Cutis

Dermatologists frequently learn about skin conditions that are directly linked to diet. For example, we know that nutritional deficiencies can impact the hair, skin, and nails, and that celiac disease manifests with dermatitis herpetiformis of the skin. Patients commonly ask their dermatologists about the impact of diet on their skin. There are many outdated myths, but research on the subject is increasingly demonstrating important associations. Dermatologists must become familiar with the data on this topic so that we can provide informed counseling for our patients. This article reviews the current literature on associations between diet and 3 common cutaneous conditions—acne, psoriasis, and atopic dermatitis [AD]—and provides tips on how to best address our patients’ questions on this topic.

Acne

Studies increasingly support an association between a high glycemic diet (foods that lead to a spike in serum glucose) and acne; Bowe et al1 provided an excellent summary of the topic in 2010. This year, a large prospective cohort study of more than 24,000 participants demonstrated an association between adult acne and a diet high in milk, sugary beverages and foods, and fatty foods.2 In prospective cohort studies of more than 6000 adolescent girls and 4000 adolescent boys, Adebamowo et al3^,4 demonstrated a correlation between skim milk consumption and acne. Whey protein supplementation also has been implicated in acne flares.^5,6 The biological mechanism of the impact of high glycemic index foods and acne is believed to be mainly via activation of the insulinlike growth factor 1 (IGF-1) pathway, which promotes androgen synthesis and increases androgen bioavailability via decreased synthesis of sex hormone binding globulin.^1,2 Insulinlike growth factor 1 also stimulates its downstream target, mammalian target of rapamycin (mTOR), leading to activation of antiapoptotic and proliferation signaling, ultimately resulting in oxidative stress and inflammation causing acne.² Penso et al² noted that patients with IGF-1 deficiency (Laron syndrome) never develop acne unless treated with exogenous IGF-1, further supporting its role in acne formation.⁷ There currently is a paucity of randomized controlled trials assessing the impact of diet on acne.

Psoriasis 

The literature consistently shows that obesity is a predisposing factor for psoriasis. Additionally, weight gain may cause flares of existing psoriasis.⁸ Promotion of a healthy diet is an important factor in the management of obesity, alongside physical activity and, in some cases, medication and bariatric surgery.⁹ Patients with psoriasis who are overweight have been shown to experience improvement in their psoriasis after weight loss secondary to diet and exercise.^8,10 The joint American Academy of Dermatology and National Psoriasis Foundation guidelines recommend that dermatologists advise patients to practice a healthy lifestyle including a healthy diet and communicate with a patient’s primary care provider so they can be appropriately evaluated and treated for comorbidities including metabolic syndrome, diabetes, and hyperlipidemia.¹¹ In the NutriNet-Santé cohort study, investigators found an inverse correlation between psoriasis severity and adherence to a Mediterranean diet, which the authors conclude supports the hypothesis that this may slow the progression of psoriasis.¹² In a single meta-analysis, it was reported that patients with psoriasis have a 3-fold increased risk for celiac disease compared to the general population.1³ It remains unknown if these data are generalizable to the US population. Dermatologists should consider screening patients with psoriasis for celiac disease based on reported symptoms. When suspected, it is necessary to order appropriate serologies and consider referral to gastroenterology prior to recommending a gluten-free diet, as elimination of gluten prior to testing may lead to false-negative results.

Atopic Dermatitis

Patients and parents/guardians of children with AD often ask about the impact of diet on the condition. A small minority of patients may experience flares of AD due to ongoing, non–IgE-mediated allergen exposure.¹⁴ Diet as a trigger for flares should be suspected in children with persistent, moderate to severe AD. In these patients, allergen avoidance may lead to improvement but not resolution of AD. Allergens ordered from most common to least common are the following: eggs, milk, peanuts/tree nuts, shellfish, soy, and wheat.¹⁵ Additionally, it is important to note that children with AD are at higher risk for developing life-threatening, IgE-mediated food allergies compared to the general population (37% vs 6.8%).^16,17 The LEAP (Learning Early about Peanut Allergy) study led to a paradigm shift in prevention of peanut allergies in high-risk children (ie, those with severe AD and/or egg allergy), providing data to support the idea that early introduction of allergenic foods such as peanuts may prevent severe allergies.¹⁸ Further studies are necessary to clarify the population in which allergen testing and recommendations on food avoidance are warranted vs early introduction.¹⁹

Conclusion

Early data support the relationship between diet and many common dermatologic conditions, including acne, psoriasis, and AD. Dermatologists should be familiar with the evidence supporting the relationship between diet and various skin conditions to best answer patients’ questions and counsel as appropriate. It is important for dermatologists to continue to stay up-to-date on the literature on this subject as new data emerge. Knowledge about the relationship between diet and skin allows dermatologists to not only support our patients’ skin health but their overall health as well.

Dermatologists frequently learn about skin conditions that are directly linked to diet. For example, we know that nutritional deficiencies can impact the hair, skin, and nails, and that celiac disease manifests with dermatitis herpetiformis of the skin. Patients commonly ask their dermatologists about the impact of diet on their skin. There are many outdated myths, but research on the subject is increasingly demonstrating important associations. Dermatologists must become familiar with the data on this topic so that we can provide informed counseling for our patients. This article reviews the current literature on associations between diet and 3 common cutaneous conditions—acne, psoriasis, and atopic dermatitis [AD]—and provides tips on how to best address our patients’ questions on this topic.

Acne

Studies increasingly support an association between a high glycemic diet (foods that lead to a spike in serum glucose) and acne; Bowe et al1 provided an excellent summary of the topic in 2010. This year, a large prospective cohort study of more than 24,000 participants demonstrated an association between adult acne and a diet high in milk, sugary beverages and foods, and fatty foods.2 In prospective cohort studies of more than 6000 adolescent girls and 4000 adolescent boys, Adebamowo et al3^,4 demonstrated a correlation between skim milk consumption and acne. Whey protein supplementation also has been implicated in acne flares.^5,6 The biological mechanism of the impact of high glycemic index foods and acne is believed to be mainly via activation of the insulinlike growth factor 1 (IGF-1) pathway, which promotes androgen synthesis and increases androgen bioavailability via decreased synthesis of sex hormone binding globulin.^1,2 Insulinlike growth factor 1 also stimulates its downstream target, mammalian target of rapamycin (mTOR), leading to activation of antiapoptotic and proliferation signaling, ultimately resulting in oxidative stress and inflammation causing acne.² Penso et al² noted that patients with IGF-1 deficiency (Laron syndrome) never develop acne unless treated with exogenous IGF-1, further supporting its role in acne formation.⁷ There currently is a paucity of randomized controlled trials assessing the impact of diet on acne.

Psoriasis 

The literature consistently shows that obesity is a predisposing factor for psoriasis. Additionally, weight gain may cause flares of existing psoriasis.⁸ Promotion of a healthy diet is an important factor in the management of obesity, alongside physical activity and, in some cases, medication and bariatric surgery.⁹ Patients with psoriasis who are overweight have been shown to experience improvement in their psoriasis after weight loss secondary to diet and exercise.^8,10 The joint American Academy of Dermatology and National Psoriasis Foundation guidelines recommend that dermatologists advise patients to practice a healthy lifestyle including a healthy diet and communicate with a patient’s primary care provider so they can be appropriately evaluated and treated for comorbidities including metabolic syndrome, diabetes, and hyperlipidemia.¹¹ In the NutriNet-Santé cohort study, investigators found an inverse correlation between psoriasis severity and adherence to a Mediterranean diet, which the authors conclude supports the hypothesis that this may slow the progression of psoriasis.¹² In a single meta-analysis, it was reported that patients with psoriasis have a 3-fold increased risk for celiac disease compared to the general population.1³ It remains unknown if these data are generalizable to the US population. Dermatologists should consider screening patients with psoriasis for celiac disease based on reported symptoms. When suspected, it is necessary to order appropriate serologies and consider referral to gastroenterology prior to recommending a gluten-free diet, as elimination of gluten prior to testing may lead to false-negative results.

Atopic Dermatitis

Patients and parents/guardians of children with AD often ask about the impact of diet on the condition. A small minority of patients may experience flares of AD due to ongoing, non–IgE-mediated allergen exposure.¹⁴ Diet as a trigger for flares should be suspected in children with persistent, moderate to severe AD. In these patients, allergen avoidance may lead to improvement but not resolution of AD. Allergens ordered from most common to least common are the following: eggs, milk, peanuts/tree nuts, shellfish, soy, and wheat.¹⁵ Additionally, it is important to note that children with AD are at higher risk for developing life-threatening, IgE-mediated food allergies compared to the general population (37% vs 6.8%).^16,17 The LEAP (Learning Early about Peanut Allergy) study led to a paradigm shift in prevention of peanut allergies in high-risk children (ie, those with severe AD and/or egg allergy), providing data to support the idea that early introduction of allergenic foods such as peanuts may prevent severe allergies.¹⁸ Further studies are necessary to clarify the population in which allergen testing and recommendations on food avoidance are warranted vs early introduction.¹⁹

Conclusion

Early data support the relationship between diet and many common dermatologic conditions, including acne, psoriasis, and AD. Dermatologists should be familiar with the evidence supporting the relationship between diet and various skin conditions to best answer patients’ questions and counsel as appropriate. It is important for dermatologists to continue to stay up-to-date on the literature on this subject as new data emerge. Knowledge about the relationship between diet and skin allows dermatologists to not only support our patients’ skin health but their overall health as well.

Dermatologists frequently learn about skin conditions that are directly linked to diet. For example, we know that nutritional deficiencies can impact the hair, skin, and nails, and that celiac disease manifests with dermatitis herpetiformis of the skin. Patients commonly ask their dermatologists about the impact of diet on their skin. There are many outdated myths, but research on the subject is increasingly demonstrating important associations. Dermatologists must become familiar with the data on this topic so that we can provide informed counseling for our patients. This article reviews the current literature on associations between diet and 3 common cutaneous conditions—acne, psoriasis, and atopic dermatitis [AD]—and provides tips on how to best address our patients’ questions on this topic.

Acne

Studies increasingly support an association between a high glycemic diet (foods that lead to a spike in serum glucose) and acne; Bowe et al1 provided an excellent summary of the topic in 2010. This year, a large prospective cohort study of more than 24,000 participants demonstrated an association between adult acne and a diet high in milk, sugary beverages and foods, and fatty foods.2 In prospective cohort studies of more than 6000 adolescent girls and 4000 adolescent boys, Adebamowo et al3^,4 demonstrated a correlation between skim milk consumption and acne. Whey protein supplementation also has been implicated in acne flares.^5,6 The biological mechanism of the impact of high glycemic index foods and acne is believed to be mainly via activation of the insulinlike growth factor 1 (IGF-1) pathway, which promotes androgen synthesis and increases androgen bioavailability via decreased synthesis of sex hormone binding globulin.^1,2 Insulinlike growth factor 1 also stimulates its downstream target, mammalian target of rapamycin (mTOR), leading to activation of antiapoptotic and proliferation signaling, ultimately resulting in oxidative stress and inflammation causing acne.² Penso et al² noted that patients with IGF-1 deficiency (Laron syndrome) never develop acne unless treated with exogenous IGF-1, further supporting its role in acne formation.⁷ There currently is a paucity of randomized controlled trials assessing the impact of diet on acne.

Psoriasis 

The literature consistently shows that obesity is a predisposing factor for psoriasis. Additionally, weight gain may cause flares of existing psoriasis.⁸ Promotion of a healthy diet is an important factor in the management of obesity, alongside physical activity and, in some cases, medication and bariatric surgery.⁹ Patients with psoriasis who are overweight have been shown to experience improvement in their psoriasis after weight loss secondary to diet and exercise.^8,10 The joint American Academy of Dermatology and National Psoriasis Foundation guidelines recommend that dermatologists advise patients to practice a healthy lifestyle including a healthy diet and communicate with a patient’s primary care provider so they can be appropriately evaluated and treated for comorbidities including metabolic syndrome, diabetes, and hyperlipidemia.¹¹ In the NutriNet-Santé cohort study, investigators found an inverse correlation between psoriasis severity and adherence to a Mediterranean diet, which the authors conclude supports the hypothesis that this may slow the progression of psoriasis.¹² In a single meta-analysis, it was reported that patients with psoriasis have a 3-fold increased risk for celiac disease compared to the general population.1³ It remains unknown if these data are generalizable to the US population. Dermatologists should consider screening patients with psoriasis for celiac disease based on reported symptoms. When suspected, it is necessary to order appropriate serologies and consider referral to gastroenterology prior to recommending a gluten-free diet, as elimination of gluten prior to testing may lead to false-negative results.

Atopic Dermatitis

Patients and parents/guardians of children with AD often ask about the impact of diet on the condition. A small minority of patients may experience flares of AD due to ongoing, non–IgE-mediated allergen exposure.¹⁴ Diet as a trigger for flares should be suspected in children with persistent, moderate to severe AD. In these patients, allergen avoidance may lead to improvement but not resolution of AD. Allergens ordered from most common to least common are the following: eggs, milk, peanuts/tree nuts, shellfish, soy, and wheat.¹⁵ Additionally, it is important to note that children with AD are at higher risk for developing life-threatening, IgE-mediated food allergies compared to the general population (37% vs 6.8%).^16,17 The LEAP (Learning Early about Peanut Allergy) study led to a paradigm shift in prevention of peanut allergies in high-risk children (ie, those with severe AD and/or egg allergy), providing data to support the idea that early introduction of allergenic foods such as peanuts may prevent severe allergies.¹⁸ Further studies are necessary to clarify the population in which allergen testing and recommendations on food avoidance are warranted vs early introduction.¹⁹

Conclusion

Early data support the relationship between diet and many common dermatologic conditions, including acne, psoriasis, and AD. Dermatologists should be familiar with the evidence supporting the relationship between diet and various skin conditions to best answer patients’ questions and counsel as appropriate. It is important for dermatologists to continue to stay up-to-date on the literature on this subject as new data emerge. Knowledge about the relationship between diet and skin allows dermatologists to not only support our patients’ skin health but their overall health as well.

