adipocytes and stimulates collagen remodeling within the tissue matrix.³³ Tissue temperatures above 56°C stimulate adipocyte necrosis while sparing nearby nerves and vessels.²⁸ Because of the short duration of the procedure, the risk for epidermal damage is minimal. Contrary to high-frequency ultrasonography, focus-pulsed ultrasonography employs low-frequency waves to induce the mechanical disruption of adipocytes, which is generally better tolerated due to its nonthermal mechanism. The latter may be advantageous in patients with SOC due to a reduced risk for thermal injury to the epidermis. Multiple treatments often are needed at 3- to 4-week intervals, resulting in gradual improvement observed over 2 to 6 months. One study of microfocused ultrasonography in 25 Asian patients for treatment of face and neck laxity reported that skin laxity was improved or much improved in 84% (21/25) of patients following treatment.³⁴ Adverse effects were reported as mild and transient, resolving within 90 days.³⁴ Ultrasound devices also were shown to improve wrinkles, texture, and overall appearance of the skin in a 71-year-old African American woman 4 months following treatment (Figure 2). These photographs highlight the clinical utility of a microfocused ultrasound skin-tightening treatment in African American patients.

Cryolipolysis—Cryolipolysis is a noninvasive body contouring procedure that employs controlled cooling to induce subcutaneous panniculitis. Through cold-induced apoptosis of adipocytes, this procedure selectively reduces adipose tissue in localized areas such as the flank, abdomen, thighs, buttocks, back, submental area, and upper arms. The temperature used in cryolipolysis is approximately –10°C.³⁵ The lethal temperature for melanocytes is –4 °C, below which melanocyte apoptosis may be induced, resulting in depigmentation. Given the prolonged contact of the skin with a cryolipolysis device for up to 60 minutes during a body-contouring procedure, there is a risk for resultant depigmentation in darker skin types. Controlled studies are needed to fully evaluate the safety and efficacy of cryolipolysis in patients with SOC. One retrospective study of cryolipolysis applied to the abdomen and upper arm of 4122 Asian patients reported a significant (P<.05) reduction in the circumference of the abdomen and the upper-arm areas. No long-term adverse effects were reported.³⁶

Laser Lipolysis—The 1060-nm diode laser for body contouring selectively destroys adipose tissue, resulting in body contouring via thermally induced inflammation. Hyperthermic exposure for 15 minutes selectively elevates adipocyte temperature between 42°C to 47°C, which triggers apoptosis and the eventual clearance of destroyed cells from the interstitial space.³⁷ The selectivity of the 1060-nm wavelength coupled with the device’s contact cooling system preserves the overlying skin and adnexa during the procedure,³⁷ which would minimize epidermal damage that may induce dyspigmentation in patients with SOC. No notable adverse effects or dyspigmentation have been reported using this device.

Injection Lipolysis—Deoxycholic acid is an injectable adipocytolytic for the reduction of submental fat. It nonselectively lyses muscle and other adjacent nonfatty tissue. One study of 50 Indian patients demonstrated a substantial reduction of submental fat in 90% (45/50).³⁸ For each treatment, 5 mL of 30 mg/mL deoxycholic acid was injected. Serial sessions were conducted at 2-month intervals, and most (64% [32/50]) patients required 3 sessions to see a treatment effect. Adverse effects included transient swelling, lumpiness, and tenderness. A phase 2a investigation of the novel injectable small-molecule drug CBL-514 in 43 Asian and White participants found a significant improvement in the reduction in abdominal fat volume (P<.00001) and thickness (P<.0001) relative to baseline at higher doses (unit dose, 2.0 mg/cm² and 1.6 mg/cm²).³⁹ In addition to the adverse effects mentioned previously, pruritus, repeated urticaria, body rash, and fever also were reported.³⁹  

Radiofrequency Lipolysis—Radiofrequency is used for adipolysis through heat-induced apoptosis. To achieve this effect, adipose tissue must sustain a temperature of 42 °C to 45 °C for at least 15 minutes.⁴⁰ In one study, 4 treatments performed at 7-day intervals resulted in a statistically significant reduction in circumference to the treated areas of the inner and outer thighs without any reported adverse effects (P<0.001).⁴¹ Of note, there was 1 cm of distance between the applicator and the skin. The absence of direct contact with the skin is likely to reduce the risk for postprocedural complications in patients with SOC.

Magnetic Resonance Contouring—Magnetic resonance contouring with high-intensity focused electromagnetic technology is an emerging treatment modality for noninvasive body contouring. One distinguishing characteristic from other currently available noninvasive fat-­reduction therapies is that magnetic resonance may improve strength, tone, and muscle thickness.⁴² This modality is FDA approved for contouring of the buttocks and abdomen and employs electromagnetic energy to stimulate approximately 20,000 muscle contractions within a time frame of 30 minutes. Though the mechanisms causing benefits to muscular and adipose tissue have not been elucidated, current findings suggest that the contractions stimulate substantial lipolysis of adipocytes, resulting in the release of large amounts of free fatty acids that cause damage to nearby adipose tissue.⁴³ Multiple treatments are required over time to maintain effect. No major adverse effects have been reported. The likely mechanism of action of magnetic resonance contouring does not appear to pose an increased risk to patients with SOC.

