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A teen presents with a severe, tender rash on the extremities
“There’s rue for you, and here’s some for me; we may call it herb of grace o’ Sundays. O, you must wear your rue with a difference.”
— Ophelia in Hamlet by William Shakespeare
The patient was admitted to the hospital for IV fluids, pain control, and observation. The following day she admitted using the leaves of a plant on the trail as a bug repellent, as one time was taught by her grandfather. She rubbed some of the leaves on the brother as well. The grandfather shared some pictures of the bushes, and the plant was identified as Ruta graveolens.
The blisters were deroofed, cleaned with saline, and wrapped with triamcinolone ointment and petrolatum. The patient was also started on a prednisone taper and received analgesics for the severe pain.
Ruta graveolens also known as common rue or herb of grace, is an ornamental plant from the Rutaceae family. This plant is also used as a medicinal herb, condiment, and as an insect repellent. If ingested in large doses, it can cause severe abdominal pain and vomiting. It also can be hepatotoxic.
The herb contains furocumarines, such as 8-methoxypsoralen and 5-methoxypsoralen and furoquinoline alkaloids. These chemicals when exposed to UVA radiation cause cell injury and inflammation of the skin. This is considered a phototoxic reaction of the skin, compared with allergic reactions, such as poison ivy dermatitis, which need a prior sensitization to the allergen for the T cells to be activated and cause injury in the skin. Other common plants and fruits that can cause phytophotodermatitis include citrus fruits, figs, carrots, celery, parsnips, parsley, and other wildflowers like hogweed.
Depending on the degree of injury, the patients can be treated with topical corticosteroids, petrolatum wraps, and pain control. In severe cases like our patient, systemic prednisone may help stop the progression of the lesions and help with the inflammation. Skin hyperpigmentation after the initial injury may take months to clear, and some patient can develop scars.
The differential diagnosis should include severe bullous contact dermatitis like exposure to urushiol in poison ivy; second- and third-degree burns; severe medications reactions such Stevens-Johnson syndrome or toxic epidermal necrolysis, and inmunobullous diseases such as bullous lupus erythematosus, pemphigus vulgaris, or bullous pemphigoid. If there is no history of exposure or there are any other systemic symptoms, consider performing a skin biopsy of one of the lesions.
In this patient’s case, the history of exposure and skin findings helped the dermatologist on call make the right diagnosis.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
J Burn Care Res. 2018 Oct 23;39(6):1064-6.
Dermatitis. 2007 Mar;18(1):52-5.
BMJ Case Rep. 2015 Dec 23;2015:bcr2015213388.
“There’s rue for you, and here’s some for me; we may call it herb of grace o’ Sundays. O, you must wear your rue with a difference.”
— Ophelia in Hamlet by William Shakespeare
The patient was admitted to the hospital for IV fluids, pain control, and observation. The following day she admitted using the leaves of a plant on the trail as a bug repellent, as one time was taught by her grandfather. She rubbed some of the leaves on the brother as well. The grandfather shared some pictures of the bushes, and the plant was identified as Ruta graveolens.
The blisters were deroofed, cleaned with saline, and wrapped with triamcinolone ointment and petrolatum. The patient was also started on a prednisone taper and received analgesics for the severe pain.
Ruta graveolens also known as common rue or herb of grace, is an ornamental plant from the Rutaceae family. This plant is also used as a medicinal herb, condiment, and as an insect repellent. If ingested in large doses, it can cause severe abdominal pain and vomiting. It also can be hepatotoxic.
The herb contains furocumarines, such as 8-methoxypsoralen and 5-methoxypsoralen and furoquinoline alkaloids. These chemicals when exposed to UVA radiation cause cell injury and inflammation of the skin. This is considered a phototoxic reaction of the skin, compared with allergic reactions, such as poison ivy dermatitis, which need a prior sensitization to the allergen for the T cells to be activated and cause injury in the skin. Other common plants and fruits that can cause phytophotodermatitis include citrus fruits, figs, carrots, celery, parsnips, parsley, and other wildflowers like hogweed.
Depending on the degree of injury, the patients can be treated with topical corticosteroids, petrolatum wraps, and pain control. In severe cases like our patient, systemic prednisone may help stop the progression of the lesions and help with the inflammation. Skin hyperpigmentation after the initial injury may take months to clear, and some patient can develop scars.