The Diagnosis: Subcutaneous Granuloma Annulare 

Subcutaneous granuloma annulare (SGA), also known as deep GA, is a rare variant of GA that usually occurs in children and young adults. It presents as single or multiple, nontender, deep dermal and/or subcutaneous nodules with normal-appearing skin usually on the anterior lower legs, dorsal aspects of the hands and fingers, scalp, or buttocks.^1-3 The pathogenesis of SGA as well as GA is not fully understood, and proposed inciting factors include trauma, insect bite reactions, tuberculin skin testing, vaccines, UV exposure, medications, and viral infections.^3-6 A cell-mediated, delayed-type hypersensitivity reaction to an unknown antigen also has been postulated as a possible mechanism.⁷ Treatment usually is not necessary, as the nature of the condition is benign and the course often is self-limited. Spontaneous resolution occurs within 2 years in 50% of patients with localized GA.^4,8 Surgery usually is not recommended due to the high recurrence rate (40%-75%).^4,9  

Absence of epidermal change in this entity obfuscates clinical recognition, and accurate diagnosis often depends on punch or excisional biopsies revealing characteristic histopathology. The histology of SGA consists of palisaded granulomas with central areas of necrobiosis composed of degenerated collagen, mucin deposition, and nuclear dust from neutrophils that extend into the deep dermis and subcutis.² The periphery of the granulomas is lined by palisading epithelioid histiocytes with occasional multinucleated giant cells.^10,11 Eosinophils often are present.¹² Colloidal iron and Alcian blue stains can be used to highlight the abundant connective tissue mucin of the granulomas.⁴  

The histologic differential diagnosis of SGA includes rheumatoid nodule, necrobiosis lipoidica, epithelioid sarcoma, and tophaceous gout.² Rheumatoid nodules are the most common dermatologic presentation of rheumatoid arthritis and are found in up to 30% to 40% of patients with the disease.^13-15 They present as firm, painless, subcutaneous papulonodules on the extensor surfaces and at sites of trauma or pressure. Histologically, rheumatoid nodules exhibit a homogenous and eosinophilic central area of necrobiosis with fibrin deposition and absent mucin deep within the dermis and subcutaneous tissue (Figure 1). In contrast, granulomas in SGA usually are pale and basophilic with abundant mucin.²  

Necrobiosis lipoidica is a rare chronic granulomatous disease of the skin that most commonly occurs in young to middle-aged adults and is strongly associated with diabetes mellitus.¹⁶ It clinically presents as yellow to red-brown papules and plaques with a peripheral erythematous to violaceous rim usually on the pretibial area. Over time, lesions become yellowish atrophic patches and plaques that sometimes can ulcerate. Histopathology reveals areas of horizontally arranged, palisaded, and interstitial granulomatous dermatitis intermixed with areas of degenerated collagen and widespread fibrosis extending from the superficial dermis into the subcutis (Figure 2).² These areas lack mucin and have an increased number of plasma cells. Eosinophils and/or lymphoid nodules occasionally can be seen.^17,18 

Epithelioid sarcoma is a rare malignant soft tissue sarcoma that tends to occur on the distal extremities in younger patients, typically aged 20 to 40 years, often with preceding trauma to the area. It usually presents as a solitary, poorly defined, hard, subcutaneous nodule. Histologic analysis shows central areas of necrosis and degenerated collagen surrounded by epithelioid and spindle cells with hyperchromatic and pleomorphic nuclei and mitoses (Figure 3).² These tumor cells express positivity for keratins, vimentin, epithelial membrane antigen, and CD34, while they usually are negative for desmin, S-100, and FLI-1 nuclear transcription factor.^2,4,19  

Tophaceous gout results from the accumulation of monosodium urate crystals in the skin. It clinically presents as firm, white-yellow, dermal and subcutaneous papulonodules on the helix of the ear and the skin overlying joints. Histopathology reveals palisaded granulomas surrounding an amorphous feathery material that corresponds to the urate crystals that were destroyed with formalin fixation (Figure 4). When the tissue is fixed with ethanol or is incompletely fixed in formalin, birefringent urate crystals are evident with polarization.²⁰

The Diagnosis: Subcutaneous Granuloma Annulare 

Subcutaneous granuloma annulare (SGA), also known as deep GA, is a rare variant of GA that usually occurs in children and young adults. It presents as single or multiple, nontender, deep dermal and/or subcutaneous nodules with normal-appearing skin usually on the anterior lower legs, dorsal aspects of the hands and fingers, scalp, or buttocks.^1-3 The pathogenesis of SGA as well as GA is not fully understood, and proposed inciting factors include trauma, insect bite reactions, tuberculin skin testing, vaccines, UV exposure, medications, and viral infections.^3-6 A cell-mediated, delayed-type hypersensitivity reaction to an unknown antigen also has been postulated as a possible mechanism.⁷ Treatment usually is not necessary, as the nature of the condition is benign and the course often is self-limited. Spontaneous resolution occurs within 2 years in 50% of patients with localized GA.^4,8 Surgery usually is not recommended due to the high recurrence rate (40%-75%).^4,9  

Absence of epidermal change in this entity obfuscates clinical recognition, and accurate diagnosis often depends on punch or excisional biopsies revealing characteristic histopathology. The histology of SGA consists of palisaded granulomas with central areas of necrobiosis composed of degenerated collagen, mucin deposition, and nuclear dust from neutrophils that extend into the deep dermis and subcutis.² The periphery of the granulomas is lined by palisading epithelioid histiocytes with occasional multinucleated giant cells.^10,11 Eosinophils often are present.¹² Colloidal iron and Alcian blue stains can be used to highlight the abundant connective tissue mucin of the granulomas.⁴  

The histologic differential diagnosis of SGA includes rheumatoid nodule, necrobiosis lipoidica, epithelioid sarcoma, and tophaceous gout.² Rheumatoid nodules are the most common dermatologic presentation of rheumatoid arthritis and are found in up to 30% to 40% of patients with the disease.^13-15 They present as firm, painless, subcutaneous papulonodules on the extensor surfaces and at sites of trauma or pressure. Histologically, rheumatoid nodules exhibit a homogenous and eosinophilic central area of necrobiosis with fibrin deposition and absent mucin deep within the dermis and subcutaneous tissue (Figure 1). In contrast, granulomas in SGA usually are pale and basophilic with abundant mucin.²  

Necrobiosis lipoidica is a rare chronic granulomatous disease of the skin that most commonly occurs in young to middle-aged adults and is strongly associated with diabetes mellitus.¹⁶ It clinically presents as yellow to red-brown papules and plaques with a peripheral erythematous to violaceous rim usually on the pretibial area. Over time, lesions become yellowish atrophic patches and plaques that sometimes can ulcerate. Histopathology reveals areas of horizontally arranged, palisaded, and interstitial granulomatous dermatitis intermixed with areas of degenerated collagen and widespread fibrosis extending from the superficial dermis into the subcutis (Figure 2).² These areas lack mucin and have an increased number of plasma cells. Eosinophils and/or lymphoid nodules occasionally can be seen.^17,18 

Epithelioid sarcoma is a rare malignant soft tissue sarcoma that tends to occur on the distal extremities in younger patients, typically aged 20 to 40 years, often with preceding trauma to the area. It usually presents as a solitary, poorly defined, hard, subcutaneous nodule. Histologic analysis shows central areas of necrosis and degenerated collagen surrounded by epithelioid and spindle cells with hyperchromatic and pleomorphic nuclei and mitoses (Figure 3).² These tumor cells express positivity for keratins, vimentin, epithelial membrane antigen, and CD34, while they usually are negative for desmin, S-100, and FLI-1 nuclear transcription factor.^2,4,19  

Tophaceous gout results from the accumulation of monosodium urate crystals in the skin. It clinically presents as firm, white-yellow, dermal and subcutaneous papulonodules on the helix of the ear and the skin overlying joints. Histopathology reveals palisaded granulomas surrounding an amorphous feathery material that corresponds to the urate crystals that were destroyed with formalin fixation (Figure 4). When the tissue is fixed with ethanol or is incompletely fixed in formalin, birefringent urate crystals are evident with polarization.²⁰

The Diagnosis: Subcutaneous Granuloma Annulare 

Subcutaneous granuloma annulare (SGA), also known as deep GA, is a rare variant of GA that usually occurs in children and young adults. It presents as single or multiple, nontender, deep dermal and/or subcutaneous nodules with normal-appearing skin usually on the anterior lower legs, dorsal aspects of the hands and fingers, scalp, or buttocks.^1-3 The pathogenesis of SGA as well as GA is not fully understood, and proposed inciting factors include trauma, insect bite reactions, tuberculin skin testing, vaccines, UV exposure, medications, and viral infections.^3-6 A cell-mediated, delayed-type hypersensitivity reaction to an unknown antigen also has been postulated as a possible mechanism.⁷ Treatment usually is not necessary, as the nature of the condition is benign and the course often is self-limited. Spontaneous resolution occurs within 2 years in 50% of patients with localized GA.^4,8 Surgery usually is not recommended due to the high recurrence rate (40%-75%).^4,9  

Absence of epidermal change in this entity obfuscates clinical recognition, and accurate diagnosis often depends on punch or excisional biopsies revealing characteristic histopathology. The histology of SGA consists of palisaded granulomas with central areas of necrobiosis composed of degenerated collagen, mucin deposition, and nuclear dust from neutrophils that extend into the deep dermis and subcutis.² The periphery of the granulomas is lined by palisading epithelioid histiocytes with occasional multinucleated giant cells.^10,11 Eosinophils often are present.¹² Colloidal iron and Alcian blue stains can be used to highlight the abundant connective tissue mucin of the granulomas.⁴  

The histologic differential diagnosis of SGA includes rheumatoid nodule, necrobiosis lipoidica, epithelioid sarcoma, and tophaceous gout.² Rheumatoid nodules are the most common dermatologic presentation of rheumatoid arthritis and are found in up to 30% to 40% of patients with the disease.^13-15 They present as firm, painless, subcutaneous papulonodules on the extensor surfaces and at sites of trauma or pressure. Histologically, rheumatoid nodules exhibit a homogenous and eosinophilic central area of necrobiosis with fibrin deposition and absent mucin deep within the dermis and subcutaneous tissue (Figure 1). In contrast, granulomas in SGA usually are pale and basophilic with abundant mucin.²  

Necrobiosis lipoidica is a rare chronic granulomatous disease of the skin that most commonly occurs in young to middle-aged adults and is strongly associated with diabetes mellitus.¹⁶ It clinically presents as yellow to red-brown papules and plaques with a peripheral erythematous to violaceous rim usually on the pretibial area. Over time, lesions become yellowish atrophic patches and plaques that sometimes can ulcerate. Histopathology reveals areas of horizontally arranged, palisaded, and interstitial granulomatous dermatitis intermixed with areas of degenerated collagen and widespread fibrosis extending from the superficial dermis into the subcutis (Figure 2).² These areas lack mucin and have an increased number of plasma cells. Eosinophils and/or lymphoid nodules occasionally can be seen.^17,18 

Epithelioid sarcoma is a rare malignant soft tissue sarcoma that tends to occur on the distal extremities in younger patients, typically aged 20 to 40 years, often with preceding trauma to the area. It usually presents as a solitary, poorly defined, hard, subcutaneous nodule. Histologic analysis shows central areas of necrosis and degenerated collagen surrounded by epithelioid and spindle cells with hyperchromatic and pleomorphic nuclei and mitoses (Figure 3).² These tumor cells express positivity for keratins, vimentin, epithelial membrane antigen, and CD34, while they usually are negative for desmin, S-100, and FLI-1 nuclear transcription factor.^2,4,19  

Tophaceous gout results from the accumulation of monosodium urate crystals in the skin. It clinically presents as firm, white-yellow, dermal and subcutaneous papulonodules on the helix of the ear and the skin overlying joints. Histopathology reveals palisaded granulomas surrounding an amorphous feathery material that corresponds to the urate crystals that were destroyed with formalin fixation (Figure 4). When the tissue is fixed with ethanol or is incompletely fixed in formalin, birefringent urate crystals are evident with polarization.²⁰

The Diagnosis: Kaposi Sarcoma 

On initial presentation, the differential diagnosis included secondary syphilis, Kaposi sarcoma (KS), lichen planus pigmentosus, sarcoidosis, and psoriasis. A laboratory workup was ordered, which included complete blood cell count, comprehensive metabolic panel, antinuclear antibodies, anti-Ro/Sjögren syndrome antigen A and anti-La/Sjögren syndrome antigen B autoantibodies, angiotensin-converting enzyme, rapid plasma reagin, and human immunodeficiency virus (HIV) antibodies. A 4-mm punch biopsy of the rash also was performed from the right upper back. Histology revealed a vascular proliferation that was diffusely positive for human herpesvirus 8 (HHV-8)(Figure 1). The patient was informed of the diagnosis, at which time he revealed he had a history of homosexual relationships, with his last sexual contact being more than 1 year prior to presentation. The laboratory workup confirmed a diagnosis of HIV, and the remainder of the tests were unremarkable. 

He was referred to our university's HIV clinic where he was started on highly active antiretroviral therapy (HAART). His facial swelling worsened, leading to hospital admission. Computed tomography (CT) of the chest, abdomen, and pelvis showed diffuse lymphadenopathy and lung nodules concerning for visceral involvement of KS. Hematology and oncology was consulted for further evaluation, and he was treated with 6 cycles of doxorubicin 20 mg/m², which led to resolution of the lung nodules on CT and improvement of the rash burden. He was then started on alitretinoin gel 0.1% twice daily, which led to continued slow improvement (Figure 2). 