Final Thoughts

One of the major roadblocks in distilling indications along with associated risks and benefits for nonsurgical cosmetic practices for patients with SOC is a void in the primary literature involving these populations. Clinical experience serves to address this deficit in combination with a thorough review of the literature. The 1064-nm Nd:YAG laser has shown clinical utility in the treatment of DPN, melanoma, and acne scars, but it poses financial constraints to the provider in comparison to modalities used for many years. Notably, NAF resurfacing is preferred for the management of acne scars in patients with SOC and continues to gain popularity for the treatment of photoaging. Regarding skin-tightening and body-contouring devices, studies performed in patients with SOC are limited and affected by factors such as small sample sizes, underrepresentation of FSTs IV through VI, short follow-up durations, and a lack of standardized outcome measures. Additionally, few studies assess pigmentary adverse effects or stratify results by skin type, which is critical given the higher risk for PIH in SOC. Ultrasound devices showed clinical utility in improvement of skin laxity, texture, and overall improvement. Patients with SOC respond well to skin-tightening devices due to the increased collagen synthesis. Regarding emerging devices for reduction of adipocytes, deoxycholic acid when injected showed notable improvement in fat reduction but also had adverse effects. As additional studies on cosmetic procedures in SOC emerge, an expansion of treatment options could be offered to this demographic group with confidence, provided proper treatment and follow-up protocols are in place.

Personal electronic devices have become more common as consumer-driven health and entertainment practices continue to increase in popularity. A wide variety of devices including smartphones, headphones and earbuds, fitness watches, and continuous glucose monitors (CGMs) allow consumers to collect data and personalize their daily activities and health practices. The global market for fitness tracking devices alone was valued at $62.03 billion in 2024 and is projected to grow to $290.85 billion by 2032.¹ Accordingly, the growing demand for continuous data tracking has led to new and prolonged skin contact with these devices, which have become emerging sources of allergic contact dermatitis (ACD). In this article, we provide a summary of the potential allergenicity of personal electronic devices with a focus on wearable devices, including clinical manifestations, reported allergens, and patch testing and management considerations (Table^2-28).

Earbuds and Headphones

Wireless earbuds and headphones are used for listening to media and may contain microphones for voice calls. Earbuds are inserted into the ears while headphones are worn over the ears with a connecting band across the scalp. These devices frequently are worn during physical activity and thus in the setting of moist sweaty environments and mechanical friction on the skin. Depending on the style of the earbuds or headphones, associated ACD may manifest as acute or chronic pruritic eczema involving the inner and/or outer ears and potentially the periauricular areas or scalp.² In a reported case of earbud ACD, the patient first presented to an otolaryngologist before being referred to a dermatologist for further evaluation and patch testing.⁹ Clinicians may be unfamiliar with these devices as a source of ACD or may potentially overlook inner ear canal manifestations, which may delay diagnosis.

Allergens reported in earbuds include (meth)acrylates,^4-6 nickel, gold,⁸ and silicone.⁹ Apple AirPods and Samsung Galaxy Buds disclose the presence of acrylates and nickel.^5,6 Cases also have been reported of ACD to gold earbud microphones⁸ and unknown allergens within silicone tips.^4,9 Acrylates, named the 2012 Allergen of the Year by the American Contact Dermatitis Society,²⁹ are used in a wide variety of consumer products as adhesives and coatings and are among the most frequently suspected headphone allergens.⁴ While fully polymerized acrylates theoretically are nonallergenic, residual acrylic monomers are potent allergens that may be found in in these products due to incomplete curing or polymer breakdown.²⁹ It remains unclear whether earbud allergen concentrations are sufficient to induce sensitization or merely elicit ACD in previously sensitized users.²⁹ Among patients with earbud ACD, the finding of inconsistent patch test reactions/cross-reactions led to the hypothesis that these headphones may contain an unidentified proprietary (meth)acrylate.⁴

Headphones, often utilized by runners and gymgoers for their comfort and fit, also have gained recent attention for their unique allergen profiles. In 2024, a case series described primary sensitization to octylisothiazolinone causing severe headphone-related ACD.³ This preservative, which is in the same family as methylchloroisothiazolinone/methylisothiazolinone, is used as a biocide in the leather or faux leather that encases the foam padding of headphones.³ Another case report highlighted ACD caused by methylisothiazolinone, methylchloroisothiazolinone, and octylisothiazolinone present in various components of a pair of headphones.² These cases are notable, as European legislation limiting the use of methylchloroisothiazolinone/methylisothiazolinone in personal care products does not apply to inclusion of isothiazolinones in other product categories, such as detergents, paints, glues, and personal electronic devices.

Mobile Phones

Mobile phones are a staple in modern society, used for a multitude of tasks including communication, internet browsing, entertainment, and activity tracking. In the early 2000s, mobile phone ACD primarily manifested on the lateral face, ears, and periauricular regions,¹² as well as the thighs from carriage in pants pockets. Early cases of mobile phone ACD were attributed to metals including chromium¹⁶ and nickel.¹⁴ At that time, lengthy and frequent phone calls with the device against the ear were thought to increase exposure to metal allergens.³⁰ More recently, as the utility of these devices has evolved, ACD has been reported to manifest on the fingers and hands associated with contact with cell phone cases, accessories, and screen protectors (Figure). In one report, a 17-year-old boy with chronic eczema of the palms was diagnosed with ACD to the rubber-related chemicals paraphenylenediamine and N-cyclohexyl-N-phenyl-4-phenylenediamine, confirmed via chemical analysis to be present in a phone case the patient used during daily gaming.¹⁷ Similarly, another case of palmar ACD resulted from thiuram rubber accelerators in a phone case.¹⁸ Most recently, a Japanese patient with a history of skin reactions to costume jewelry developed ACD involving the proximal middle finger due to exposure to nickel in a ring-grip phone case.¹¹ While the European Union has enacted regulations regarding maximum nickel leaching in products that come into direct and prolonged contact with the skin, such regulations have not been implemented in Japan or the United States.¹¹ International e-commerce makes these grips widely available, even in regions where strict metal regulations are in place. As screen time increases, it is important to consider all phone-related exposures including components of the case, screen protector, and main device body.

Watches

Smart watches and fitness bands are widely available to consumers and serve a variety of health and lifestyle functions. Features include fitness tracking, notification management, mobile payment, electrocardiography, navigation, and sleep and oxygen sensors. Multiple companies have produced hand- and wrist-based sensors for detailed wellness tracking within these categories. Allergic contact dermatitis to smart watches and wristbands manifests as eczematous lesions on the wrist (dorsal,^21,22 volar,²⁰ or circumferential involvement^23,24).