The differential diagnosis should include severe bullous contact dermatitis like exposure to urushiol in poison ivy; second- and third-degree burns; severe medications reactions such Stevens-Johnson syndrome or toxic epidermal necrolysis, and inmunobullous diseases such as bullous lupus erythematosus, pemphigus vulgaris, or bullous pemphigoid. If there is no history of exposure or there are any other systemic symptoms, consider performing a skin biopsy of one of the lesions.
In this patient’s case, the history of exposure and skin findings helped the dermatologist on call make the right diagnosis.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
J Burn Care Res. 2018 Oct 23;39(6):1064-6.
Dermatitis. 2007 Mar;18(1):52-5.
BMJ Case Rep. 2015 Dec 23;2015:bcr2015213388.
“There’s rue for you, and here’s some for me; we may call it herb of grace o’ Sundays. O, you must wear your rue with a difference.”
— Ophelia in Hamlet by William Shakespeare
The patient was admitted to the hospital for IV fluids, pain control, and observation. The following day she admitted using the leaves of a plant on the trail as a bug repellent, as one time was taught by her grandfather. She rubbed some of the leaves on the brother as well. The grandfather shared some pictures of the bushes, and the plant was identified as Ruta graveolens.
The blisters were deroofed, cleaned with saline, and wrapped with triamcinolone ointment and petrolatum. The patient was also started on a prednisone taper and received analgesics for the severe pain.
Ruta graveolens also known as common rue or herb of grace, is an ornamental plant from the Rutaceae family. This plant is also used as a medicinal herb, condiment, and as an insect repellent. If ingested in large doses, it can cause severe abdominal pain and vomiting. It also can be hepatotoxic.
The herb contains furocumarines, such as 8-methoxypsoralen and 5-methoxypsoralen and furoquinoline alkaloids. These chemicals when exposed to UVA radiation cause cell injury and inflammation of the skin. This is considered a phototoxic reaction of the skin, compared with allergic reactions, such as poison ivy dermatitis, which need a prior sensitization to the allergen for the T cells to be activated and cause injury in the skin. Other common plants and fruits that can cause phytophotodermatitis include citrus fruits, figs, carrots, celery, parsnips, parsley, and other wildflowers like hogweed.
Depending on the degree of injury, the patients can be treated with topical corticosteroids, petrolatum wraps, and pain control. In severe cases like our patient, systemic prednisone may help stop the progression of the lesions and help with the inflammation. Skin hyperpigmentation after the initial injury may take months to clear, and some patient can develop scars.
The differential diagnosis should include severe bullous contact dermatitis like exposure to urushiol in poison ivy; second- and third-degree burns; severe medications reactions such Stevens-Johnson syndrome or toxic epidermal necrolysis, and inmunobullous diseases such as bullous lupus erythematosus, pemphigus vulgaris, or bullous pemphigoid. If there is no history of exposure or there are any other systemic symptoms, consider performing a skin biopsy of one of the lesions.
In this patient’s case, the history of exposure and skin findings helped the dermatologist on call make the right diagnosis.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. Email her at pdnews@mdedge.com.
References
J Burn Care Res. 2018 Oct 23;39(6):1064-6.
Dermatitis. 2007 Mar;18(1):52-5.
BMJ Case Rep. 2015 Dec 23;2015:bcr2015213388.
She started taking lithium for depression and anxiety 3 weeks prior to her developing the rash. She denies taking any other medications, supplements, or recreational drugs.
She denied any prior history of photosensitivity, no history of mouth ulcers, joint pain, muscle weakness, hair loss, or any other symptoms.
Besides her brother, there are no other affected family members, and no history of immune bullous disorders or other skin conditions.
On physical exam, the girl appears in a lot of pain and is uncomfortable. The skin is red and hot, and there are tense bullae on the neck, arms, and legs. There are no ocular or mucosal lesions.
A 31-year-old with a 3-week history of a waxing and waning, mildly pruritic eruption on his neck, chest, and back
Prurigo pigmentosa is an inflammatory disorder of uncertain etiology characterized by the eruption of erythematous, markedly pruritic, urticaria-like papules and vesicles on the posterior neck, mid- to upper back, and chest. Crops of papules appear rapidly and then involute within days, leaving behind postinflammatory hyperpigmentation in a netlike configuration. New papules may appear prior to resolution of hyperpigmented macules, resulting in a mixed presentation of erythematous papules overlying reticulated hyperpigmentation.1
The condition was initially described in Japanese individuals, and to date, most cases have occurred in this population.2 However, the incidence of prurigo pigmentosa is increasing worldwide, including in the United States, which has led to the identification of several metabolic risk factors including diabetes mellitus, fasting, and dieting, with the common etiologic endpoint of ketosis.3With the increasing popularity of diets with strict carbohydrate limits, often with the goal of ketosis, dermatologists should be aware of the clinical appearance and common history of this rash to facilitate prompt diagnosis and treatment.