Kaposi sarcoma is a vascular neoplasm that occurs from infection with HHV-8. It typically presents as painless, reddish to violaceous macules or patches involving the skin and mucosa that often progress to plaques or nodules with possible visceral involvement. Kaposi sarcoma is classified into 4 subtypes based on epidemiology and clinical presentation: classic, endemic, iatrogenic, and AIDS associated.^1,2  

Classic KS primarily affects elderly males of Mediterranean or Eastern European descent, with a mean age of 64.¹ years and a male to female ratio of 3 to 1. It has an indolent course and a strong predilection for the skin of the lower extremities. The endemic form occurs mainly in Africa and has a more aggressive course, especially the lymphadenopathic type that affects children younger than 10 years.³ Iatrogenic KS develops in immunosuppressed patients, such as transplant recipients, and may regress if the immunosuppressive agent is stopped.¹ Kaposi sarcoma is an AIDS-defining illness and is the most common malignancy in AIDS patients. It is strongly associated with a low CD4 count, which accounts for the notable decline in its incidence after the widespread introduction of HAART.¹ Among HIV patients, KS has the highest incidence in men who have sex with men. This population has a higher seroprevalence of HHV-8, which suggests possible sexual transmission of HHV-8. AIDS-associated KS most commonly involves the lower extremities, face, and oral mucosa. It may have visceral involvement, particularly of the gastrointestinal and respiratory systems, which carries a poor prognosis.^4,5 

Approximately 40% of patients presenting with KS have gastrointestinal tract involvement.⁶ Of these patients, up to 80% are asymptomatic, with diagnosis usually being made on endoscopy.⁷ In contrast, pulmonary KS is less common and typically is symptomatic. It can involve the lung parenchyma, airways, or pleura and is diagnosed by chest radiography or CT scans. Glucocorticoid therapy is a known trigger for pulmonary KS exacerbation.⁸  

All 4 subtypes share the same histopathologic findings consisting of spindled endothelial cell proliferation, inflammation, and angiogenesis. Immunohistochemistry reveals tumor cells that are CD34 and CD31 positive but are factor VIII negative. Staining for HHV-8 antigen is used to confirm the diagnosis. The inflammatory infiltrate predominantly is lymphocytic with scattered plasma cells.⁹  

The laboratory results and histopathologic findings clearly indicated a diagnosis of KS in our patient. Other entities in the clinical differential would have shown notably different histopathologic findings and laboratory results. Lichen planus pigmentosus displays a lichenoid infiltrate and pigment dropout on histology. Histologic findings of psoriasis include psoriasiform acanthosis, dilated vessels in the dermal papillae, thinning of suprapapillary plates, and neutrophilic microabscesses. Sarcoidosis would demonstrate naked granulomas on histopathology. Syphilis displays variable but often psoriasiform or lichenoid findings on histology, and a positive rapid plasma reagin also would be noted.  

First-line treatment of AIDS-related KS is HAART. For patients with severe and rapidly progressive KS or with visceral involvement, cytotoxic chemotherapy with doxorubicin or taxanes often is required. Additional therapies include radiotherapy, topical alitretinoin, and cryotherapy.^1,10 

The Diagnosis: Kaposi Sarcoma 

On initial presentation, the differential diagnosis included secondary syphilis, Kaposi sarcoma (KS), lichen planus pigmentosus, sarcoidosis, and psoriasis. A laboratory workup was ordered, which included complete blood cell count, comprehensive metabolic panel, antinuclear antibodies, anti-Ro/Sjögren syndrome antigen A and anti-La/Sjögren syndrome antigen B autoantibodies, angiotensin-converting enzyme, rapid plasma reagin, and human immunodeficiency virus (HIV) antibodies. A 4-mm punch biopsy of the rash also was performed from the right upper back. Histology revealed a vascular proliferation that was diffusely positive for human herpesvirus 8 (HHV-8)(Figure 1). The patient was informed of the diagnosis, at which time he revealed he had a history of homosexual relationships, with his last sexual contact being more than 1 year prior to presentation. The laboratory workup confirmed a diagnosis of HIV, and the remainder of the tests were unremarkable. 

He was referred to our university's HIV clinic where he was started on highly active antiretroviral therapy (HAART). His facial swelling worsened, leading to hospital admission. Computed tomography (CT) of the chest, abdomen, and pelvis showed diffuse lymphadenopathy and lung nodules concerning for visceral involvement of KS. Hematology and oncology was consulted for further evaluation, and he was treated with 6 cycles of doxorubicin 20 mg/m², which led to resolution of the lung nodules on CT and improvement of the rash burden. He was then started on alitretinoin gel 0.1% twice daily, which led to continued slow improvement (Figure 2). 

Kaposi sarcoma is a vascular neoplasm that occurs from infection with HHV-8. It typically presents as painless, reddish to violaceous macules or patches involving the skin and mucosa that often progress to plaques or nodules with possible visceral involvement. Kaposi sarcoma is classified into 4 subtypes based on epidemiology and clinical presentation: classic, endemic, iatrogenic, and AIDS associated.^1,2  

Classic KS primarily affects elderly males of Mediterranean or Eastern European descent, with a mean age of 64.¹ years and a male to female ratio of 3 to 1. It has an indolent course and a strong predilection for the skin of the lower extremities. The endemic form occurs mainly in Africa and has a more aggressive course, especially the lymphadenopathic type that affects children younger than 10 years.³ Iatrogenic KS develops in immunosuppressed patients, such as transplant recipients, and may regress if the immunosuppressive agent is stopped.¹ Kaposi sarcoma is an AIDS-defining illness and is the most common malignancy in AIDS patients. It is strongly associated with a low CD4 count, which accounts for the notable decline in its incidence after the widespread introduction of HAART.¹ Among HIV patients, KS has the highest incidence in men who have sex with men. This population has a higher seroprevalence of HHV-8, which suggests possible sexual transmission of HHV-8. AIDS-associated KS most commonly involves the lower extremities, face, and oral mucosa. It may have visceral involvement, particularly of the gastrointestinal and respiratory systems, which carries a poor prognosis.^4,5 

Approximately 40% of patients presenting with KS have gastrointestinal tract involvement.⁶ Of these patients, up to 80% are asymptomatic, with diagnosis usually being made on endoscopy.⁷ In contrast, pulmonary KS is less common and typically is symptomatic. It can involve the lung parenchyma, airways, or pleura and is diagnosed by chest radiography or CT scans. Glucocorticoid therapy is a known trigger for pulmonary KS exacerbation.⁸  

All 4 subtypes share the same histopathologic findings consisting of spindled endothelial cell proliferation, inflammation, and angiogenesis. Immunohistochemistry reveals tumor cells that are CD34 and CD31 positive but are factor VIII negative. Staining for HHV-8 antigen is used to confirm the diagnosis. The inflammatory infiltrate predominantly is lymphocytic with scattered plasma cells.⁹  

The laboratory results and histopathologic findings clearly indicated a diagnosis of KS in our patient. Other entities in the clinical differential would have shown notably different histopathologic findings and laboratory results. Lichen planus pigmentosus displays a lichenoid infiltrate and pigment dropout on histology. Histologic findings of psoriasis include psoriasiform acanthosis, dilated vessels in the dermal papillae, thinning of suprapapillary plates, and neutrophilic microabscesses. Sarcoidosis would demonstrate naked granulomas on histopathology. Syphilis displays variable but often psoriasiform or lichenoid findings on histology, and a positive rapid plasma reagin also would be noted.  

First-line treatment of AIDS-related KS is HAART. For patients with severe and rapidly progressive KS or with visceral involvement, cytotoxic chemotherapy with doxorubicin or taxanes often is required. Additional therapies include radiotherapy, topical alitretinoin, and cryotherapy.^1,10 

The Diagnosis: Kaposi Sarcoma 

On initial presentation, the differential diagnosis included secondary syphilis, Kaposi sarcoma (KS), lichen planus pigmentosus, sarcoidosis, and psoriasis. A laboratory workup was ordered, which included complete blood cell count, comprehensive metabolic panel, antinuclear antibodies, anti-Ro/Sjögren syndrome antigen A and anti-La/Sjögren syndrome antigen B autoantibodies, angiotensin-converting enzyme, rapid plasma reagin, and human immunodeficiency virus (HIV) antibodies. A 4-mm punch biopsy of the rash also was performed from the right upper back. Histology revealed a vascular proliferation that was diffusely positive for human herpesvirus 8 (HHV-8)(Figure 1). The patient was informed of the diagnosis, at which time he revealed he had a history of homosexual relationships, with his last sexual contact being more than 1 year prior to presentation. The laboratory workup confirmed a diagnosis of HIV, and the remainder of the tests were unremarkable. 

He was referred to our university's HIV clinic where he was started on highly active antiretroviral therapy (HAART). His facial swelling worsened, leading to hospital admission. Computed tomography (CT) of the chest, abdomen, and pelvis showed diffuse lymphadenopathy and lung nodules concerning for visceral involvement of KS. Hematology and oncology was consulted for further evaluation, and he was treated with 6 cycles of doxorubicin 20 mg/m², which led to resolution of the lung nodules on CT and improvement of the rash burden. He was then started on alitretinoin gel 0.1% twice daily, which led to continued slow improvement (Figure 2). 

Kaposi sarcoma is a vascular neoplasm that occurs from infection with HHV-8. It typically presents as painless, reddish to violaceous macules or patches involving the skin and mucosa that often progress to plaques or nodules with possible visceral involvement. Kaposi sarcoma is classified into 4 subtypes based on epidemiology and clinical presentation: classic, endemic, iatrogenic, and AIDS associated.^1,2  

Classic KS primarily affects elderly males of Mediterranean or Eastern European descent, with a mean age of 64.¹ years and a male to female ratio of 3 to 1. It has an indolent course and a strong predilection for the skin of the lower extremities. The endemic form occurs mainly in Africa and has a more aggressive course, especially the lymphadenopathic type that affects children younger than 10 years.³ Iatrogenic KS develops in immunosuppressed patients, such as transplant recipients, and may regress if the immunosuppressive agent is stopped.¹ Kaposi sarcoma is an AIDS-defining illness and is the most common malignancy in AIDS patients. It is strongly associated with a low CD4 count, which accounts for the notable decline in its incidence after the widespread introduction of HAART.¹ Among HIV patients, KS has the highest incidence in men who have sex with men. This population has a higher seroprevalence of HHV-8, which suggests possible sexual transmission of HHV-8. AIDS-associated KS most commonly involves the lower extremities, face, and oral mucosa. It may have visceral involvement, particularly of the gastrointestinal and respiratory systems, which carries a poor prognosis.^4,5 

Approximately 40% of patients presenting with KS have gastrointestinal tract involvement.⁶ Of these patients, up to 80% are asymptomatic, with diagnosis usually being made on endoscopy.⁷ In contrast, pulmonary KS is less common and typically is symptomatic. It can involve the lung parenchyma, airways, or pleura and is diagnosed by chest radiography or CT scans. Glucocorticoid therapy is a known trigger for pulmonary KS exacerbation.⁸  

All 4 subtypes share the same histopathologic findings consisting of spindled endothelial cell proliferation, inflammation, and angiogenesis. Immunohistochemistry reveals tumor cells that are CD34 and CD31 positive but are factor VIII negative. Staining for HHV-8 antigen is used to confirm the diagnosis. The inflammatory infiltrate predominantly is lymphocytic with scattered plasma cells.⁹  

The laboratory results and histopathologic findings clearly indicated a diagnosis of KS in our patient. Other entities in the clinical differential would have shown notably different histopathologic findings and laboratory results. Lichen planus pigmentosus displays a lichenoid infiltrate and pigment dropout on histology. Histologic findings of psoriasis include psoriasiform acanthosis, dilated vessels in the dermal papillae, thinning of suprapapillary plates, and neutrophilic microabscesses. Sarcoidosis would demonstrate naked granulomas on histopathology. Syphilis displays variable but often psoriasiform or lichenoid findings on histology, and a positive rapid plasma reagin also would be noted.  

First-line treatment of AIDS-related KS is HAART. For patients with severe and rapidly progressive KS or with visceral involvement, cytotoxic chemotherapy with doxorubicin or taxanes often is required. Additional therapies include radiotherapy, topical alitretinoin, and cryotherapy.^1,10 

The Diagnosis: Warty Dyskeratoma 

Warty dyskeratoma (WD) is a benign cutaneous tumor that was first described in 1954 as isolated Darier disease (DD). In 1957, Szymanski¹ renamed it warty dyskeratoma as a distinct condition from DD. Warty dyskeratoma typically presents as a flesh-colored to brownish, round, well-demarcated, and slightly elevated papule or nodule accompanied by an umbilical invagination at the center. It most commonly arises on the scalp, face, or neck.² In contrast to DD, familial occurrence is uncommon. It usually is difficult to distinguish WD from other conditions such as seborrheic keratosis, verruca vulgaris, or keratoacanthoma due to its macroscopic features. Therefore, histopathologic investigation is necessary for a precise diagnosis. 

In our case, histologic investigation revealed a symmetric cup-shaped invagination filled with acantholytic and dyskeratotic keratinocytes with no atypia or mitotic figures (Figure, A). The bottom of the invagination was occupied with numerous villi covered by a single layer of basal cells (Figure, B). At the edge of the invagination, corps ronds and grains were observed in the granular and cornified layers, respectively (Figure, C).

The hallmark histopathologic findings are acantholysis and dyskeratosis just above the basal cell layer, called focal acantholytic dyskeratosis. The differential diagnosis includes other disorders associated with focal acantholytic dyskeratosis, such as DD and acantholytic squamous cell carcinoma.³ Distinguishing WD from DD may be difficult in rare cases with multiple lesions.⁴ In such cases, an autosomal-dominant inheritance pattern and younger age of onset should prompt clinicians to seek for mutations in the ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 gene, ATP2A2, for the diagnosis of DD.⁵ Additionally, the presence of atypia or mitotic figures will rule out malignant disorders such as squamous cell carcinoma.  