(Meth)acrylates used to adhere screen protectors, house lithium ion batteries, and bind metal to plastic have been reported to cause ACD in smart watch users.^22,25 In addition, there are at least 2 published reports of ACD to nickel in Apple Watches.^21,31 Apple, having sold more than 229 million watches worldwide, has acknowledged the presence of trace acrylates and nickel in their watches (the latter falling below European Registration, Evaluation, Authorization, and Restriction of Chemicals limits).³² Hosoki et al²⁰ identified ACD resulting from chromium exposure in the clasp of an Apple Watch band, which remains unreported by the manufacturer as a potential allergen.

Continuous Glucose Monitors

Continuous glucose monitoring systems provide users with dynamic information on their glycemic status and are associated with lower glycated hemoglobin and reduced episodes of hypoglycemia in patients with diabetes.³³ Recently, growing interest in personalized health monitoring and performance optimization has expanded CGM use to individuals without diabetes; there are 2 over-the-counter CGM options currently available in the United States.³⁴

Allergic contact dermatitis to CGMs in patients with diabetes is well characterized, manifesting as pruritic acute or chronic dermatitis at the sensor site.²⁷ To date, we are unaware of published cases of ACD associated with use of CGM in individuals without diabetes; however, wearing a CGM during athletic activities and sweating could potentially increase adhesive degradation and/or penetration of allergens in the skin.⁶

Isobornyl acrylate, named the 2020 Allergen of the Year,³⁵ is the most well-known contact allergen in glucose sensors.^36,33 Initially suspected as a component of the CGM skin adhesive, isobornyl acrylate was found to leach from the device body onto the skin in users of one CGM device.³⁶ Other reported allergens in CGM devices include colophony and related rosin derivatives, ethyl cyanoacrylate, and several chemicals that are not available as commercial patch test substances.²⁷ Understanding these potential allergens is important for patch testing considerations as CGM use increases in individuals without diabetes.

Final Thoughts

Allergic contact dermatitis to personal electronic devices including wearables, sensors, and fitness trackers is an emerging problem that should be considered in cases of dermatitis of the wrists, hands, face, ears, or in any area that comes into contact with such devices. Although in-depth studies are lacking, certain wearable devices appear to introduce continuous, low-level allergen exposure that may be below the sensitization threshold but still is capable of eliciting ACD in previously sensitized users.^21,26 Furthermore, increased allergen exposure is facilitated by prolonged skin contact, mechanical friction, and sweat.

Comprehensive patch testing often is necessary to diagnose cases of ACD to personal electronic devices.³³ The thin-layer rapid use epicutaneous (T.R.U.E.) test does not include (meth)acrylates, which repeatedly have come up as culprit allergens.³⁷ Isobornyl acrylate, a key allergen related to CGMs, is absent from standard patch test series.²⁶ Nickel remains a common culprit in these devices despite adherence to European regulations.²¹ Since there is no obligation for manufacturers to declare all possible ingredients, chemical analysis can be useful in identifying potential allergens and directing the patch test strategy, but this is not feasible in general clinical practice outside the research setting.²

Following patch testing, patient education is essential to managing personal electronic device—induced ACD. Informed patients should switch to products that do not contain their triggers—although this may be more easily said than done, since incomplete ingredient disclosure from manufacturers may necessitate a frustrating and expensive trial-and-error approach. As wearable technology proliferates, device composition and potential contact allergen transparency must be prioritized by manufacturers and regulatory bodies. Until then, clinicians should stay on their toes regarding new and emerging clinical presentations and contact allergens in hopes of improving patient outcomes.

Personal electronic devices have become more common as consumer-driven health and entertainment practices continue to increase in popularity. A wide variety of devices including smartphones, headphones and earbuds, fitness watches, and continuous glucose monitors (CGMs) allow consumers to collect data and personalize their daily activities and health practices. The global market for fitness tracking devices alone was valued at $62.03 billion in 2024 and is projected to grow to $290.85 billion by 2032.¹ Accordingly, the growing demand for continuous data tracking has led to new and prolonged skin contact with these devices, which have become emerging sources of allergic contact dermatitis (ACD). In this article, we provide a summary of the potential allergenicity of personal electronic devices with a focus on wearable devices, including clinical manifestations, reported allergens, and patch testing and management considerations (Table^2-28).

Earbuds and Headphones

Wireless earbuds and headphones are used for listening to media and may contain microphones for voice calls. Earbuds are inserted into the ears while headphones are worn over the ears with a connecting band across the scalp. These devices frequently are worn during physical activity and thus in the setting of moist sweaty environments and mechanical friction on the skin. Depending on the style of the earbuds or headphones, associated ACD may manifest as acute or chronic pruritic eczema involving the inner and/or outer ears and potentially the periauricular areas or scalp.² In a reported case of earbud ACD, the patient first presented to an otolaryngologist before being referred to a dermatologist for further evaluation and patch testing.⁹ Clinicians may be unfamiliar with these devices as a source of ACD or may potentially overlook inner ear canal manifestations, which may delay diagnosis.