Clinical exam with appropriate history is usually sufficient for diagnosis. However, biopsy with histopathologic analysis can be utilized to confirm atypical cases. Histopathologic findings depend on the stage of the lesion biopsied. The earliest finding is a shallow perivascular neutrophilic infiltrate, neutrophil exocytosis, and epidermal and superficial dermal edema. As lesions progress, the prominent findings include epidermal vesiculation with necrotic keratinocytes and a lichenoid infiltrate dominated by lymphocytes and eosinophils. In the final stages, lesions demonstrate variable parakeratosis and acanthosis, as well as prominent dermal melanophagia.1
Treatment of prurigo pigmentosa includes modification of the patient’s underlying health issues to avoid ketosis, and in the case of diet-induced ketosis, reinstitution of a more balanced diet with sufficient carbohydrates. In the case of the patient presented here, rash resolved 1 week following instruction to include more carbohydrates in his diet. For recalcitrant cases or those without a clear precipitating factor, the addition of oral antibiotics is often helpful. Tetracyclines or dapsone are typically employed, usually in courses of 1-2 months.3,4
Dr. Johnson is a PGY-4 dermatology resident at Carilion Clinic in Roanoke, Va. He provided the case and photos. Donna Bilu Martin, MD, is the editor of the column.
References
1. Boer A et al. Am J Dermatopathol. 2003 Apr;25(2):117-292.
2. Satter E et al. J Cutan Pathol. 2016 Oct;43(10):809-14.
3. Alshaya M et al. JAAD Case Rep. 2019 Jun 8;5(6):504-7.
4. Hartman M et al. Cutis. 2019 Mar;103(3):E10-3.
Prurigo pigmentosa is an inflammatory disorder of uncertain etiology characterized by the eruption of erythematous, markedly pruritic, urticaria-like papules and vesicles on the posterior neck, mid- to upper back, and chest. Crops of papules appear rapidly and then involute within days, leaving behind postinflammatory hyperpigmentation in a netlike configuration. New papules may appear prior to resolution of hyperpigmented macules, resulting in a mixed presentation of erythematous papules overlying reticulated hyperpigmentation.1
The condition was initially described in Japanese individuals, and to date, most cases have occurred in this population.2 However, the incidence of prurigo pigmentosa is increasing worldwide, including in the United States, which has led to the identification of several metabolic risk factors including diabetes mellitus, fasting, and dieting, with the common etiologic endpoint of ketosis.3With the increasing popularity of diets with strict carbohydrate limits, often with the goal of ketosis, dermatologists should be aware of the clinical appearance and common history of this rash to facilitate prompt diagnosis and treatment.
Clinical exam with appropriate history is usually sufficient for diagnosis. However, biopsy with histopathologic analysis can be utilized to confirm atypical cases. Histopathologic findings depend on the stage of the lesion biopsied. The earliest finding is a shallow perivascular neutrophilic infiltrate, neutrophil exocytosis, and epidermal and superficial dermal edema. As lesions progress, the prominent findings include epidermal vesiculation with necrotic keratinocytes and a lichenoid infiltrate dominated by lymphocytes and eosinophils. In the final stages, lesions demonstrate variable parakeratosis and acanthosis, as well as prominent dermal melanophagia.1
Treatment of prurigo pigmentosa includes modification of the patient’s underlying health issues to avoid ketosis, and in the case of diet-induced ketosis, reinstitution of a more balanced diet with sufficient carbohydrates. In the case of the patient presented here, rash resolved 1 week following instruction to include more carbohydrates in his diet. For recalcitrant cases or those without a clear precipitating factor, the addition of oral antibiotics is often helpful. Tetracyclines or dapsone are typically employed, usually in courses of 1-2 months.3,4
Dr. Johnson is a PGY-4 dermatology resident at Carilion Clinic in Roanoke, Va. He provided the case and photos. Donna Bilu Martin, MD, is the editor of the column.