Although the pathogenesis of WD is not fully understood, most clinicians consider it a follicular adnexal neoplasm because the lesions often are connected to the pilosebaceous unit on microscopic observation.⁶ Although WD-like lesions arising from the oral mucosa have been reported,⁷ their etiology may be different from WD because the oral mucosa lacks hair follicles.⁸ The term warty leads to speculation of the contribution of human papillomavirus to the pathogenesis of WD, but this has been questioned due to the negative result of viral DNA detection from WD lesions by polymerase chain reaction analysis.² Therefore, the term follicular dyskeratoma has been suggested as a novel denomination that reflects its etiology more precisely.²  

The efficacy of topical treatment has not yet been established. Cryosurgery is another therapeutic option, but it sometimes fails.⁹ As performed in our patient, excisional biopsy is the most reasonable treatment option to obtain both complete removal and precise diagnosis.  
 

The Diagnosis: Warty Dyskeratoma 

Warty dyskeratoma (WD) is a benign cutaneous tumor that was first described in 1954 as isolated Darier disease (DD). In 1957, Szymanski¹ renamed it warty dyskeratoma as a distinct condition from DD. Warty dyskeratoma typically presents as a flesh-colored to brownish, round, well-demarcated, and slightly elevated papule or nodule accompanied by an umbilical invagination at the center. It most commonly arises on the scalp, face, or neck.² In contrast to DD, familial occurrence is uncommon. It usually is difficult to distinguish WD from other conditions such as seborrheic keratosis, verruca vulgaris, or keratoacanthoma due to its macroscopic features. Therefore, histopathologic investigation is necessary for a precise diagnosis. 

In our case, histologic investigation revealed a symmetric cup-shaped invagination filled with acantholytic and dyskeratotic keratinocytes with no atypia or mitotic figures (Figure, A). The bottom of the invagination was occupied with numerous villi covered by a single layer of basal cells (Figure, B). At the edge of the invagination, corps ronds and grains were observed in the granular and cornified layers, respectively (Figure, C).

The hallmark histopathologic findings are acantholysis and dyskeratosis just above the basal cell layer, called focal acantholytic dyskeratosis. The differential diagnosis includes other disorders associated with focal acantholytic dyskeratosis, such as DD and acantholytic squamous cell carcinoma.³ Distinguishing WD from DD may be difficult in rare cases with multiple lesions.⁴ In such cases, an autosomal-dominant inheritance pattern and younger age of onset should prompt clinicians to seek for mutations in the ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 gene, ATP2A2, for the diagnosis of DD.⁵ Additionally, the presence of atypia or mitotic figures will rule out malignant disorders such as squamous cell carcinoma.  

Although the pathogenesis of WD is not fully understood, most clinicians consider it a follicular adnexal neoplasm because the lesions often are connected to the pilosebaceous unit on microscopic observation.⁶ Although WD-like lesions arising from the oral mucosa have been reported,⁷ their etiology may be different from WD because the oral mucosa lacks hair follicles.⁸ The term warty leads to speculation of the contribution of human papillomavirus to the pathogenesis of WD, but this has been questioned due to the negative result of viral DNA detection from WD lesions by polymerase chain reaction analysis.² Therefore, the term follicular dyskeratoma has been suggested as a novel denomination that reflects its etiology more precisely.²  

The efficacy of topical treatment has not yet been established. Cryosurgery is another therapeutic option, but it sometimes fails.⁹ As performed in our patient, excisional biopsy is the most reasonable treatment option to obtain both complete removal and precise diagnosis.  
 

The Diagnosis: Warty Dyskeratoma 

Warty dyskeratoma (WD) is a benign cutaneous tumor that was first described in 1954 as isolated Darier disease (DD). In 1957, Szymanski¹ renamed it warty dyskeratoma as a distinct condition from DD. Warty dyskeratoma typically presents as a flesh-colored to brownish, round, well-demarcated, and slightly elevated papule or nodule accompanied by an umbilical invagination at the center. It most commonly arises on the scalp, face, or neck.² In contrast to DD, familial occurrence is uncommon. It usually is difficult to distinguish WD from other conditions such as seborrheic keratosis, verruca vulgaris, or keratoacanthoma due to its macroscopic features. Therefore, histopathologic investigation is necessary for a precise diagnosis. 

In our case, histologic investigation revealed a symmetric cup-shaped invagination filled with acantholytic and dyskeratotic keratinocytes with no atypia or mitotic figures (Figure, A). The bottom of the invagination was occupied with numerous villi covered by a single layer of basal cells (Figure, B). At the edge of the invagination, corps ronds and grains were observed in the granular and cornified layers, respectively (Figure, C).

The hallmark histopathologic findings are acantholysis and dyskeratosis just above the basal cell layer, called focal acantholytic dyskeratosis. The differential diagnosis includes other disorders associated with focal acantholytic dyskeratosis, such as DD and acantholytic squamous cell carcinoma.³ Distinguishing WD from DD may be difficult in rare cases with multiple lesions.⁴ In such cases, an autosomal-dominant inheritance pattern and younger age of onset should prompt clinicians to seek for mutations in the ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2 gene, ATP2A2, for the diagnosis of DD.⁵ Additionally, the presence of atypia or mitotic figures will rule out malignant disorders such as squamous cell carcinoma.  

Although the pathogenesis of WD is not fully understood, most clinicians consider it a follicular adnexal neoplasm because the lesions often are connected to the pilosebaceous unit on microscopic observation.⁶ Although WD-like lesions arising from the oral mucosa have been reported,⁷ their etiology may be different from WD because the oral mucosa lacks hair follicles.⁸ The term warty leads to speculation of the contribution of human papillomavirus to the pathogenesis of WD, but this has been questioned due to the negative result of viral DNA detection from WD lesions by polymerase chain reaction analysis.² Therefore, the term follicular dyskeratoma has been suggested as a novel denomination that reflects its etiology more precisely.²  

The efficacy of topical treatment has not yet been established. Cryosurgery is another therapeutic option, but it sometimes fails.⁹ As performed in our patient, excisional biopsy is the most reasonable treatment option to obtain both complete removal and precise diagnosis.  
 

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the most recently identified member of the zoonotic pathogens of coronaviruses. It caused an outbreak of pneumonia in December 2019 in Wuhan, China.¹ Among all related acute respiratory syndromes (SARS-CoV, Middle East respiratory syndrome coronavirus), SARS-CoV-2 remains to be the most infectious, has the highest potential for human transmission, and can eventually result in acute respiratory distress syndrome.^2,3

Only 15% of coronavirus disease 2019 (COVID-19) cases progress to pneumonia, and approximately 5% of these cases develop acute respiratory distress syndrome, septic shock, and/or multiple organ failure. The majority of cases only exhibit mild to moderate symptoms.^4,5 A wide array of skin manifestations in COVID-19 infection have been reported, including maculopapular eruptions, morbilliform rashes, urticaria, chickenpoxlike lesions, livedo reticularis, COVID toes, erythema multiforme, pityriasis rosea, and several other patterns.⁶ We report a case of herpes zoster (HZ) complication in a COVID-19–positive woman who was 27 weeks pregnant.

Case Report

A 36-year-old woman who was 27 weeks pregnant was referred by her obstetrician to the dermatology clinic. She presented with a low-grade fever and a vesicular painful rash. Physical examination revealed painful, itchy, dysesthetic papules and vesicles on the left side of the forehead along with mild edema of the left upper eyelid but no watering of the eye or photophobia. She reported episodes of fever (temperature, 38.9°C), fatigue, and myalgia over the last week. She had bouts of dyspnea and tachycardia that she thought were related to being in the late second trimester of pregnancy. The area surrounding the vesicular eruption was tender to touch. No dry cough or any gastrointestinal or urinary tract symptoms were noted. She reported a burning sensation when splashing water on the face or when exposed to air currents. One week following the initial symptoms, she experienced a painful vesicular rash along the upper left forehead (Figure) associated with eyelid edema. Oral and ocular mucosae were free of any presentations. She had no relevant history and had not experienced any complications during pregnancy. A diagnosis of HZ was made, and she was prescribed valacyclovir 1 g 3 times daily for 7 days, acetaminophen for the fever, and calamine lotion. We recommended COVID-19 testing based on her symptoms. A chest radiograph and a positive nasopharyngeal smear were consistent with COVID-19 infection. She reported via telephone follow-up 1 week after presentation that her skin condition had improved following the treatment course and that the vesicles eventually dried, leaving a crusting appearance after 5 to 7 days. Regarding her SARS-CoV-2 condition, her oxygen saturation was 95% at presentation; she self-quarantined at home; and she was treated with oseltamivir 75 mg orally every 12 hours for 5 days, azithromycin 500 mg orally daily, acetaminophen, and vitamin C. Electronic fetal heart rate monitoring and ultrasound examinations were performed to assess the condition of the fetus and were reported normal. At the time of writing this article, she was 32 weeks pregnant and tested negative to 2 consecutive nasopharyngeal swabs for COVID-19 and was in good general condition. She continued her pregnancy according to her obstetrician’s recommendations.

Comment

The incubation time of COVID-19 can be up to 14 days. Fever, dry cough, fatigue, and diarrhea have been speculated to be clinical symptoms; however, many cases may be asymptomatic. Aside from a medical or travel history at risk for COVID-19, diagnosis can be confirmed by detection of viral RNA by reverse transcriptase–polymerase chain reaction for nasopharyngeal swabs or bronchoalveolar fluid. Patients who are immunocompromised, older, or male or who have a history of cardiovascular conditions or debilitating chronic conditions are at an increased risk for severe disease and poor outcome compared to younger healthy individuals.⁷

The vesicular rash of COVID-19 has been reported to have different forms of presentation. A diffuse widespread pattern resembling hand-foot-and-mouth disease and a localized monomorphic pattern resembling chickenpox but with predilection to the trunk has been described.⁸

Physiologic changes in the immune and cardiopulmonary systems during pregnancy (eg, diaphragm elevation, increased oxygen consumption, edema of the respiratory tract mucosae) make pregnant women intolerant to hypoxia. The mortality rate of the 1918 influenza pandemic was 2.6% in the overall population but 37% among pregnant women.⁹ In 2009, pregnant women were reported to be at an increased risk for complications from the H1N1 influenza virus pandemic, with a higher estimated rate of hospital admission than the general population.¹⁰ In 2003, approximately 50% of pregnant women who received a diagnosis of SARS-CoV were admitted to the intensive care unit, approximately 33% of pregnant women with SARS-CoV required mechanical ventilation, and the mortality rate was as high as 25% for these women.¹¹ To date, data on the effects of COVID-19 in pregnancy are limited to small case series.^12-15

It was confirmed that COVID-19 infection is accompanied by a reduction in lymphocytes, monocytes, and eosinophils, along with a notable reduction of CD4/CD8 T cells, B cells, and natural killer cells. It was further revealed that nonsurvivor COVID-19 patients continued to show a decrease in lymphocyte counts along the course of their disease until death.^16-18

Different mechanisms for lymphocyte depletion and deficiency were speculated among COVID-19 patients and include direct lymphocyte death through coronavirus angiotensin-converting enzyme 2–lymphocyte-expressed receptors; direct damage to lymphatic organs, such as the thymus and spleen, but this theory needs to be further investigated; direct lymphocyte apoptosis mediated by tumor necrosis factor α, IL-6, and other proinflammatory cytokines; and direct inhibition of lymphocytes by metabolic upset, such as acidosis.^19,20

These causes may precipitate lymphopenia and impaired antiviral responses.²¹ It also has been postulated that the functional damage of CD4⁺ T cells may predispose patients with COVID-19 to severe disease.²² Such immune changes can render a patient more susceptible to developing shingles by reactivating varicella-zoster virus, which could be a sign of undiagnosed COVID-19 infection in younger age groups.

Two earlier reports discussed HZ among COVID-19–diagnosed patients. Shors²³ presented a case of a patient who developed varicella-zoster virus reactivation of the V2 dermatome during the course of COVID-19 infection. In addition, the patient developed severe acute herpetic neuralgia despite the early initiation of antiviral therapy.²³ Elsaie et al²⁴ described 2 cases of patients during the pandemic who first presented with HZ before later being diagnosed with COVID-19 infection.

New information and cutaneous manifestations possibly related to COVID-19 are emerging every day. We report a pregnant female presenting with HZ during the course of COVID-19 infection, which suggests that the clinical presentation of HZ at the time of the current pandemic, especially if associated with other signs of COVID-19 infection, should be carefully monitored and reported for further assessment.

Acknowledgment
The authors would like to thank all the health care workers who have been fighting COVID-19 in Egypt and worldwide.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the most recently identified member of the zoonotic pathogens of coronaviruses. It caused an outbreak of pneumonia in December 2019 in Wuhan, China.¹ Among all related acute respiratory syndromes (SARS-CoV, Middle East respiratory syndrome coronavirus), SARS-CoV-2 remains to be the most infectious, has the highest potential for human transmission, and can eventually result in acute respiratory distress syndrome.^2,3

Only 15% of coronavirus disease 2019 (COVID-19) cases progress to pneumonia, and approximately 5% of these cases develop acute respiratory distress syndrome, septic shock, and/or multiple organ failure. The majority of cases only exhibit mild to moderate symptoms.^4,5 A wide array of skin manifestations in COVID-19 infection have been reported, including maculopapular eruptions, morbilliform rashes, urticaria, chickenpoxlike lesions, livedo reticularis, COVID toes, erythema multiforme, pityriasis rosea, and several other patterns.⁶ We report a case of herpes zoster (HZ) complication in a COVID-19–positive woman who was 27 weeks pregnant.