Allergens reported in earbuds include (meth)acrylates,^4-6 nickel, gold,⁸ and silicone.⁹ Apple AirPods and Samsung Galaxy Buds disclose the presence of acrylates and nickel.^5,6 Cases also have been reported of ACD to gold earbud microphones⁸ and unknown allergens within silicone tips.^4,9 Acrylates, named the 2012 Allergen of the Year by the American Contact Dermatitis Society,²⁹ are used in a wide variety of consumer products as adhesives and coatings and are among the most frequently suspected headphone allergens.⁴ While fully polymerized acrylates theoretically are nonallergenic, residual acrylic monomers are potent allergens that may be found in in these products due to incomplete curing or polymer breakdown.²⁹ It remains unclear whether earbud allergen concentrations are sufficient to induce sensitization or merely elicit ACD in previously sensitized users.²⁹ Among patients with earbud ACD, the finding of inconsistent patch test reactions/cross-reactions led to the hypothesis that these headphones may contain an unidentified proprietary (meth)acrylate.⁴

Headphones, often utilized by runners and gymgoers for their comfort and fit, also have gained recent attention for their unique allergen profiles. In 2024, a case series described primary sensitization to octylisothiazolinone causing severe headphone-related ACD.³ This preservative, which is in the same family as methylchloroisothiazolinone/methylisothiazolinone, is used as a biocide in the leather or faux leather that encases the foam padding of headphones.³ Another case report highlighted ACD caused by methylisothiazolinone, methylchloroisothiazolinone, and octylisothiazolinone present in various components of a pair of headphones.² These cases are notable, as European legislation limiting the use of methylchloroisothiazolinone/methylisothiazolinone in personal care products does not apply to inclusion of isothiazolinones in other product categories, such as detergents, paints, glues, and personal electronic devices.

Mobile Phones

Mobile phones are a staple in modern society, used for a multitude of tasks including communication, internet browsing, entertainment, and activity tracking. In the early 2000s, mobile phone ACD primarily manifested on the lateral face, ears, and periauricular regions,¹² as well as the thighs from carriage in pants pockets. Early cases of mobile phone ACD were attributed to metals including chromium¹⁶ and nickel.¹⁴ At that time, lengthy and frequent phone calls with the device against the ear were thought to increase exposure to metal allergens.³⁰ More recently, as the utility of these devices has evolved, ACD has been reported to manifest on the fingers and hands associated with contact with cell phone cases, accessories, and screen protectors (Figure). In one report, a 17-year-old boy with chronic eczema of the palms was diagnosed with ACD to the rubber-related chemicals paraphenylenediamine and N-cyclohexyl-N-phenyl-4-phenylenediamine, confirmed via chemical analysis to be present in a phone case the patient used during daily gaming.¹⁷ Similarly, another case of palmar ACD resulted from thiuram rubber accelerators in a phone case.¹⁸ Most recently, a Japanese patient with a history of skin reactions to costume jewelry developed ACD involving the proximal middle finger due to exposure to nickel in a ring-grip phone case.¹¹ While the European Union has enacted regulations regarding maximum nickel leaching in products that come into direct and prolonged contact with the skin, such regulations have not been implemented in Japan or the United States.¹¹ International e-commerce makes these grips widely available, even in regions where strict metal regulations are in place. As screen time increases, it is important to consider all phone-related exposures including components of the case, screen protector, and main device body.

Watches

Smart watches and fitness bands are widely available to consumers and serve a variety of health and lifestyle functions. Features include fitness tracking, notification management, mobile payment, electrocardiography, navigation, and sleep and oxygen sensors. Multiple companies have produced hand- and wrist-based sensors for detailed wellness tracking within these categories. Allergic contact dermatitis to smart watches and wristbands manifests as eczematous lesions on the wrist (dorsal,^21,22 volar,²⁰ or circumferential involvement^23,24).

(Meth)acrylates used to adhere screen protectors, house lithium ion batteries, and bind metal to plastic have been reported to cause ACD in smart watch users.^22,25 In addition, there are at least 2 published reports of ACD to nickel in Apple Watches.^21,31 Apple, having sold more than 229 million watches worldwide, has acknowledged the presence of trace acrylates and nickel in their watches (the latter falling below European Registration, Evaluation, Authorization, and Restriction of Chemicals limits).³² Hosoki et al²⁰ identified ACD resulting from chromium exposure in the clasp of an Apple Watch band, which remains unreported by the manufacturer as a potential allergen.

Continuous Glucose Monitors

Continuous glucose monitoring systems provide users with dynamic information on their glycemic status and are associated with lower glycated hemoglobin and reduced episodes of hypoglycemia in patients with diabetes.³³ Recently, growing interest in personalized health monitoring and performance optimization has expanded CGM use to individuals without diabetes; there are 2 over-the-counter CGM options currently available in the United States.³⁴

Allergic contact dermatitis to CGMs in patients with diabetes is well characterized, manifesting as pruritic acute or chronic dermatitis at the sensor site.²⁷ To date, we are unaware of published cases of ACD associated with use of CGM in individuals without diabetes; however, wearing a CGM during athletic activities and sweating could potentially increase adhesive degradation and/or penetration of allergens in the skin.⁶

Isobornyl acrylate, named the 2020 Allergen of the Year,³⁵ is the most well-known contact allergen in glucose sensors.^36,33 Initially suspected as a component of the CGM skin adhesive, isobornyl acrylate was found to leach from the device body onto the skin in users of one CGM device.³⁶ Other reported allergens in CGM devices include colophony and related rosin derivatives, ethyl cyanoacrylate, and several chemicals that are not available as commercial patch test substances.²⁷ Understanding these potential allergens is important for patch testing considerations as CGM use increases in individuals without diabetes.

Final Thoughts

Allergic contact dermatitis to personal electronic devices including wearables, sensors, and fitness trackers is an emerging problem that should be considered in cases of dermatitis of the wrists, hands, face, ears, or in any area that comes into contact with such devices. Although in-depth studies are lacking, certain wearable devices appear to introduce continuous, low-level allergen exposure that may be below the sensitization threshold but still is capable of eliciting ACD in previously sensitized users.^21,26 Furthermore, increased allergen exposure is facilitated by prolonged skin contact, mechanical friction, and sweat.