References
1. Boer A et al. Am J Dermatopathol. 2003 Apr;25(2):117-292.
2. Satter E et al. J Cutan Pathol. 2016 Oct;43(10):809-14.
3. Alshaya M et al. JAAD Case Rep. 2019 Jun 8;5(6):504-7.
4. Hartman M et al. Cutis. 2019 Mar;103(3):E10-3.
Prurigo pigmentosa is an inflammatory disorder of uncertain etiology characterized by the eruption of erythematous, markedly pruritic, urticaria-like papules and vesicles on the posterior neck, mid- to upper back, and chest. Crops of papules appear rapidly and then involute within days, leaving behind postinflammatory hyperpigmentation in a netlike configuration. New papules may appear prior to resolution of hyperpigmented macules, resulting in a mixed presentation of erythematous papules overlying reticulated hyperpigmentation.1
The condition was initially described in Japanese individuals, and to date, most cases have occurred in this population.2 However, the incidence of prurigo pigmentosa is increasing worldwide, including in the United States, which has led to the identification of several metabolic risk factors including diabetes mellitus, fasting, and dieting, with the common etiologic endpoint of ketosis.3With the increasing popularity of diets with strict carbohydrate limits, often with the goal of ketosis, dermatologists should be aware of the clinical appearance and common history of this rash to facilitate prompt diagnosis and treatment.
Clinical exam with appropriate history is usually sufficient for diagnosis. However, biopsy with histopathologic analysis can be utilized to confirm atypical cases. Histopathologic findings depend on the stage of the lesion biopsied. The earliest finding is a shallow perivascular neutrophilic infiltrate, neutrophil exocytosis, and epidermal and superficial dermal edema. As lesions progress, the prominent findings include epidermal vesiculation with necrotic keratinocytes and a lichenoid infiltrate dominated by lymphocytes and eosinophils. In the final stages, lesions demonstrate variable parakeratosis and acanthosis, as well as prominent dermal melanophagia.1
Treatment of prurigo pigmentosa includes modification of the patient’s underlying health issues to avoid ketosis, and in the case of diet-induced ketosis, reinstitution of a more balanced diet with sufficient carbohydrates. In the case of the patient presented here, rash resolved 1 week following instruction to include more carbohydrates in his diet. For recalcitrant cases or those without a clear precipitating factor, the addition of oral antibiotics is often helpful. Tetracyclines or dapsone are typically employed, usually in courses of 1-2 months.3,4
Dr. Johnson is a PGY-4 dermatology resident at Carilion Clinic in Roanoke, Va. He provided the case and photos. Donna Bilu Martin, MD, is the editor of the column.
References
1. Boer A et al. Am J Dermatopathol. 2003 Apr;25(2):117-292.
2. Satter E et al. J Cutan Pathol. 2016 Oct;43(10):809-14.
3. Alshaya M et al. JAAD Case Rep. 2019 Jun 8;5(6):504-7.
4. Hartman M et al. Cutis. 2019 Mar;103(3):E10-3.
A teen girl presents with a pinkish-red bump on her right leg
This atypical lesion might warrant a biopsy. However, upon closer examination, you can appreciate a small papule with a whitish center, at the inferior margin of the tumor (6 o’clock), and another flat-topped papule with a white center several centimeters inferior-lateral to the lesion, both consistent with molluscum lesions. Therefore, the tumor is consistent with a giant molluscum contagiosum.
Molluscum contagiosum is a cutaneous viral infection caused by the poxvirus, which commonly affects children. It can spread easily by direct physical contact, fomites, and autoinoculation.1 It usually presents with skin-colored or pink pearly dome-shaped papules with central umbilication that can occur anywhere on the face or body. The skin lesions can be asymptomatic or pruritic. When the size of the molluscum is 0.5 cm or more in diameter, it is considered a giant molluscum. Atypical size and appearance may be seen in patients with altered or impaired immunity such as those with HIV.2,3 Giant molluscum has been reported in immunocompetent patients as well.4,5
The diagnosis of molluscum contagiosum usually is made clinically. Our patient had typically appearing molluscum lesions approximate to the larger lesion of concern. She was overall healthy without any history of impaired immunity so no further work-up was pursued. However, a biopsy of the skin lesion may be considered if the diagnosis is unclear.
What’s the treatment plan?
Treatment may not be necessary for molluscum contagiosum because it is often self-limited in immunocompetent children, although it can take many months to years to resolve. Treatment may be considered to reduce autoinoculation or risk of transmission because of close contact to others, to alleviate discomfort, including itching, to reduce cosmetic concerns and to prevent secondary infection.6
The most common treatments for molluscum contagiosum are cantharidin or cryotherapy. Other treatment available include topical retinoids, immunomodulators such as cimetidine, or antivirals such as cidofovir.1 Lesions with or without treatment may exhibit the BOTE (beginning of the end) sign, which is an apparent worsening associated with the body’s immune response to the molluscum virus and generally indicates imminent resolution.
What’s the differential diagnosis?