Case Report

A 36-year-old woman who was 27 weeks pregnant was referred by her obstetrician to the dermatology clinic. She presented with a low-grade fever and a vesicular painful rash. Physical examination revealed painful, itchy, dysesthetic papules and vesicles on the left side of the forehead along with mild edema of the left upper eyelid but no watering of the eye or photophobia. She reported episodes of fever (temperature, 38.9°C), fatigue, and myalgia over the last week. She had bouts of dyspnea and tachycardia that she thought were related to being in the late second trimester of pregnancy. The area surrounding the vesicular eruption was tender to touch. No dry cough or any gastrointestinal or urinary tract symptoms were noted. She reported a burning sensation when splashing water on the face or when exposed to air currents. One week following the initial symptoms, she experienced a painful vesicular rash along the upper left forehead (Figure) associated with eyelid edema. Oral and ocular mucosae were free of any presentations. She had no relevant history and had not experienced any complications during pregnancy. A diagnosis of HZ was made, and she was prescribed valacyclovir 1 g 3 times daily for 7 days, acetaminophen for the fever, and calamine lotion. We recommended COVID-19 testing based on her symptoms. A chest radiograph and a positive nasopharyngeal smear were consistent with COVID-19 infection. She reported via telephone follow-up 1 week after presentation that her skin condition had improved following the treatment course and that the vesicles eventually dried, leaving a crusting appearance after 5 to 7 days. Regarding her SARS-CoV-2 condition, her oxygen saturation was 95% at presentation; she self-quarantined at home; and she was treated with oseltamivir 75 mg orally every 12 hours for 5 days, azithromycin 500 mg orally daily, acetaminophen, and vitamin C. Electronic fetal heart rate monitoring and ultrasound examinations were performed to assess the condition of the fetus and were reported normal. At the time of writing this article, she was 32 weeks pregnant and tested negative to 2 consecutive nasopharyngeal swabs for COVID-19 and was in good general condition. She continued her pregnancy according to her obstetrician’s recommendations.

Comment

The incubation time of COVID-19 can be up to 14 days. Fever, dry cough, fatigue, and diarrhea have been speculated to be clinical symptoms; however, many cases may be asymptomatic. Aside from a medical or travel history at risk for COVID-19, diagnosis can be confirmed by detection of viral RNA by reverse transcriptase–polymerase chain reaction for nasopharyngeal swabs or bronchoalveolar fluid. Patients who are immunocompromised, older, or male or who have a history of cardiovascular conditions or debilitating chronic conditions are at an increased risk for severe disease and poor outcome compared to younger healthy individuals.⁷

The vesicular rash of COVID-19 has been reported to have different forms of presentation. A diffuse widespread pattern resembling hand-foot-and-mouth disease and a localized monomorphic pattern resembling chickenpox but with predilection to the trunk has been described.⁸

Physiologic changes in the immune and cardiopulmonary systems during pregnancy (eg, diaphragm elevation, increased oxygen consumption, edema of the respiratory tract mucosae) make pregnant women intolerant to hypoxia. The mortality rate of the 1918 influenza pandemic was 2.6% in the overall population but 37% among pregnant women.⁹ In 2009, pregnant women were reported to be at an increased risk for complications from the H1N1 influenza virus pandemic, with a higher estimated rate of hospital admission than the general population.¹⁰ In 2003, approximately 50% of pregnant women who received a diagnosis of SARS-CoV were admitted to the intensive care unit, approximately 33% of pregnant women with SARS-CoV required mechanical ventilation, and the mortality rate was as high as 25% for these women.¹¹ To date, data on the effects of COVID-19 in pregnancy are limited to small case series.^12-15

It was confirmed that COVID-19 infection is accompanied by a reduction in lymphocytes, monocytes, and eosinophils, along with a notable reduction of CD4/CD8 T cells, B cells, and natural killer cells. It was further revealed that nonsurvivor COVID-19 patients continued to show a decrease in lymphocyte counts along the course of their disease until death.^16-18

Different mechanisms for lymphocyte depletion and deficiency were speculated among COVID-19 patients and include direct lymphocyte death through coronavirus angiotensin-converting enzyme 2–lymphocyte-expressed receptors; direct damage to lymphatic organs, such as the thymus and spleen, but this theory needs to be further investigated; direct lymphocyte apoptosis mediated by tumor necrosis factor α, IL-6, and other proinflammatory cytokines; and direct inhibition of lymphocytes by metabolic upset, such as acidosis.^19,20

These causes may precipitate lymphopenia and impaired antiviral responses.²¹ It also has been postulated that the functional damage of CD4⁺ T cells may predispose patients with COVID-19 to severe disease.²² Such immune changes can render a patient more susceptible to developing shingles by reactivating varicella-zoster virus, which could be a sign of undiagnosed COVID-19 infection in younger age groups.

Two earlier reports discussed HZ among COVID-19–diagnosed patients. Shors²³ presented a case of a patient who developed varicella-zoster virus reactivation of the V2 dermatome during the course of COVID-19 infection. In addition, the patient developed severe acute herpetic neuralgia despite the early initiation of antiviral therapy.²³ Elsaie et al²⁴ described 2 cases of patients during the pandemic who first presented with HZ before later being diagnosed with COVID-19 infection.

New information and cutaneous manifestations possibly related to COVID-19 are emerging every day. We report a pregnant female presenting with HZ during the course of COVID-19 infection, which suggests that the clinical presentation of HZ at the time of the current pandemic, especially if associated with other signs of COVID-19 infection, should be carefully monitored and reported for further assessment.

Acknowledgment
The authors would like to thank all the health care workers who have been fighting COVID-19 in Egypt and worldwide.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the most recently identified member of the zoonotic pathogens of coronaviruses. It caused an outbreak of pneumonia in December 2019 in Wuhan, China.¹ Among all related acute respiratory syndromes (SARS-CoV, Middle East respiratory syndrome coronavirus), SARS-CoV-2 remains to be the most infectious, has the highest potential for human transmission, and can eventually result in acute respiratory distress syndrome.^2,3

Only 15% of coronavirus disease 2019 (COVID-19) cases progress to pneumonia, and approximately 5% of these cases develop acute respiratory distress syndrome, septic shock, and/or multiple organ failure. The majority of cases only exhibit mild to moderate symptoms.^4,5 A wide array of skin manifestations in COVID-19 infection have been reported, including maculopapular eruptions, morbilliform rashes, urticaria, chickenpoxlike lesions, livedo reticularis, COVID toes, erythema multiforme, pityriasis rosea, and several other patterns.⁶ We report a case of herpes zoster (HZ) complication in a COVID-19–positive woman who was 27 weeks pregnant.

Case Report

A 36-year-old woman who was 27 weeks pregnant was referred by her obstetrician to the dermatology clinic. She presented with a low-grade fever and a vesicular painful rash. Physical examination revealed painful, itchy, dysesthetic papules and vesicles on the left side of the forehead along with mild edema of the left upper eyelid but no watering of the eye or photophobia. She reported episodes of fever (temperature, 38.9°C), fatigue, and myalgia over the last week. She had bouts of dyspnea and tachycardia that she thought were related to being in the late second trimester of pregnancy. The area surrounding the vesicular eruption was tender to touch. No dry cough or any gastrointestinal or urinary tract symptoms were noted. She reported a burning sensation when splashing water on the face or when exposed to air currents. One week following the initial symptoms, she experienced a painful vesicular rash along the upper left forehead (Figure) associated with eyelid edema. Oral and ocular mucosae were free of any presentations. She had no relevant history and had not experienced any complications during pregnancy. A diagnosis of HZ was made, and she was prescribed valacyclovir 1 g 3 times daily for 7 days, acetaminophen for the fever, and calamine lotion. We recommended COVID-19 testing based on her symptoms. A chest radiograph and a positive nasopharyngeal smear were consistent with COVID-19 infection. She reported via telephone follow-up 1 week after presentation that her skin condition had improved following the treatment course and that the vesicles eventually dried, leaving a crusting appearance after 5 to 7 days. Regarding her SARS-CoV-2 condition, her oxygen saturation was 95% at presentation; she self-quarantined at home; and she was treated with oseltamivir 75 mg orally every 12 hours for 5 days, azithromycin 500 mg orally daily, acetaminophen, and vitamin C. Electronic fetal heart rate monitoring and ultrasound examinations were performed to assess the condition of the fetus and were reported normal. At the time of writing this article, she was 32 weeks pregnant and tested negative to 2 consecutive nasopharyngeal swabs for COVID-19 and was in good general condition. She continued her pregnancy according to her obstetrician’s recommendations.

Comment

The incubation time of COVID-19 can be up to 14 days. Fever, dry cough, fatigue, and diarrhea have been speculated to be clinical symptoms; however, many cases may be asymptomatic. Aside from a medical or travel history at risk for COVID-19, diagnosis can be confirmed by detection of viral RNA by reverse transcriptase–polymerase chain reaction for nasopharyngeal swabs or bronchoalveolar fluid. Patients who are immunocompromised, older, or male or who have a history of cardiovascular conditions or debilitating chronic conditions are at an increased risk for severe disease and poor outcome compared to younger healthy individuals.⁷

The vesicular rash of COVID-19 has been reported to have different forms of presentation. A diffuse widespread pattern resembling hand-foot-and-mouth disease and a localized monomorphic pattern resembling chickenpox but with predilection to the trunk has been described.⁸

Physiologic changes in the immune and cardiopulmonary systems during pregnancy (eg, diaphragm elevation, increased oxygen consumption, edema of the respiratory tract mucosae) make pregnant women intolerant to hypoxia. The mortality rate of the 1918 influenza pandemic was 2.6% in the overall population but 37% among pregnant women.⁹ In 2009, pregnant women were reported to be at an increased risk for complications from the H1N1 influenza virus pandemic, with a higher estimated rate of hospital admission than the general population.¹⁰ In 2003, approximately 50% of pregnant women who received a diagnosis of SARS-CoV were admitted to the intensive care unit, approximately 33% of pregnant women with SARS-CoV required mechanical ventilation, and the mortality rate was as high as 25% for these women.¹¹ To date, data on the effects of COVID-19 in pregnancy are limited to small case series.^12-15

It was confirmed that COVID-19 infection is accompanied by a reduction in lymphocytes, monocytes, and eosinophils, along with a notable reduction of CD4/CD8 T cells, B cells, and natural killer cells. It was further revealed that nonsurvivor COVID-19 patients continued to show a decrease in lymphocyte counts along the course of their disease until death.^16-18

Different mechanisms for lymphocyte depletion and deficiency were speculated among COVID-19 patients and include direct lymphocyte death through coronavirus angiotensin-converting enzyme 2–lymphocyte-expressed receptors; direct damage to lymphatic organs, such as the thymus and spleen, but this theory needs to be further investigated; direct lymphocyte apoptosis mediated by tumor necrosis factor α, IL-6, and other proinflammatory cytokines; and direct inhibition of lymphocytes by metabolic upset, such as acidosis.^19,20

These causes may precipitate lymphopenia and impaired antiviral responses.²¹ It also has been postulated that the functional damage of CD4⁺ T cells may predispose patients with COVID-19 to severe disease.²² Such immune changes can render a patient more susceptible to developing shingles by reactivating varicella-zoster virus, which could be a sign of undiagnosed COVID-19 infection in younger age groups.

Two earlier reports discussed HZ among COVID-19–diagnosed patients. Shors²³ presented a case of a patient who developed varicella-zoster virus reactivation of the V2 dermatome during the course of COVID-19 infection. In addition, the patient developed severe acute herpetic neuralgia despite the early initiation of antiviral therapy.²³ Elsaie et al²⁴ described 2 cases of patients during the pandemic who first presented with HZ before later being diagnosed with COVID-19 infection.

New information and cutaneous manifestations possibly related to COVID-19 are emerging every day. We report a pregnant female presenting with HZ during the course of COVID-19 infection, which suggests that the clinical presentation of HZ at the time of the current pandemic, especially if associated with other signs of COVID-19 infection, should be carefully monitored and reported for further assessment.

Acknowledgment
The authors would like to thank all the health care workers who have been fighting COVID-19 in Egypt and worldwide.

Although physicians commit themselves to providing equitable treatment to all patients, significant disparities remain in the dermatologic care of Black patients, who constitute 13% of the US population, which continues to grow increasingly diverse.¹ Despite these changes in the population, the literature demonstrates that dermatologic training does not adequately focus on unique presentations of cutaneous pathology in the Black population.^2,3 Accordingly, medical students lack proper training in how skin disorders manifest in people of color. Compounding the problem, only 3% of dermatologists are Black, creating a cultural barrier that can compromise care for Black patients.^2,4 Racial disparities in dermatology training can compromise treatment, patient satisfaction, and outcomes.³

Issues in Medical Education Training and Resources

Lack of diversity in the resources used for dermatology training in medical schools affects diagnosis and treatment, as skin manifestations such as hypersensitivity reactions, rashes, and cancer can appear differently on different skin tones.⁵ A study of medical students’ ability to diagnose common dermatologic pathologies found that when trainees were presented with photographs of dark skin, their accuracy in identifying urticaria, squamous cell carcinoma, and even atopic dermatitis was reduced, despite these diseases being more prevalent in children of African American ancestry.^4,6

Dermatologic diseases also can have different distributions in different races; for example, on non–sun-exposed sites, squamous cell carcinoma in Black patients occurs at 8.5 times the frequency of White patients.⁷ Failure to identify diseases accurately due to insufficient training can have grave consequences for patients. Although skin cancer is less common in individuals with skin of color, it is associated with greater morbidity and mortality, in part due to delayed diagnosis.⁷

Inadequate research, reporting, and instruction on dermatologic findings in patients with darker complexions further compound racial disparities in dermatology. A 2006 study of the representation of darker skin in major dermatology educational resources found that only 2% of teaching events at American Academy of Dermatology annual meetings focused on skin of color. Furthermore, the study determined that many common diseases in patients with dark skin, such as acne vulgaris and pityriasis rosea, were completely absent or limited in dermatology textbooks.⁸

Impact on the Black Patient Experience

Patients’ therapeutic relationship with their physician also is damaged by limitations in training in diverse skin color. A study that assessed Black patients seen in a skin of color clinic (SOCC) compared to Black patients seen in a non-SOCC found that non-SOCC patients reported a lower degree of respect, dignity, understanding, and trust compared to the patients seen in a SOCC. Black patients expressed specific concerns about non-SOCC dermatologists’ knowledge of abnormalities that present in darker skin and Black hair.³ These findings are compounded by reports suggesting that, independent of care, structural racism contributes to dermatologic disease severity by influencing patient education level, household income, and degree of exposure to harmful environmental irritants.⁶