Comprehensive patch testing often is necessary to diagnose cases of ACD to personal electronic devices.³³ The thin-layer rapid use epicutaneous (T.R.U.E.) test does not include (meth)acrylates, which repeatedly have come up as culprit allergens.³⁷ Isobornyl acrylate, a key allergen related to CGMs, is absent from standard patch test series.²⁶ Nickel remains a common culprit in these devices despite adherence to European regulations.²¹ Since there is no obligation for manufacturers to declare all possible ingredients, chemical analysis can be useful in identifying potential allergens and directing the patch test strategy, but this is not feasible in general clinical practice outside the research setting.²

Following patch testing, patient education is essential to managing personal electronic device—induced ACD. Informed patients should switch to products that do not contain their triggers—although this may be more easily said than done, since incomplete ingredient disclosure from manufacturers may necessitate a frustrating and expensive trial-and-error approach. As wearable technology proliferates, device composition and potential contact allergen transparency must be prioritized by manufacturers and regulatory bodies. Until then, clinicians should stay on their toes regarding new and emerging clinical presentations and contact allergens in hopes of improving patient outcomes.

Personal electronic devices have become more common as consumer-driven health and entertainment practices continue to increase in popularity. A wide variety of devices including smartphones, headphones and earbuds, fitness watches, and continuous glucose monitors (CGMs) allow consumers to collect data and personalize their daily activities and health practices. The global market for fitness tracking devices alone was valued at $62.03 billion in 2024 and is projected to grow to $290.85 billion by 2032.¹ Accordingly, the growing demand for continuous data tracking has led to new and prolonged skin contact with these devices, which have become emerging sources of allergic contact dermatitis (ACD). In this article, we provide a summary of the potential allergenicity of personal electronic devices with a focus on wearable devices, including clinical manifestations, reported allergens, and patch testing and management considerations (Table^2-28).

Earbuds and Headphones

Wireless earbuds and headphones are used for listening to media and may contain microphones for voice calls. Earbuds are inserted into the ears while headphones are worn over the ears with a connecting band across the scalp. These devices frequently are worn during physical activity and thus in the setting of moist sweaty environments and mechanical friction on the skin. Depending on the style of the earbuds or headphones, associated ACD may manifest as acute or chronic pruritic eczema involving the inner and/or outer ears and potentially the periauricular areas or scalp.² In a reported case of earbud ACD, the patient first presented to an otolaryngologist before being referred to a dermatologist for further evaluation and patch testing.⁹ Clinicians may be unfamiliar with these devices as a source of ACD or may potentially overlook inner ear canal manifestations, which may delay diagnosis.

Allergens reported in earbuds include (meth)acrylates,^4-6 nickel, gold,⁸ and silicone.⁹ Apple AirPods and Samsung Galaxy Buds disclose the presence of acrylates and nickel.^5,6 Cases also have been reported of ACD to gold earbud microphones⁸ and unknown allergens within silicone tips.^4,9 Acrylates, named the 2012 Allergen of the Year by the American Contact Dermatitis Society,²⁹ are used in a wide variety of consumer products as adhesives and coatings and are among the most frequently suspected headphone allergens.⁴ While fully polymerized acrylates theoretically are nonallergenic, residual acrylic monomers are potent allergens that may be found in in these products due to incomplete curing or polymer breakdown.²⁹ It remains unclear whether earbud allergen concentrations are sufficient to induce sensitization or merely elicit ACD in previously sensitized users.²⁹ Among patients with earbud ACD, the finding of inconsistent patch test reactions/cross-reactions led to the hypothesis that these headphones may contain an unidentified proprietary (meth)acrylate.⁴

Headphones, often utilized by runners and gymgoers for their comfort and fit, also have gained recent attention for their unique allergen profiles. In 2024, a case series described primary sensitization to octylisothiazolinone causing severe headphone-related ACD.³ This preservative, which is in the same family as methylchloroisothiazolinone/methylisothiazolinone, is used as a biocide in the leather or faux leather that encases the foam padding of headphones.³ Another case report highlighted ACD caused by methylisothiazolinone, methylchloroisothiazolinone, and octylisothiazolinone present in various components of a pair of headphones.² These cases are notable, as European legislation limiting the use of methylchloroisothiazolinone/methylisothiazolinone in personal care products does not apply to inclusion of isothiazolinones in other product categories, such as detergents, paints, glues, and personal electronic devices.

Mobile Phones

Mobile phones are a staple in modern society, used for a multitude of tasks including communication, internet browsing, entertainment, and activity tracking. In the early 2000s, mobile phone ACD primarily manifested on the lateral face, ears, and periauricular regions,¹² as well as the thighs from carriage in pants pockets. Early cases of mobile phone ACD were attributed to metals including chromium¹⁶ and nickel.¹⁴ At that time, lengthy and frequent phone calls with the device against the ear were thought to increase exposure to metal allergens.³⁰ More recently, as the utility of these devices has evolved, ACD has been reported to manifest on the fingers and hands associated with contact with cell phone cases, accessories, and screen protectors (Figure). In one report, a 17-year-old boy with chronic eczema of the palms was diagnosed with ACD to the rubber-related chemicals paraphenylenediamine and N-cyclohexyl-N-phenyl-4-phenylenediamine, confirmed via chemical analysis to be present in a phone case the patient used during daily gaming.¹⁷ Similarly, another case of palmar ACD resulted from thiuram rubber accelerators in a phone case.¹⁸ Most recently, a Japanese patient with a history of skin reactions to costume jewelry developed ACD involving the proximal middle finger due to exposure to nickel in a ring-grip phone case.¹¹ While the European Union has enacted regulations regarding maximum nickel leaching in products that come into direct and prolonged contact with the skin, such regulations have not been implemented in Japan or the United States.¹¹ International e-commerce makes these grips widely available, even in regions where strict metal regulations are in place. As screen time increases, it is important to consider all phone-related exposures including components of the case, screen protector, and main device body.