The differential diagnosis for giant molluscum contagiosum includes epidermal inclusion cyst, skin tag, pilomatrixoma, and amelanotic melanoma.
Epidermal inclusion cyst typically presents as a firm, mobile nodule under the skin with central punctum, which can enlarge and become inflamed. It can be painful, especially when infected. Definitive treatment is surgical excision because it rarely resolves spontaneously.
Skin tags, also known as acrochordons, are benign skin-colored papules most often found in the skin folds. People with obesity and type 2 diabetes are at higher risk for skin tags. Skin tags may be treated with cryotherapy, surgical excision, or ligation.
Pilomatrixoma is a benign skin tumor derived from hair matrix cells. It is usually a nontender, firm, skin-colored or red-purple subcutaneous nodule that may have calcifications. Treatment is surgical excision.
Amelanotic melanoma is a melanoma with little or no pigment and can present as a skin- or red-colored nodule. While these are quite uncommon, recognition that many pediatric melanomas present as amelanotic lesions makes it important to consider this in the differential diagnosis of growing papules and nodules.7 Treatment and prognosis is similar to that of pigmented melanoma, but as it is often clinically challenging to diagnose because of atypical features, it may be detected in more advanced stages.
Our patient underwent cryotherapy with liquid nitrogen to the nodule given the large size of the lesion, with resolution without recurrence.
Dr. Lee is a pediatric dermatology research fellow in the division of pediatric and adolescent dermatology at the University of California, San Diego and Rady Children’s Hospital–San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Lee nor Dr. Eichenfield had any relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Recent Pat Inflamm Allergy Drug Discov. 2017. doi: 10.2174/1872213X11666170518114456.
2. J Epidemiol Glob Health. 2013 Dec. doi: 10.1016/j.jegh.2013.06.002.
3. Trop Doct. 2015 Apr. doi: 10.1177/0049475514568133.
4. J Pak Med Assoc. 2013 Jun;63(6):778-9.
5. Dermatol Pract Concept. 2016 Jul. doi: 10.5826/dpc.0603a15.
6 Molluscum Contagiosum, in “Red Book: 2018 Report of the Committee on Infectious Diseases,” 31st ed. (Itasca, Ill.: American Academy of Pediatrics, 2018, pp. 565-66).
7. J Am Acad Dermatol. 2013 Jun. doi: 10.1016/j.jaad.2012.12.953.
This atypical lesion might warrant a biopsy. However, upon closer examination, you can appreciate a small papule with a whitish center, at the inferior margin of the tumor (6 o’clock), and another flat-topped papule with a white center several centimeters inferior-lateral to the lesion, both consistent with molluscum lesions. Therefore, the tumor is consistent with a giant molluscum contagiosum.
Molluscum contagiosum is a cutaneous viral infection caused by the poxvirus, which commonly affects children. It can spread easily by direct physical contact, fomites, and autoinoculation.1 It usually presents with skin-colored or pink pearly dome-shaped papules with central umbilication that can occur anywhere on the face or body. The skin lesions can be asymptomatic or pruritic. When the size of the molluscum is 0.5 cm or more in diameter, it is considered a giant molluscum. Atypical size and appearance may be seen in patients with altered or impaired immunity such as those with HIV.2,3 Giant molluscum has been reported in immunocompetent patients as well.4,5
The diagnosis of molluscum contagiosum usually is made clinically. Our patient had typically appearing molluscum lesions approximate to the larger lesion of concern. She was overall healthy without any history of impaired immunity so no further work-up was pursued. However, a biopsy of the skin lesion may be considered if the diagnosis is unclear.
What’s the treatment plan?
Treatment may not be necessary for molluscum contagiosum because it is often self-limited in immunocompetent children, although it can take many months to years to resolve. Treatment may be considered to reduce autoinoculation or risk of transmission because of close contact to others, to alleviate discomfort, including itching, to reduce cosmetic concerns and to prevent secondary infection.6
The most common treatments for molluscum contagiosum are cantharidin or cryotherapy. Other treatment available include topical retinoids, immunomodulators such as cimetidine, or antivirals such as cidofovir.1 Lesions with or without treatment may exhibit the BOTE (beginning of the end) sign, which is an apparent worsening associated with the body’s immune response to the molluscum virus and generally indicates imminent resolution.
What’s the differential diagnosis?
The differential diagnosis for giant molluscum contagiosum includes epidermal inclusion cyst, skin tag, pilomatrixoma, and amelanotic melanoma.