Racial disparities continue to be seen in the makeup of the universe of dermatologists and skin researchers. As of 2016, only 3% of dermatologists were Black, making dermatology one of the least diverse medical specialties.² Increasing the diversity of the dermatology workforce is important to improve patient satisfaction and treatment, both for minority and nonminority patients. Compared to race-discordant medical visits, race-concordant visits were shown to have a higher rate of satisfaction and better shared decision-making.⁹ Also, minority physicians are more likely to practice health care in areas that are traditionally underserved and to care for patients who do not have health insurance, making their participation essential in addressing some of the baseline disparities Black patients face in securing quality dermatologic care.¹

Structural Racism in Medicine

Changing dermatology training to ensure improved treatment of Black patients requires not only increased attention to differences in disease presentation but also heightened awareness of underlying genetic, environmental, and structural factors that contribute to the disease course.⁶ For example, there is evidence suggesting that structural racism in the form of residential segregation, lower socioeconomic status, and lower educational attainment contribute to disease severity in conditions such as atopic dermatitis. There is additional evidence suggesting that White patients are more readily offered therapeutic options than Black patients. A study of racial disparities in psoriasis treatment found that Black patients with moderate to severe psoriasis were 70% less likely to receive treatment with a biologic than White patients, independent of socioeconomic factors, comorbidities, and insurance plans.¹⁰

Moving Forward

Although research continues to underscore racial disparities in dermatology, some leaders in the field are actively combating these problems. A recent study that looked at representations of dark skin images in medical educational resources found far greater representation of dark pigmented skin in web-based resources than in traditional printed texts. Specifically, the online resource VisualDx (https://www.visualdx.com/) features 28.5% dark skin images compared to 10.3% (on average) in printed dermatology books.¹¹ There also is increasing public awareness of these issues, with organizations such as the Skin of Color Society (http://skinofcolorsociety.org/) helping to promote interest in racial disparities in dermatology. Physicians also have created textbooks and social media accounts focused on dermatologic manifestations in skin of color.¹² The Instagram account Brown Skin Matters (@brownskinmatters) has created a publicly accessible online resource where physicians and patients can see and post dermatologic diseases in skin of color.⁵

Final Thoughts

It is critical that physicians be trained to identify skin and hair manifestations of disease and disorders in Black patients. Training can be improved by including more images of skin manifestations in dark skin, both in medical school curricula and in new editions of dermatology textbooks. Training also must teach students about hair in Black individuals and how to properly treat it as well as related conditions of the hair and scalp.¹³ More research also is needed to better understand how dermatologists can improve the patient experience for Black patients. Residency programs must work to increase diversity among dermatology trainees.

Lastly, dermatology education should increasingly be supplemented with newer, web-based resources that show dermatologic manifestations across the spectrum of skin tones. Dermatology training must be adapted to better account for diverse patient populations and increase its focus on the systems that produce baseline disparities in disease morbidity and mortality.

Although physicians commit themselves to providing equitable treatment to all patients, significant disparities remain in the dermatologic care of Black patients, who constitute 13% of the US population, which continues to grow increasingly diverse.¹ Despite these changes in the population, the literature demonstrates that dermatologic training does not adequately focus on unique presentations of cutaneous pathology in the Black population.^2,3 Accordingly, medical students lack proper training in how skin disorders manifest in people of color. Compounding the problem, only 3% of dermatologists are Black, creating a cultural barrier that can compromise care for Black patients.^2,4 Racial disparities in dermatology training can compromise treatment, patient satisfaction, and outcomes.³

Issues in Medical Education Training and Resources

Lack of diversity in the resources used for dermatology training in medical schools affects diagnosis and treatment, as skin manifestations such as hypersensitivity reactions, rashes, and cancer can appear differently on different skin tones.⁵ A study of medical students’ ability to diagnose common dermatologic pathologies found that when trainees were presented with photographs of dark skin, their accuracy in identifying urticaria, squamous cell carcinoma, and even atopic dermatitis was reduced, despite these diseases being more prevalent in children of African American ancestry.^4,6

Dermatologic diseases also can have different distributions in different races; for example, on non–sun-exposed sites, squamous cell carcinoma in Black patients occurs at 8.5 times the frequency of White patients.⁷ Failure to identify diseases accurately due to insufficient training can have grave consequences for patients. Although skin cancer is less common in individuals with skin of color, it is associated with greater morbidity and mortality, in part due to delayed diagnosis.⁷

Inadequate research, reporting, and instruction on dermatologic findings in patients with darker complexions further compound racial disparities in dermatology. A 2006 study of the representation of darker skin in major dermatology educational resources found that only 2% of teaching events at American Academy of Dermatology annual meetings focused on skin of color. Furthermore, the study determined that many common diseases in patients with dark skin, such as acne vulgaris and pityriasis rosea, were completely absent or limited in dermatology textbooks.⁸

Impact on the Black Patient Experience

Patients’ therapeutic relationship with their physician also is damaged by limitations in training in diverse skin color. A study that assessed Black patients seen in a skin of color clinic (SOCC) compared to Black patients seen in a non-SOCC found that non-SOCC patients reported a lower degree of respect, dignity, understanding, and trust compared to the patients seen in a SOCC. Black patients expressed specific concerns about non-SOCC dermatologists’ knowledge of abnormalities that present in darker skin and Black hair.³ These findings are compounded by reports suggesting that, independent of care, structural racism contributes to dermatologic disease severity by influencing patient education level, household income, and degree of exposure to harmful environmental irritants.⁶

Racial disparities continue to be seen in the makeup of the universe of dermatologists and skin researchers. As of 2016, only 3% of dermatologists were Black, making dermatology one of the least diverse medical specialties.² Increasing the diversity of the dermatology workforce is important to improve patient satisfaction and treatment, both for minority and nonminority patients. Compared to race-discordant medical visits, race-concordant visits were shown to have a higher rate of satisfaction and better shared decision-making.⁹ Also, minority physicians are more likely to practice health care in areas that are traditionally underserved and to care for patients who do not have health insurance, making their participation essential in addressing some of the baseline disparities Black patients face in securing quality dermatologic care.¹

Structural Racism in Medicine

Changing dermatology training to ensure improved treatment of Black patients requires not only increased attention to differences in disease presentation but also heightened awareness of underlying genetic, environmental, and structural factors that contribute to the disease course.⁶ For example, there is evidence suggesting that structural racism in the form of residential segregation, lower socioeconomic status, and lower educational attainment contribute to disease severity in conditions such as atopic dermatitis. There is additional evidence suggesting that White patients are more readily offered therapeutic options than Black patients. A study of racial disparities in psoriasis treatment found that Black patients with moderate to severe psoriasis were 70% less likely to receive treatment with a biologic than White patients, independent of socioeconomic factors, comorbidities, and insurance plans.¹⁰

Moving Forward

Although research continues to underscore racial disparities in dermatology, some leaders in the field are actively combating these problems. A recent study that looked at representations of dark skin images in medical educational resources found far greater representation of dark pigmented skin in web-based resources than in traditional printed texts. Specifically, the online resource VisualDx (https://www.visualdx.com/) features 28.5% dark skin images compared to 10.3% (on average) in printed dermatology books.¹¹ There also is increasing public awareness of these issues, with organizations such as the Skin of Color Society (http://skinofcolorsociety.org/) helping to promote interest in racial disparities in dermatology. Physicians also have created textbooks and social media accounts focused on dermatologic manifestations in skin of color.¹² The Instagram account Brown Skin Matters (@brownskinmatters) has created a publicly accessible online resource where physicians and patients can see and post dermatologic diseases in skin of color.⁵

Final Thoughts

It is critical that physicians be trained to identify skin and hair manifestations of disease and disorders in Black patients. Training can be improved by including more images of skin manifestations in dark skin, both in medical school curricula and in new editions of dermatology textbooks. Training also must teach students about hair in Black individuals and how to properly treat it as well as related conditions of the hair and scalp.¹³ More research also is needed to better understand how dermatologists can improve the patient experience for Black patients. Residency programs must work to increase diversity among dermatology trainees.

Lastly, dermatology education should increasingly be supplemented with newer, web-based resources that show dermatologic manifestations across the spectrum of skin tones. Dermatology training must be adapted to better account for diverse patient populations and increase its focus on the systems that produce baseline disparities in disease morbidity and mortality.

Although physicians commit themselves to providing equitable treatment to all patients, significant disparities remain in the dermatologic care of Black patients, who constitute 13% of the US population, which continues to grow increasingly diverse.¹ Despite these changes in the population, the literature demonstrates that dermatologic training does not adequately focus on unique presentations of cutaneous pathology in the Black population.^2,3 Accordingly, medical students lack proper training in how skin disorders manifest in people of color. Compounding the problem, only 3% of dermatologists are Black, creating a cultural barrier that can compromise care for Black patients.^2,4 Racial disparities in dermatology training can compromise treatment, patient satisfaction, and outcomes.³

Issues in Medical Education Training and Resources

Lack of diversity in the resources used for dermatology training in medical schools affects diagnosis and treatment, as skin manifestations such as hypersensitivity reactions, rashes, and cancer can appear differently on different skin tones.⁵ A study of medical students’ ability to diagnose common dermatologic pathologies found that when trainees were presented with photographs of dark skin, their accuracy in identifying urticaria, squamous cell carcinoma, and even atopic dermatitis was reduced, despite these diseases being more prevalent in children of African American ancestry.^4,6

Dermatologic diseases also can have different distributions in different races; for example, on non–sun-exposed sites, squamous cell carcinoma in Black patients occurs at 8.5 times the frequency of White patients.⁷ Failure to identify diseases accurately due to insufficient training can have grave consequences for patients. Although skin cancer is less common in individuals with skin of color, it is associated with greater morbidity and mortality, in part due to delayed diagnosis.⁷

Inadequate research, reporting, and instruction on dermatologic findings in patients with darker complexions further compound racial disparities in dermatology. A 2006 study of the representation of darker skin in major dermatology educational resources found that only 2% of teaching events at American Academy of Dermatology annual meetings focused on skin of color. Furthermore, the study determined that many common diseases in patients with dark skin, such as acne vulgaris and pityriasis rosea, were completely absent or limited in dermatology textbooks.⁸

Impact on the Black Patient Experience

Patients’ therapeutic relationship with their physician also is damaged by limitations in training in diverse skin color. A study that assessed Black patients seen in a skin of color clinic (SOCC) compared to Black patients seen in a non-SOCC found that non-SOCC patients reported a lower degree of respect, dignity, understanding, and trust compared to the patients seen in a SOCC. Black patients expressed specific concerns about non-SOCC dermatologists’ knowledge of abnormalities that present in darker skin and Black hair.³ These findings are compounded by reports suggesting that, independent of care, structural racism contributes to dermatologic disease severity by influencing patient education level, household income, and degree of exposure to harmful environmental irritants.⁶

Racial disparities continue to be seen in the makeup of the universe of dermatologists and skin researchers. As of 2016, only 3% of dermatologists were Black, making dermatology one of the least diverse medical specialties.² Increasing the diversity of the dermatology workforce is important to improve patient satisfaction and treatment, both for minority and nonminority patients. Compared to race-discordant medical visits, race-concordant visits were shown to have a higher rate of satisfaction and better shared decision-making.⁹ Also, minority physicians are more likely to practice health care in areas that are traditionally underserved and to care for patients who do not have health insurance, making their participation essential in addressing some of the baseline disparities Black patients face in securing quality dermatologic care.¹

Structural Racism in Medicine

Changing dermatology training to ensure improved treatment of Black patients requires not only increased attention to differences in disease presentation but also heightened awareness of underlying genetic, environmental, and structural factors that contribute to the disease course.⁶ For example, there is evidence suggesting that structural racism in the form of residential segregation, lower socioeconomic status, and lower educational attainment contribute to disease severity in conditions such as atopic dermatitis. There is additional evidence suggesting that White patients are more readily offered therapeutic options than Black patients. A study of racial disparities in psoriasis treatment found that Black patients with moderate to severe psoriasis were 70% less likely to receive treatment with a biologic than White patients, independent of socioeconomic factors, comorbidities, and insurance plans.¹⁰

Moving Forward

Although research continues to underscore racial disparities in dermatology, some leaders in the field are actively combating these problems. A recent study that looked at representations of dark skin images in medical educational resources found far greater representation of dark pigmented skin in web-based resources than in traditional printed texts. Specifically, the online resource VisualDx (https://www.visualdx.com/) features 28.5% dark skin images compared to 10.3% (on average) in printed dermatology books.¹¹ There also is increasing public awareness of these issues, with organizations such as the Skin of Color Society (http://skinofcolorsociety.org/) helping to promote interest in racial disparities in dermatology. Physicians also have created textbooks and social media accounts focused on dermatologic manifestations in skin of color.¹² The Instagram account Brown Skin Matters (@brownskinmatters) has created a publicly accessible online resource where physicians and patients can see and post dermatologic diseases in skin of color.⁵

Final Thoughts

It is critical that physicians be trained to identify skin and hair manifestations of disease and disorders in Black patients. Training can be improved by including more images of skin manifestations in dark skin, both in medical school curricula and in new editions of dermatology textbooks. Training also must teach students about hair in Black individuals and how to properly treat it as well as related conditions of the hair and scalp.¹³ More research also is needed to better understand how dermatologists can improve the patient experience for Black patients. Residency programs must work to increase diversity among dermatology trainees.

Lastly, dermatology education should increasingly be supplemented with newer, web-based resources that show dermatologic manifestations across the spectrum of skin tones. Dermatology training must be adapted to better account for diverse patient populations and increase its focus on the systems that produce baseline disparities in disease morbidity and mortality.

To the Editor:

Onychomycosis is the most common nail disorder, affecting approximately 5.5% of the world’s population.¹ There are a limited number of topical and systemic therapies approved by the US Food and Drug Administration (FDA), but no consensus guidelines exist for the management of onychomycosis. Therefore, we hypothesized that prescribing patterns would vary among different groups.