Watches

Smart watches and fitness bands are widely available to consumers and serve a variety of health and lifestyle functions. Features include fitness tracking, notification management, mobile payment, electrocardiography, navigation, and sleep and oxygen sensors. Multiple companies have produced hand- and wrist-based sensors for detailed wellness tracking within these categories. Allergic contact dermatitis to smart watches and wristbands manifests as eczematous lesions on the wrist (dorsal,^21,22 volar,²⁰ or circumferential involvement^23,24).

(Meth)acrylates used to adhere screen protectors, house lithium ion batteries, and bind metal to plastic have been reported to cause ACD in smart watch users.^22,25 In addition, there are at least 2 published reports of ACD to nickel in Apple Watches.^21,31 Apple, having sold more than 229 million watches worldwide, has acknowledged the presence of trace acrylates and nickel in their watches (the latter falling below European Registration, Evaluation, Authorization, and Restriction of Chemicals limits).³² Hosoki et al²⁰ identified ACD resulting from chromium exposure in the clasp of an Apple Watch band, which remains unreported by the manufacturer as a potential allergen.

Continuous Glucose Monitors

Continuous glucose monitoring systems provide users with dynamic information on their glycemic status and are associated with lower glycated hemoglobin and reduced episodes of hypoglycemia in patients with diabetes.³³ Recently, growing interest in personalized health monitoring and performance optimization has expanded CGM use to individuals without diabetes; there are 2 over-the-counter CGM options currently available in the United States.³⁴

Allergic contact dermatitis to CGMs in patients with diabetes is well characterized, manifesting as pruritic acute or chronic dermatitis at the sensor site.²⁷ To date, we are unaware of published cases of ACD associated with use of CGM in individuals without diabetes; however, wearing a CGM during athletic activities and sweating could potentially increase adhesive degradation and/or penetration of allergens in the skin.⁶

Isobornyl acrylate, named the 2020 Allergen of the Year,³⁵ is the most well-known contact allergen in glucose sensors.^36,33 Initially suspected as a component of the CGM skin adhesive, isobornyl acrylate was found to leach from the device body onto the skin in users of one CGM device.³⁶ Other reported allergens in CGM devices include colophony and related rosin derivatives, ethyl cyanoacrylate, and several chemicals that are not available as commercial patch test substances.²⁷ Understanding these potential allergens is important for patch testing considerations as CGM use increases in individuals without diabetes.

Final Thoughts

Allergic contact dermatitis to personal electronic devices including wearables, sensors, and fitness trackers is an emerging problem that should be considered in cases of dermatitis of the wrists, hands, face, ears, or in any area that comes into contact with such devices. Although in-depth studies are lacking, certain wearable devices appear to introduce continuous, low-level allergen exposure that may be below the sensitization threshold but still is capable of eliciting ACD in previously sensitized users.^21,26 Furthermore, increased allergen exposure is facilitated by prolonged skin contact, mechanical friction, and sweat.

Comprehensive patch testing often is necessary to diagnose cases of ACD to personal electronic devices.³³ The thin-layer rapid use epicutaneous (T.R.U.E.) test does not include (meth)acrylates, which repeatedly have come up as culprit allergens.³⁷ Isobornyl acrylate, a key allergen related to CGMs, is absent from standard patch test series.²⁶ Nickel remains a common culprit in these devices despite adherence to European regulations.²¹ Since there is no obligation for manufacturers to declare all possible ingredients, chemical analysis can be useful in identifying potential allergens and directing the patch test strategy, but this is not feasible in general clinical practice outside the research setting.²

Following patch testing, patient education is essential to managing personal electronic device—induced ACD. Informed patients should switch to products that do not contain their triggers—although this may be more easily said than done, since incomplete ingredient disclosure from manufacturers may necessitate a frustrating and expensive trial-and-error approach. As wearable technology proliferates, device composition and potential contact allergen transparency must be prioritized by manufacturers and regulatory bodies. Until then, clinicians should stay on their toes regarding new and emerging clinical presentations and contact allergens in hopes of improving patient outcomes.

Practice Gap

Many dermatology practices utilize pens and markers to label biopsy specimen containers, but the ink may have variable susceptibility to fading and smearing when exposed to moisture before processing. Specimen containers often are placed in plastic bags for transport. If formalin accidentally spills into the bag during this time, the labels may be exposed to moisture for hours, overnight, or even over a weekend. Effective labeling with formalin-resistant ink is crucial for maintaining the clarity of anatomic location and planning treatment, especially when multiple samples are obtained.

The Technique

We tested 12 pens and markers commonly used when labeling specimen containers to determine their susceptibility to fading due to accidental formalin exposure (Figure). Various inks were allowed to dry on sample specimen labels for 5 minutes before a thin layer of 10% buffered formalin was evenly distributed over the dried ink. Photographs of the labels were taken at baseline as well as 15 minutes, 1 hour, 3 hours, and 24 hours after formalin exposure.

Fading was observed in both the skin marker and gel panes after 15 minutes and peaked after 1 hour. Gel pens were most susceptible to fading on exposure to formalin, and the level of fading varied by ink color, with certain colors disappearing almost entirely (Figure). The solvent-resistant marker had a robust defense to formalin, as did both ballpoint pens.

Practice Implications

Given our findings, dermatology practices should avoid using gel pens to label specimen containers. Solvent-resistant markers performed as expected; however, ballpoint pens appeared to withstand formalin exposure to a similar degree and often are more readily available. Labeling biopsy specimens with an appropriate ink ensures that each sample is clearly identified with the appropriate anatomic location and any other relevant patient information.

Practice Gap

Many dermatology practices utilize pens and markers to label biopsy specimen containers, but the ink may have variable susceptibility to fading and smearing when exposed to moisture before processing. Specimen containers often are placed in plastic bags for transport. If formalin accidentally spills into the bag during this time, the labels may be exposed to moisture for hours, overnight, or even over a weekend. Effective labeling with formalin-resistant ink is crucial for maintaining the clarity of anatomic location and planning treatment, especially when multiple samples are obtained.