Epidermal inclusion cyst typically presents as a firm, mobile nodule under the skin with central punctum, which can enlarge and become inflamed. It can be painful, especially when infected. Definitive treatment is surgical excision because it rarely resolves spontaneously.
Skin tags, also known as acrochordons, are benign skin-colored papules most often found in the skin folds. People with obesity and type 2 diabetes are at higher risk for skin tags. Skin tags may be treated with cryotherapy, surgical excision, or ligation.
Pilomatrixoma is a benign skin tumor derived from hair matrix cells. It is usually a nontender, firm, skin-colored or red-purple subcutaneous nodule that may have calcifications. Treatment is surgical excision.
Amelanotic melanoma is a melanoma with little or no pigment and can present as a skin- or red-colored nodule. While these are quite uncommon, recognition that many pediatric melanomas present as amelanotic lesions makes it important to consider this in the differential diagnosis of growing papules and nodules.7 Treatment and prognosis is similar to that of pigmented melanoma, but as it is often clinically challenging to diagnose because of atypical features, it may be detected in more advanced stages.
Our patient underwent cryotherapy with liquid nitrogen to the nodule given the large size of the lesion, with resolution without recurrence.
Dr. Lee is a pediatric dermatology research fellow in the division of pediatric and adolescent dermatology at the University of California, San Diego and Rady Children’s Hospital–San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Lee nor Dr. Eichenfield had any relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Recent Pat Inflamm Allergy Drug Discov. 2017. doi: 10.2174/1872213X11666170518114456.
2. J Epidemiol Glob Health. 2013 Dec. doi: 10.1016/j.jegh.2013.06.002.
3. Trop Doct. 2015 Apr. doi: 10.1177/0049475514568133.
4. J Pak Med Assoc. 2013 Jun;63(6):778-9.
5. Dermatol Pract Concept. 2016 Jul. doi: 10.5826/dpc.0603a15.
6 Molluscum Contagiosum, in “Red Book: 2018 Report of the Committee on Infectious Diseases,” 31st ed. (Itasca, Ill.: American Academy of Pediatrics, 2018, pp. 565-66).
7. J Am Acad Dermatol. 2013 Jun. doi: 10.1016/j.jaad.2012.12.953.
This atypical lesion might warrant a biopsy. However, upon closer examination, you can appreciate a small papule with a whitish center, at the inferior margin of the tumor (6 o’clock), and another flat-topped papule with a white center several centimeters inferior-lateral to the lesion, both consistent with molluscum lesions. Therefore, the tumor is consistent with a giant molluscum contagiosum.
Molluscum contagiosum is a cutaneous viral infection caused by the poxvirus, which commonly affects children. It can spread easily by direct physical contact, fomites, and autoinoculation.1 It usually presents with skin-colored or pink pearly dome-shaped papules with central umbilication that can occur anywhere on the face or body. The skin lesions can be asymptomatic or pruritic. When the size of the molluscum is 0.5 cm or more in diameter, it is considered a giant molluscum. Atypical size and appearance may be seen in patients with altered or impaired immunity such as those with HIV.2,3 Giant molluscum has been reported in immunocompetent patients as well.4,5
The diagnosis of molluscum contagiosum usually is made clinically. Our patient had typically appearing molluscum lesions approximate to the larger lesion of concern. She was overall healthy without any history of impaired immunity so no further work-up was pursued. However, a biopsy of the skin lesion may be considered if the diagnosis is unclear.
What’s the treatment plan?
Treatment may not be necessary for molluscum contagiosum because it is often self-limited in immunocompetent children, although it can take many months to years to resolve. Treatment may be considered to reduce autoinoculation or risk of transmission because of close contact to others, to alleviate discomfort, including itching, to reduce cosmetic concerns and to prevent secondary infection.6
The most common treatments for molluscum contagiosum are cantharidin or cryotherapy. Other treatment available include topical retinoids, immunomodulators such as cimetidine, or antivirals such as cidofovir.1 Lesions with or without treatment may exhibit the BOTE (beginning of the end) sign, which is an apparent worsening associated with the body’s immune response to the molluscum virus and generally indicates imminent resolution.
What’s the differential diagnosis?
The differential diagnosis for giant molluscum contagiosum includes epidermal inclusion cyst, skin tag, pilomatrixoma, and amelanotic melanoma.
Epidermal inclusion cyst typically presents as a firm, mobile nodule under the skin with central punctum, which can enlarge and become inflamed. It can be painful, especially when infected. Definitive treatment is surgical excision because it rarely resolves spontaneously.