We examined data from the Centers for Medicare & Medicaid Services’ Part D Prescriber Public Use Files for 2013 to 2016.² Prescribing patterns were assessed for dermatologists, nurse practitioners, physician assistants, and podiatrists prescribing systemic (ie, terbinafine, itraconazole) or topical (ie, efinaconazole, tavaborole, ciclopirox) therapies. A cut-off of systemic therapy lasting 84 days or more (reflecting FDA-approved treatment regimens for toenail onychomycosis) was used to exclude prescriptions for other fungal conditions that require shorter treatment courses. Statistical analysis with χ² tests identified differences among specialties’ prescribing patterns.

Overall, onychomycosis medications accounted for $85.4 million in expenditures from 2013 to 2016, with spending increasing at a rate of 21.2% annually (Table 1). The greatest single-year increase was observed from 2014 to 2015, with a 40.6% surge in overall expenditures for onychomycosis medications—increasing from $17.8 million to $25.0 million in spending. Dermatologists’ prescriptions accounted for 14.8% of all claims for onychomycosis medications and 18.3% of total expenditures during the study period, totaling $15.7 million in costs. Dermatologists’ claims increased at a rate of 7.4% annually, while expenditures increased at 15.4% annually. A greater proportion of dermatologists (96.4%) prescribed topicals for onychomycosis relative to nurse practitioners (90.2%) and podiatrists (91.3%)(P<.01)(Table 2). No significant difference was observed in the prescribing patterns of dermatologists and physician assistants (P=.99).

Ciclopirox is the most commonly prescribed therapy for onychomycosis across all groups, prescribed by more than 88% of prescribers in all studied specialties. Although ciclopirox is one of the least expensive treatment options available for onychomycosis, it has the lowest relative cure rate.⁵ Onychomycosis management requires understanding of drug efficacy and disease severity.⁶ Inappropriate treatment selection may result in prolonged treatment courses and increased costs. Consensus guidelines for onychomycosis therapies across specialties may yield more cost-effective treatment for this common nail condition.

Acknowledgment
The authors thank Paul J. Christos, DrPH, MS (New York, New York), for his advisement regarding statistical analysis for this manuscript.

To the Editor:

Onychomycosis is the most common nail disorder, affecting approximately 5.5% of the world’s population.¹ There are a limited number of topical and systemic therapies approved by the US Food and Drug Administration (FDA), but no consensus guidelines exist for the management of onychomycosis. Therefore, we hypothesized that prescribing patterns would vary among different groups.

We examined data from the Centers for Medicare & Medicaid Services’ Part D Prescriber Public Use Files for 2013 to 2016.² Prescribing patterns were assessed for dermatologists, nurse practitioners, physician assistants, and podiatrists prescribing systemic (ie, terbinafine, itraconazole) or topical (ie, efinaconazole, tavaborole, ciclopirox) therapies. A cut-off of systemic therapy lasting 84 days or more (reflecting FDA-approved treatment regimens for toenail onychomycosis) was used to exclude prescriptions for other fungal conditions that require shorter treatment courses. Statistical analysis with χ² tests identified differences among specialties’ prescribing patterns.

Overall, onychomycosis medications accounted for $85.4 million in expenditures from 2013 to 2016, with spending increasing at a rate of 21.2% annually (Table 1). The greatest single-year increase was observed from 2014 to 2015, with a 40.6% surge in overall expenditures for onychomycosis medications—increasing from $17.8 million to $25.0 million in spending. Dermatologists’ prescriptions accounted for 14.8% of all claims for onychomycosis medications and 18.3% of total expenditures during the study period, totaling $15.7 million in costs. Dermatologists’ claims increased at a rate of 7.4% annually, while expenditures increased at 15.4% annually. A greater proportion of dermatologists (96.4%) prescribed topicals for onychomycosis relative to nurse practitioners (90.2%) and podiatrists (91.3%)(P<.01)(Table 2). No significant difference was observed in the prescribing patterns of dermatologists and physician assistants (P=.99).

Ciclopirox is the most commonly prescribed therapy for onychomycosis across all groups, prescribed by more than 88% of prescribers in all studied specialties. Although ciclopirox is one of the least expensive treatment options available for onychomycosis, it has the lowest relative cure rate.⁵ Onychomycosis management requires understanding of drug efficacy and disease severity.⁶ Inappropriate treatment selection may result in prolonged treatment courses and increased costs. Consensus guidelines for onychomycosis therapies across specialties may yield more cost-effective treatment for this common nail condition.

Acknowledgment
The authors thank Paul J. Christos, DrPH, MS (New York, New York), for his advisement regarding statistical analysis for this manuscript.

To the Editor:

Onychomycosis is the most common nail disorder, affecting approximately 5.5% of the world’s population.¹ There are a limited number of topical and systemic therapies approved by the US Food and Drug Administration (FDA), but no consensus guidelines exist for the management of onychomycosis. Therefore, we hypothesized that prescribing patterns would vary among different groups.

We examined data from the Centers for Medicare & Medicaid Services’ Part D Prescriber Public Use Files for 2013 to 2016.² Prescribing patterns were assessed for dermatologists, nurse practitioners, physician assistants, and podiatrists prescribing systemic (ie, terbinafine, itraconazole) or topical (ie, efinaconazole, tavaborole, ciclopirox) therapies. A cut-off of systemic therapy lasting 84 days or more (reflecting FDA-approved treatment regimens for toenail onychomycosis) was used to exclude prescriptions for other fungal conditions that require shorter treatment courses. Statistical analysis with χ² tests identified differences among specialties’ prescribing patterns.

Overall, onychomycosis medications accounted for $85.4 million in expenditures from 2013 to 2016, with spending increasing at a rate of 21.2% annually (Table 1). The greatest single-year increase was observed from 2014 to 2015, with a 40.6% surge in overall expenditures for onychomycosis medications—increasing from $17.8 million to $25.0 million in spending. Dermatologists’ prescriptions accounted for 14.8% of all claims for onychomycosis medications and 18.3% of total expenditures during the study period, totaling $15.7 million in costs. Dermatologists’ claims increased at a rate of 7.4% annually, while expenditures increased at 15.4% annually. A greater proportion of dermatologists (96.4%) prescribed topicals for onychomycosis relative to nurse practitioners (90.2%) and podiatrists (91.3%)(P<.01)(Table 2). No significant difference was observed in the prescribing patterns of dermatologists and physician assistants (P=.99).

Ciclopirox is the most commonly prescribed therapy for onychomycosis across all groups, prescribed by more than 88% of prescribers in all studied specialties. Although ciclopirox is one of the least expensive treatment options available for onychomycosis, it has the lowest relative cure rate.⁵ Onychomycosis management requires understanding of drug efficacy and disease severity.⁶ Inappropriate treatment selection may result in prolonged treatment courses and increased costs. Consensus guidelines for onychomycosis therapies across specialties may yield more cost-effective treatment for this common nail condition.

Acknowledgment
The authors thank Paul J. Christos, DrPH, MS (New York, New York), for his advisement regarding statistical analysis for this manuscript.

We are in unprecedented times. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is attacking our communities and, as with any battle, we face unexpected challenges from the global pandemic. What can dermatologists, as highly skilled health care experts, do to support the fight against coronavirus disease 2019 (COVID-19)?

In early 2020, I became involved in a fulfilling and stimulating opportunity to contribute as a US Navy reservist, having just returned from a 3-month deployment. I served in the Medical Operations Center aboard the hospital ship USNS Comfort, which was docked in New York Harbor, as liaison to surrounding New York City hospitals. I also served as sole dermatologist on the ship, caring for the dermatologic needs of our team and consulting on numerous COVID-19 inpatients.

In May 2020, upon return to Virginia from New York City, I served as senior medical officer to medically clear other Navy Reserve health care workers returning from the field hospital at the Jacob K. Javits Convention Center of New York and from serving as embedded caregivers in existing New York City hospitals. I share 2 very important observations from my work there: First, COVID-19 is devastatingly real; second, we dermatologists can be valuable team members in the fight against this disease.

It is normal for us to feel scared, confused, and helpless; as 1% of the physician population, dermatologists represent a small focused fraction of the health care force. Nevertheless, we are all well-trained medical professionals who have taken the same Hippocratic Oath as other physicians. As members of the global health care team, we can each play a role in defeating COVID-19: We can be a trusted voice of reason, set an example, implement safe and effective distancing and hygiene precautions, and assist our local overburdened medical teams.

The magnitude and severity of COVID-19 can create a mass casualty–type phenomenon, overwhelming health care systems if the disease curve is not flattened. We can help flatten that curve by lengthening the pulse duration (to use dermatology jargon): that is, slowing the abrupt impact of cases to allow health care systems to triage, treat, and discharge in a more controlled manner.

How We Can Make a Difference

Despite representing a fraction of the health care team, we see a larger percentage of the population. On the Comfort, for example, dermatology visits accounted for approximately 20% of outpatient crew visits. We have an opportunity and a voice to reach a large percentage of the population directly. Whether we are now seeing patients face-to-face or virtually, we can spread the public health message and set an example. Wearing masks and social distancing do help to slow and markedly decrease the spread of SARS-CoV-2.

When you see patients in your office, consider the following:

• Have patients wait outside the office in their car and call the receptionist upon arrival.

• Have the receptionist call back the patient when the office is ready.

• Prescreen the patient before having him/her enter the clinic.

• Do not allow handshaking.

• Require everyone to wear a mask.

• Wear gloves.

• Have ample hand sanitizer openly available for all.

• Thoroughly clean or disinfect surfaces between patients.

Recalling the Difficult Experience of a Colleague-Patient

I think back to a crew member of Comfort who presented with new-onset pruritus and erythematous papules on the arms, legs, and torso. She was an intensive care unit nurse working 13-hour days, every day, for weeks on a COVID-positive unit—double-masked, gowned, wearing eye protection, in a warmer than usual intensive care unit, managing the most critically ill patients she’s ever cared for. Outside work, her life consisted of a commute on a government-chartered bus between Comfort and a contracted hotel while eating boxed meals. For 6 hours daily, she would—unsuccessfully—attempt to sleep with raging pruritus. Treating this routine case of eczema had a domino effect, improving her quality of life and thus allowing her to provide better care for the critically ill.

Let Us All Join in the Fight

As well-educated medical experts, we have the ability and the opportunity to reach outside our comfort zone and assist our medical colleagues. As I saw in New York City, the spectrum of specialists bravely worked together to meet overwhelming demand on the health care system and care for thousands of critically ill and dying patients. Dermatologists treated extensive eczema, ulcers, and other dermatoses on caretakers; triaged patients for appropriate allocation of care; and delivered care outside their comfort zone as physician extenders on inpatient and critical care units.

We are all in this together. I encourage all dermatologists who are in an area of need to ask your health care system how you can join the fight against SARS-CoV-2. Let’s step forward to help, in recognition of the oath we took to “prevent disease whenever we can.”

We are in unprecedented times. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is attacking our communities and, as with any battle, we face unexpected challenges from the global pandemic. What can dermatologists, as highly skilled health care experts, do to support the fight against coronavirus disease 2019 (COVID-19)?

In early 2020, I became involved in a fulfilling and stimulating opportunity to contribute as a US Navy reservist, having just returned from a 3-month deployment. I served in the Medical Operations Center aboard the hospital ship USNS Comfort, which was docked in New York Harbor, as liaison to surrounding New York City hospitals. I also served as sole dermatologist on the ship, caring for the dermatologic needs of our team and consulting on numerous COVID-19 inpatients.

In May 2020, upon return to Virginia from New York City, I served as senior medical officer to medically clear other Navy Reserve health care workers returning from the field hospital at the Jacob K. Javits Convention Center of New York and from serving as embedded caregivers in existing New York City hospitals. I share 2 very important observations from my work there: First, COVID-19 is devastatingly real; second, we dermatologists can be valuable team members in the fight against this disease.

It is normal for us to feel scared, confused, and helpless; as 1% of the physician population, dermatologists represent a small focused fraction of the health care force. Nevertheless, we are all well-trained medical professionals who have taken the same Hippocratic Oath as other physicians. As members of the global health care team, we can each play a role in defeating COVID-19: We can be a trusted voice of reason, set an example, implement safe and effective distancing and hygiene precautions, and assist our local overburdened medical teams.

The magnitude and severity of COVID-19 can create a mass casualty–type phenomenon, overwhelming health care systems if the disease curve is not flattened. We can help flatten that curve by lengthening the pulse duration (to use dermatology jargon): that is, slowing the abrupt impact of cases to allow health care systems to triage, treat, and discharge in a more controlled manner.

How We Can Make a Difference

Despite representing a fraction of the health care team, we see a larger percentage of the population. On the Comfort, for example, dermatology visits accounted for approximately 20% of outpatient crew visits. We have an opportunity and a voice to reach a large percentage of the population directly. Whether we are now seeing patients face-to-face or virtually, we can spread the public health message and set an example. Wearing masks and social distancing do help to slow and markedly decrease the spread of SARS-CoV-2.

When you see patients in your office, consider the following:

• Have patients wait outside the office in their car and call the receptionist upon arrival.

• Have the receptionist call back the patient when the office is ready.

• Prescreen the patient before having him/her enter the clinic.

• Do not allow handshaking.

• Require everyone to wear a mask.

• Wear gloves.

• Have ample hand sanitizer openly available for all.

• Thoroughly clean or disinfect surfaces between patients.

Recalling the Difficult Experience of a Colleague-Patient

I think back to a crew member of Comfort who presented with new-onset pruritus and erythematous papules on the arms, legs, and torso. She was an intensive care unit nurse working 13-hour days, every day, for weeks on a COVID-positive unit—double-masked, gowned, wearing eye protection, in a warmer than usual intensive care unit, managing the most critically ill patients she’s ever cared for. Outside work, her life consisted of a commute on a government-chartered bus between Comfort and a contracted hotel while eating boxed meals. For 6 hours daily, she would—unsuccessfully—attempt to sleep with raging pruritus. Treating this routine case of eczema had a domino effect, improving her quality of life and thus allowing her to provide better care for the critically ill.