The Technique

We tested 12 pens and markers commonly used when labeling specimen containers to determine their susceptibility to fading due to accidental formalin exposure (Figure). Various inks were allowed to dry on sample specimen labels for 5 minutes before a thin layer of 10% buffered formalin was evenly distributed over the dried ink. Photographs of the labels were taken at baseline as well as 15 minutes, 1 hour, 3 hours, and 24 hours after formalin exposure.

Fading was observed in both the skin marker and gel panes after 15 minutes and peaked after 1 hour. Gel pens were most susceptible to fading on exposure to formalin, and the level of fading varied by ink color, with certain colors disappearing almost entirely (Figure). The solvent-resistant marker had a robust defense to formalin, as did both ballpoint pens.

Practice Implications

Given our findings, dermatology practices should avoid using gel pens to label specimen containers. Solvent-resistant markers performed as expected; however, ballpoint pens appeared to withstand formalin exposure to a similar degree and often are more readily available. Labeling biopsy specimens with an appropriate ink ensures that each sample is clearly identified with the appropriate anatomic location and any other relevant patient information.

Practice Gap

Many dermatology practices utilize pens and markers to label biopsy specimen containers, but the ink may have variable susceptibility to fading and smearing when exposed to moisture before processing. Specimen containers often are placed in plastic bags for transport. If formalin accidentally spills into the bag during this time, the labels may be exposed to moisture for hours, overnight, or even over a weekend. Effective labeling with formalin-resistant ink is crucial for maintaining the clarity of anatomic location and planning treatment, especially when multiple samples are obtained.

The Technique

We tested 12 pens and markers commonly used when labeling specimen containers to determine their susceptibility to fading due to accidental formalin exposure (Figure). Various inks were allowed to dry on sample specimen labels for 5 minutes before a thin layer of 10% buffered formalin was evenly distributed over the dried ink. Photographs of the labels were taken at baseline as well as 15 minutes, 1 hour, 3 hours, and 24 hours after formalin exposure.

Fading was observed in both the skin marker and gel panes after 15 minutes and peaked after 1 hour. Gel pens were most susceptible to fading on exposure to formalin, and the level of fading varied by ink color, with certain colors disappearing almost entirely (Figure). The solvent-resistant marker had a robust defense to formalin, as did both ballpoint pens.

Practice Implications

Given our findings, dermatology practices should avoid using gel pens to label specimen containers. Solvent-resistant markers performed as expected; however, ballpoint pens appeared to withstand formalin exposure to a similar degree and often are more readily available. Labeling biopsy specimens with an appropriate ink ensures that each sample is clearly identified with the appropriate anatomic location and any other relevant patient information.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.

The umbrella term skin of color (SOC) includes individuals identifying as Black/African, Hispanic, Asian, Native American, Middle Eastern, and Mediterranean as well as multiracial groups. While the Fitzpatrick skin typing system is not an accurate proxy for describing skin tone, SOC populations typically correspond to Fitzpatrick skin types IV to VI, and clinical researchers often report the Fitzpatrick skin type of their study populations.¹

Over the past several decades, the underrepresentation of diverse skin tones in educational resources has limited clinical training.² For example, only 10.3% of conditions featured in contemporary dermatology textbooks are shown in darker skin tones.³ This educational resource gap has spurred a transformative movement toward inclusivity in dermatologic education, research, and clinical practice. Notable examples include VisualDx⁴ and Dermatology for Skin of Color.⁵ In addition, Cutis began publishing the Dx Across the Skin Color Spectrum fact sheet series in 2022 to highlight differences in how cutaneous conditions manifest in various skin tones (https://www.mdedge.com/cutis/dx-across-skin-color-spectrum).

These resources play a critical role in advancing dermatologic knowledge, ensuring that dermatologists and other health care professionals are well equipped to diagnose and treat dermatologic conditions in SOC populations with accuracy and cultural humility. These innovations also have enhanced our understanding of how common dermatologic conditions manifest and respond to treatment in SOC populations. Herein, we highlight advances in diagnostic and therapeutic approaches for the most common concerns among SOC populations in the United States, including acne vulgaris, atopic dermatitis (AD), seborrheic dermatitis (SD), melasma, postinflammatory hyperpigmentation, psoriasis, and seborrheic keratosis.

Chief Concerns Common Among SOC Populations in the United States

Acne Vulgaris—In patients with SOC, acne frequently results in pigmentary changes and scarring that can manifest as both hypertrophic and keloidal scars.⁶ Clinical evidence from randomized controlled studies supports the use of topical dapsone gel as a safe and effective frontline treatment for acne in patients with SOC.^7,8 Notably, the US Food and Drug Administration–approved 1726-nm laser with a contact-cooling sapphire window has demonstrated safety and efficacy in the management of acne across Fitzpatrick skin types II to VI.^9-11 To manage atrophic acne scars, cutting-edge laser and radiofrequency devices including erbium-doped yttrium aluminum garnet, fractional CO₂, and picosecond lasers have been effectively employed in SOC populations. When these energy-based treatments are combined with cooling systems, they substantially reduce the risk for thermal damage in darker skin tones.^12,13