Skin tags, also known as acrochordons, are benign skin-colored papules most often found in the skin folds. People with obesity and type 2 diabetes are at higher risk for skin tags. Skin tags may be treated with cryotherapy, surgical excision, or ligation.
Pilomatrixoma is a benign skin tumor derived from hair matrix cells. It is usually a nontender, firm, skin-colored or red-purple subcutaneous nodule that may have calcifications. Treatment is surgical excision.
Amelanotic melanoma is a melanoma with little or no pigment and can present as a skin- or red-colored nodule. While these are quite uncommon, recognition that many pediatric melanomas present as amelanotic lesions makes it important to consider this in the differential diagnosis of growing papules and nodules.7 Treatment and prognosis is similar to that of pigmented melanoma, but as it is often clinically challenging to diagnose because of atypical features, it may be detected in more advanced stages.
Our patient underwent cryotherapy with liquid nitrogen to the nodule given the large size of the lesion, with resolution without recurrence.
Dr. Lee is a pediatric dermatology research fellow in the division of pediatric and adolescent dermatology at the University of California, San Diego and Rady Children’s Hospital–San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. Neither Dr. Lee nor Dr. Eichenfield had any relevant financial disclosures. Email them at pdnews@mdedge.com.
References
1. Recent Pat Inflamm Allergy Drug Discov. 2017. doi: 10.2174/1872213X11666170518114456.
2. J Epidemiol Glob Health. 2013 Dec. doi: 10.1016/j.jegh.2013.06.002.
3. Trop Doct. 2015 Apr. doi: 10.1177/0049475514568133.
4. J Pak Med Assoc. 2013 Jun;63(6):778-9.
5. Dermatol Pract Concept. 2016 Jul. doi: 10.5826/dpc.0603a15.
6 Molluscum Contagiosum, in “Red Book: 2018 Report of the Committee on Infectious Diseases,” 31st ed. (Itasca, Ill.: American Academy of Pediatrics, 2018, pp. 565-66).
7. J Am Acad Dermatol. 2013 Jun. doi: 10.1016/j.jaad.2012.12.953.
A woman with an asymptomatic eruption on her palms after exposure to water
This eruption can be accompanied by a mild burning or tingling sensation, which will subside with the rest of the symptoms in minutes to hours after drying.1
AWP is most frequently associated with cystic fibrosis (CF).2 It can be observed in up to 80% of CF patients and is considered a clinical sign of the disease. AWP can be present in CF carriers to a lesser extent,2,4 and has also been associated with focal hyperhidrosis, atopic dermatitis, Raynaud phenomenon, and COX-2 inhibitor use.5
While a definitive cause is unknown, it is thought that AWP is caused by dysregulation of sweat glands in the palms through increased expression of aquaporin, a protein crucial in the transport of water between cells.3
AWP is quite rare and benign in nature. However, because of its strong association with CF, genetic screening should be considered in asymptomatic patients. Our patient had been screened in the past and is not a CF carrier. Often, the itching or burning associated with CF is mild and easily controlled. The patient was placed on low dose isotretinoin for treatment of her acne. Interestingly, the patient claimed her eruption no longer appeared after starting isotretinoin therapy. To our knowledge, this is the first reported case of AWP resolving with isotretinoin use.
This case and photo were submitted by Mr. Birk, University of Texas, Austin, Texas; and Dr. Mamelak, Sanova Dermatology, in Austin. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Katz M, Ramot Y. CMAJ. 2015 Dec 8;187(18):E515.
2. Tolland JP et al. Dermatology. 2010;221(4):326-30.
3. Kabashima K et al. J Am Acad Dermatol. 2008 Aug;59(2 Suppl 1):S28-32.
4. Gild R et al. Br J Dermatol. 2010 Nov;163(5):1082-4.
5. Glatz M and Muellegger RR. BMJ Case Rep. 2014. doi: 10.1136/bcr-2014-203929.
This eruption can be accompanied by a mild burning or tingling sensation, which will subside with the rest of the symptoms in minutes to hours after drying.1
AWP is most frequently associated with cystic fibrosis (CF).2 It can be observed in up to 80% of CF patients and is considered a clinical sign of the disease. AWP can be present in CF carriers to a lesser extent,2,4 and has also been associated with focal hyperhidrosis, atopic dermatitis, Raynaud phenomenon, and COX-2 inhibitor use.5
While a definitive cause is unknown, it is thought that AWP is caused by dysregulation of sweat glands in the palms through increased expression of aquaporin, a protein crucial in the transport of water between cells.3
AWP is quite rare and benign in nature. However, because of its strong association with CF, genetic screening should be considered in asymptomatic patients. Our patient had been screened in the past and is not a CF carrier. Often, the itching or burning associated with CF is mild and easily controlled. The patient was placed on low dose isotretinoin for treatment of her acne. Interestingly, the patient claimed her eruption no longer appeared after starting isotretinoin therapy. To our knowledge, this is the first reported case of AWP resolving with isotretinoin use.