Let Us All Join in the Fight

As well-educated medical experts, we have the ability and the opportunity to reach outside our comfort zone and assist our medical colleagues. As I saw in New York City, the spectrum of specialists bravely worked together to meet overwhelming demand on the health care system and care for thousands of critically ill and dying patients. Dermatologists treated extensive eczema, ulcers, and other dermatoses on caretakers; triaged patients for appropriate allocation of care; and delivered care outside their comfort zone as physician extenders on inpatient and critical care units.

We are all in this together. I encourage all dermatologists who are in an area of need to ask your health care system how you can join the fight against SARS-CoV-2. Let’s step forward to help, in recognition of the oath we took to “prevent disease whenever we can.”

We are in unprecedented times. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is attacking our communities and, as with any battle, we face unexpected challenges from the global pandemic. What can dermatologists, as highly skilled health care experts, do to support the fight against coronavirus disease 2019 (COVID-19)?

In early 2020, I became involved in a fulfilling and stimulating opportunity to contribute as a US Navy reservist, having just returned from a 3-month deployment. I served in the Medical Operations Center aboard the hospital ship USNS Comfort, which was docked in New York Harbor, as liaison to surrounding New York City hospitals. I also served as sole dermatologist on the ship, caring for the dermatologic needs of our team and consulting on numerous COVID-19 inpatients.

In May 2020, upon return to Virginia from New York City, I served as senior medical officer to medically clear other Navy Reserve health care workers returning from the field hospital at the Jacob K. Javits Convention Center of New York and from serving as embedded caregivers in existing New York City hospitals. I share 2 very important observations from my work there: First, COVID-19 is devastatingly real; second, we dermatologists can be valuable team members in the fight against this disease.

It is normal for us to feel scared, confused, and helpless; as 1% of the physician population, dermatologists represent a small focused fraction of the health care force. Nevertheless, we are all well-trained medical professionals who have taken the same Hippocratic Oath as other physicians. As members of the global health care team, we can each play a role in defeating COVID-19: We can be a trusted voice of reason, set an example, implement safe and effective distancing and hygiene precautions, and assist our local overburdened medical teams.

The magnitude and severity of COVID-19 can create a mass casualty–type phenomenon, overwhelming health care systems if the disease curve is not flattened. We can help flatten that curve by lengthening the pulse duration (to use dermatology jargon): that is, slowing the abrupt impact of cases to allow health care systems to triage, treat, and discharge in a more controlled manner.

How We Can Make a Difference

Despite representing a fraction of the health care team, we see a larger percentage of the population. On the Comfort, for example, dermatology visits accounted for approximately 20% of outpatient crew visits. We have an opportunity and a voice to reach a large percentage of the population directly. Whether we are now seeing patients face-to-face or virtually, we can spread the public health message and set an example. Wearing masks and social distancing do help to slow and markedly decrease the spread of SARS-CoV-2.

When you see patients in your office, consider the following:

• Have patients wait outside the office in their car and call the receptionist upon arrival.

• Have the receptionist call back the patient when the office is ready.

• Prescreen the patient before having him/her enter the clinic.

• Do not allow handshaking.

• Require everyone to wear a mask.

• Wear gloves.

• Have ample hand sanitizer openly available for all.

• Thoroughly clean or disinfect surfaces between patients.

Recalling the Difficult Experience of a Colleague-Patient

I think back to a crew member of Comfort who presented with new-onset pruritus and erythematous papules on the arms, legs, and torso. She was an intensive care unit nurse working 13-hour days, every day, for weeks on a COVID-positive unit—double-masked, gowned, wearing eye protection, in a warmer than usual intensive care unit, managing the most critically ill patients she’s ever cared for. Outside work, her life consisted of a commute on a government-chartered bus between Comfort and a contracted hotel while eating boxed meals. For 6 hours daily, she would—unsuccessfully—attempt to sleep with raging pruritus. Treating this routine case of eczema had a domino effect, improving her quality of life and thus allowing her to provide better care for the critically ill.

Let Us All Join in the Fight

As well-educated medical experts, we have the ability and the opportunity to reach outside our comfort zone and assist our medical colleagues. As I saw in New York City, the spectrum of specialists bravely worked together to meet overwhelming demand on the health care system and care for thousands of critically ill and dying patients. Dermatologists treated extensive eczema, ulcers, and other dermatoses on caretakers; triaged patients for appropriate allocation of care; and delivered care outside their comfort zone as physician extenders on inpatient and critical care units.

We are all in this together. I encourage all dermatologists who are in an area of need to ask your health care system how you can join the fight against SARS-CoV-2. Let’s step forward to help, in recognition of the oath we took to “prevent disease whenever we can.”

In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) started an outbreak of respiratory illnesses in Wuhan, China. The respiratory disease was termed coronavirus disease 2019 (COVID-19) and rapidly spread worldwide, resulting in a pandemic classification on March 11, 2020. ¹ Recently, several cutaneous manifestations of COVID-19 have been reported. Skin manifestations have been reported to be similar to other common viral infections. ² However, there is a paucity of published clinical images of more atypical presentations.

Case Report

A 52-year-old black man presented via urgent store-and-forward teledermatology consultation from his primary care provider with a self-described “vesicular,” highly pruritic rash of both arms and legs of 1 week’s duration without involvement of the trunk, axillae, groin, face, genitalia, or any mucous membranes. He noted nausea, loss of appetite, and nonbloody diarrhea 4 days later. He denied fever, chills, dry cough, shortness of breath, or dyspnea. He had a history of hypertension and type 2 diabetes mellitus. There were no changes in medications; no outdoor activities, gardening, or yard work; no exposure to plants or metals; and no use of new personal care products.

The digital images showed zones of flesh-colored to slightly erythematous, somewhat “juicy” papules with some coalescence into ill-defined plaques. There were scattered foci of scale and hemorrhagic crust that involved both palms, forearms (Figure, A), and legs (Figure, B). There were no intact vesicles, and a herald patch was not identified. Vital signs at the time of imaging were normal, with the exception of a low-grade fever (temperature, 37.3°C). Basic laboratory testing showed only mild leukocytosis with mild neutropenia and mild aspartate aminotransaminase elevation. A skin biopsy was not performed. Pulmonary imaging and workup were not performed because of the lack of respiratory symptoms.

Comment

Coronavirus disease 2019 is caused by SARS-CoV2, an enveloped, nonsegmented, positive-sense RNA virus of the coronavirus family. It is currently believed that SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to gain entry into human cells, leading to infection primarily affecting the lower respiratory tract.³ Patients suspected of COVID-19 infection most often present with fever, dry cough, dyspnea, and fatigue, while GI symptoms such as nausea, vomiting, and diarrhea are uncommon.⁴ More recently, several reports describe a variety of skin findings associated with COVID-19. A current theory suggests that the virus does not directly target keratinocytes but triggers a systemic immune response, leading to a diversity of skin morphologies.⁵ The main types of described cutaneous findings include pseudochilblains, overtly vesicular, urticarial, maculopapular, and livedo/necrosis.⁶ Others have described petechial⁷ and papulosquamous eruptions.⁸ Most of these patients initially presented with typical COVID-19 symptoms and frequently represented more severe cases of the disease. Additionally, the vesicular and papulosquamous eruptions reportedly occurred on the trunk and not the limbs, as in our case.

This confirmed COVID-19–positive patient presented with an ill-defined vesicular and papulosquamous-type eruption on the arms and legs and later developed only mild GI symptoms. By sharing this case, we report yet another skin manifestation of COVID-19 and propose the possible expansion of testing for SARS-CoV-2 in patients presenting with rash and GI symptoms, which holds the potential to increase the identification of COVID-19 in the population, thereby increasing strict contact tracing and slowing the spread of this pandemic.

In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) started an outbreak of respiratory illnesses in Wuhan, China. The respiratory disease was termed coronavirus disease 2019 (COVID-19) and rapidly spread worldwide, resulting in a pandemic classification on March 11, 2020. ¹ Recently, several cutaneous manifestations of COVID-19 have been reported. Skin manifestations have been reported to be similar to other common viral infections. ² However, there is a paucity of published clinical images of more atypical presentations.

Case Report

A 52-year-old black man presented via urgent store-and-forward teledermatology consultation from his primary care provider with a self-described “vesicular,” highly pruritic rash of both arms and legs of 1 week’s duration without involvement of the trunk, axillae, groin, face, genitalia, or any mucous membranes. He noted nausea, loss of appetite, and nonbloody diarrhea 4 days later. He denied fever, chills, dry cough, shortness of breath, or dyspnea. He had a history of hypertension and type 2 diabetes mellitus. There were no changes in medications; no outdoor activities, gardening, or yard work; no exposure to plants or metals; and no use of new personal care products.

The digital images showed zones of flesh-colored to slightly erythematous, somewhat “juicy” papules with some coalescence into ill-defined plaques. There were scattered foci of scale and hemorrhagic crust that involved both palms, forearms (Figure, A), and legs (Figure, B). There were no intact vesicles, and a herald patch was not identified. Vital signs at the time of imaging were normal, with the exception of a low-grade fever (temperature, 37.3°C). Basic laboratory testing showed only mild leukocytosis with mild neutropenia and mild aspartate aminotransaminase elevation. A skin biopsy was not performed. Pulmonary imaging and workup were not performed because of the lack of respiratory symptoms.

Comment

Coronavirus disease 2019 is caused by SARS-CoV2, an enveloped, nonsegmented, positive-sense RNA virus of the coronavirus family. It is currently believed that SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to gain entry into human cells, leading to infection primarily affecting the lower respiratory tract.³ Patients suspected of COVID-19 infection most often present with fever, dry cough, dyspnea, and fatigue, while GI symptoms such as nausea, vomiting, and diarrhea are uncommon.⁴ More recently, several reports describe a variety of skin findings associated with COVID-19. A current theory suggests that the virus does not directly target keratinocytes but triggers a systemic immune response, leading to a diversity of skin morphologies.⁵ The main types of described cutaneous findings include pseudochilblains, overtly vesicular, urticarial, maculopapular, and livedo/necrosis.⁶ Others have described petechial⁷ and papulosquamous eruptions.⁸ Most of these patients initially presented with typical COVID-19 symptoms and frequently represented more severe cases of the disease. Additionally, the vesicular and papulosquamous eruptions reportedly occurred on the trunk and not the limbs, as in our case.

This confirmed COVID-19–positive patient presented with an ill-defined vesicular and papulosquamous-type eruption on the arms and legs and later developed only mild GI symptoms. By sharing this case, we report yet another skin manifestation of COVID-19 and propose the possible expansion of testing for SARS-CoV-2 in patients presenting with rash and GI symptoms, which holds the potential to increase the identification of COVID-19 in the population, thereby increasing strict contact tracing and slowing the spread of this pandemic.

In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) started an outbreak of respiratory illnesses in Wuhan, China. The respiratory disease was termed coronavirus disease 2019 (COVID-19) and rapidly spread worldwide, resulting in a pandemic classification on March 11, 2020. ¹ Recently, several cutaneous manifestations of COVID-19 have been reported. Skin manifestations have been reported to be similar to other common viral infections. ² However, there is a paucity of published clinical images of more atypical presentations.

Case Report

A 52-year-old black man presented via urgent store-and-forward teledermatology consultation from his primary care provider with a self-described “vesicular,” highly pruritic rash of both arms and legs of 1 week’s duration without involvement of the trunk, axillae, groin, face, genitalia, or any mucous membranes. He noted nausea, loss of appetite, and nonbloody diarrhea 4 days later. He denied fever, chills, dry cough, shortness of breath, or dyspnea. He had a history of hypertension and type 2 diabetes mellitus. There were no changes in medications; no outdoor activities, gardening, or yard work; no exposure to plants or metals; and no use of new personal care products.

The digital images showed zones of flesh-colored to slightly erythematous, somewhat “juicy” papules with some coalescence into ill-defined plaques. There were scattered foci of scale and hemorrhagic crust that involved both palms, forearms (Figure, A), and legs (Figure, B). There were no intact vesicles, and a herald patch was not identified. Vital signs at the time of imaging were normal, with the exception of a low-grade fever (temperature, 37.3°C). Basic laboratory testing showed only mild leukocytosis with mild neutropenia and mild aspartate aminotransaminase elevation. A skin biopsy was not performed. Pulmonary imaging and workup were not performed because of the lack of respiratory symptoms.

Comment

Coronavirus disease 2019 is caused by SARS-CoV2, an enveloped, nonsegmented, positive-sense RNA virus of the coronavirus family. It is currently believed that SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to gain entry into human cells, leading to infection primarily affecting the lower respiratory tract.³ Patients suspected of COVID-19 infection most often present with fever, dry cough, dyspnea, and fatigue, while GI symptoms such as nausea, vomiting, and diarrhea are uncommon.⁴ More recently, several reports describe a variety of skin findings associated with COVID-19. A current theory suggests that the virus does not directly target keratinocytes but triggers a systemic immune response, leading to a diversity of skin morphologies.⁵ The main types of described cutaneous findings include pseudochilblains, overtly vesicular, urticarial, maculopapular, and livedo/necrosis.⁶ Others have described petechial⁷ and papulosquamous eruptions.⁸ Most of these patients initially presented with typical COVID-19 symptoms and frequently represented more severe cases of the disease. Additionally, the vesicular and papulosquamous eruptions reportedly occurred on the trunk and not the limbs, as in our case.

This confirmed COVID-19–positive patient presented with an ill-defined vesicular and papulosquamous-type eruption on the arms and legs and later developed only mild GI symptoms. By sharing this case, we report yet another skin manifestation of COVID-19 and propose the possible expansion of testing for SARS-CoV-2 in patients presenting with rash and GI symptoms, which holds the potential to increase the identification of COVID-19 in the population, thereby increasing strict contact tracing and slowing the spread of this pandemic.