Atopic Dermatitis—While epidemiologic data indicate that Black patients experience a higher prevalence (19.3%) of AD than Asian (17.8%), White (16.1%), or Hispanic (7.8%) groups in the United States, this disparity may be influenced by factors such as access to care and environmental stressors, which require further study.^14-16 The pathogenesis of AD involves a complex interaction between skin barrier dysfunction, immune dysregulation, and environmental triggers, with patients with SOC exhibiting distinct endotypes.^14,17 For example, East Asian individuals have elevated T_H17-related cytokines and a blended T_H17/T_H2 AD-psoriasis endotype,^14,18 while Black individuals have greater T_H2 skewing and filaggrin variations and higher serum IgE levels.¹⁷ Diagnostic advancements, including a modified Eczema Area and Severity Index using grayscale rather than erythema-based assessments for patients with SOC as well as a novel SOC dermatology atlas that includes AD have increased equity in disease evaluation.^19,20 Recent clinical trials support the efficacy of topical crisaborole, topical ruxolitinib, and biologics such as dupilumab, tralokinumab, lebrikizumab, and fezakinumab for AD in SOC populations, with dupilumab also improving postinflammatory hyperpigmentation.^20-22

Seborrheic Dermatitis—Seborrheic dermatitis is common in patients with SOC, though its manifestations vary by racial/ethnic background.²³ In Black patients, petaloid SD is more prevalent and can resemble secondary syphilis, making accurate diagnosis essential to rule out potential mimickers.²⁴ Effective treatments remain limited, as current therapies often fail to address both the underlying yeast-driven inflammation and the resulting pigmentary changes that commonly affect SOC populations.²⁵ Roflumilast foam 0.3%, a phosphodiesterase 4 inhibitor, has emerged as a promising option, offering both anti-inflammatory benefits and improvements in pigmentary alterations—making it particularly valuable for treatment of SD in patients with SOC.²⁶

Melasma—Melasma is more prevalent in women with darker skin types, particularly those of African descent and those from East and Southeast Asia or Latin America.^27,28 Standard treatments including hydroquinone, retinoids, azelaic acid, kojic acid, ascorbic acid, arbutin, alpha hydroxy acids, niacinamide, and the Kligman formula (5% hydroquinone, 0.1% tretinoin, and 0.1% dexamethasone) remain therapeutic foundations in patients with SOC.²⁹ Newer alternatives that are effective in SOC populations include topical metformin 30%30; topical isobutylamido thiazolyl resorcinol or thiamidol31; and tranexamic acid cream 5%, which has comparable efficacy to hydroquinone 4% with fewer adverse effects.³² Laser therapies such as the 675-nm and 1064-nm Q-switched neodymium-doped yttrium aluminum garnet lasers, offer effective pigment reduction and are safe in darker skin tones.^33,34

Postinflammatory Hyperpigmentation—Postinflammatory hyperpigmentation, often triggered by acne in SOC populations,²³ manifests as brown, tan, or gray discoloration and is managed using similar topical agents as melasma, with the 1927-nm laser providing an additional treatment option for patients with SOC.^27,35,36

Psoriasis—In patients with SOC, psoriasis often manifests with thicker plaques, increased scaling, and greater body surface area involvement, leading to considerable quality-of-life implications.³⁷ Although prevalence is highest in White populations (3.6%), Asian (2.5%) and Hispanic/Latino (1.9%) patients experience increased disease severity, potentially explaining why psoriasis is among the top chief complaints for these racial/ ethnic groups in the United States.^23,38 Greater diversity in clinical trials has improved our understanding of the efficacy of biologics for psoriasis in SOC populations. The VISIBLE trial—the first SOC-exclusive psoriasis trial—demonstrated a Psoriasis Area and Severity Index 90 response in 57.1% (44/77) of participants receiving guselkumab vs 3.8% (1/26) of participants receiving placebo by week 16 (P<.001).³⁹ Other biologics such as risankizumab, secukinumab, and brodalumab also have shown efficacy in SOC populations.^40-42 Additionally, topical therapies such as calcipotriene-betamethasone dipropionate cream/aerosol foam and halobetasol propionatetazarotene lotion have proven effective, with minimal adverse effects and low discontinuation rates in patients with SOC.^43-46

Seborrheic Keratosis—In SOC, seborrheic keratosis (SK) often appears as a variant known as dermatosis papulosa nigra (DPN), manifesting as small, benign, hyperpigmented papules, particularly on the face and neck.⁴⁷ Dermatosis papulosa nigra is common in Black, Hispanic, and some Asian populations, with variations in color and distribution among different racial/ethnic groups.⁴⁸ For example, in Korean populations, SKs commonly affect males, and in contrast to the dark brown color common in White populations, SKs in Korean patients often appear lighter brown or sometimes pink.⁴⁹ In contrast to the verrucous and stuck-on appearance often seen in White populations, South Asian populations more often have variants including pedunculated SKs, flat SKs, and stucco keratoses.⁵⁰ High-resolution dermoscopy improves differentiation from malignant lesions; however, a sudden SK eruption in any population warrants evaluation for underlying malignancy. Cryotherapy, though effective for removal of SKs, can cause pigmentary changes in SOC populations, making laser therapy and electrosurgery preferable for these patients due to the lower risk for pigmentary sequela. If hyperpigmentation occurs, topical treatments such as hydroquinone, tretinoin, or azelaic acid can help. New laser technologies and hydrogen-peroxide–based therapies offer safer and more effective removal options while minimizing pigmentary risks in SOC populations.^47,50 While DPNs are common in patients with darker skin tones, there are limited data on optimal treatment frequency, insurance coverage, and efficacy. This literature gap hinders our understanding of treatment accessibility and economic impact on our patients.⁵¹

Final Thoughts

Innovations such as standardized scoring systems and customized therapeutic strategies for conditions including acne, pigmentary disorders, and atopic dermatitis have markedly enhanced patient care and outcomes for the most common chief concerns in SOC populations. In addition, population-specific advancements have addressed unique diagnostic and therapeutic developments in Black, Asian/Pacific Islander, and Hispanic groups, from the nuanced presentations of atopic and seborrheic dermatitis in Black patients, to those of psoriasis in Asian/Pacific Islander and Hispanic populations. Finally, updated epidemiologic studies are essential to capture the current and evolving dermatologic concerns pertinent to patients with SOC, ensuring that future clinical and research efforts align with the unique needs of these populations.