This case and photo were submitted by Mr. Birk, University of Texas, Austin, Texas; and Dr. Mamelak, Sanova Dermatology, in Austin. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Katz M, Ramot Y. CMAJ. 2015 Dec 8;187(18):E515.
2. Tolland JP et al. Dermatology. 2010;221(4):326-30.
3. Kabashima K et al. J Am Acad Dermatol. 2008 Aug;59(2 Suppl 1):S28-32.
4. Gild R et al. Br J Dermatol. 2010 Nov;163(5):1082-4.
5. Glatz M and Muellegger RR. BMJ Case Rep. 2014. doi: 10.1136/bcr-2014-203929.
This eruption can be accompanied by a mild burning or tingling sensation, which will subside with the rest of the symptoms in minutes to hours after drying.1
AWP is most frequently associated with cystic fibrosis (CF).2 It can be observed in up to 80% of CF patients and is considered a clinical sign of the disease. AWP can be present in CF carriers to a lesser extent,2,4 and has also been associated with focal hyperhidrosis, atopic dermatitis, Raynaud phenomenon, and COX-2 inhibitor use.5
While a definitive cause is unknown, it is thought that AWP is caused by dysregulation of sweat glands in the palms through increased expression of aquaporin, a protein crucial in the transport of water between cells.3
AWP is quite rare and benign in nature. However, because of its strong association with CF, genetic screening should be considered in asymptomatic patients. Our patient had been screened in the past and is not a CF carrier. Often, the itching or burning associated with CF is mild and easily controlled. The patient was placed on low dose isotretinoin for treatment of her acne. Interestingly, the patient claimed her eruption no longer appeared after starting isotretinoin therapy. To our knowledge, this is the first reported case of AWP resolving with isotretinoin use.
This case and photo were submitted by Mr. Birk, University of Texas, Austin, Texas; and Dr. Mamelak, Sanova Dermatology, in Austin. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Katz M, Ramot Y. CMAJ. 2015 Dec 8;187(18):E515.
2. Tolland JP et al. Dermatology. 2010;221(4):326-30.
3. Kabashima K et al. J Am Acad Dermatol. 2008 Aug;59(2 Suppl 1):S28-32.
4. Gild R et al. Br J Dermatol. 2010 Nov;163(5):1082-4.
5. Glatz M and Muellegger RR. BMJ Case Rep. 2014. doi: 10.1136/bcr-2014-203929.
A 36-year-old presents with a mildly pruritic rash consisting of pink papules on his hand
. MG is a dermatophytic folliculitis that classically presents as folliculocentric plaque, in which there are papules, pustules, and nodules, usually found on the lower leg and almost exclusively in adults.1 Wrists are commonly affected as well.
MG is typically caused by mechanical disruption of hair follicles that allows fungi to penetrate deep into dermal tissue.2 Quite often, the source of infection is typically the patient’s skin or nails. Associated risk factors include longstanding fungal infection, shaving or other cutaneous trauma, topical steroids, and immunosuppressive therapy.3,4 Although MG can be caused by other fungal species, it is most often caused by Trichophyton rubrum or Trichophyton tonsurans.1 There are two types of MG, the perifollicular papular form, which is localized and typically occurs in healthy individuals, and the deep subcutaneous plaque or nodular forms that usually occur in immunocompromised individuals.5
MG is an important clinical manifestation to be familiar with because of the increase in the numbers of solid-organ transplants and patients on immunosuppressive therapies. These patients are highly predisposed to opportunistic infections with aggressive clinical courses and will usually require prolonged treatment as relapses are common.3,5
Tissue culture and skin biopsy are often needed to establish the diagnosis. If a topical antifungal has been used, KOH (potassium hydroxide) and culture may be negative. This patient’s tissue culture was positive for T. rubrum. The histopathology revealed hyperkeratosis and acanthosis with focal parakeratosis and a lymphohistiocytic infiltrate in the dermis. On PAS (Periodic acid–Schiff ) stain, PAS-positive hyphae were identified in the keratin layer, confirming a diagnosis of tinea infection.
First line treatment includes systemic antifungals such as griseofulvin, ketoconazole, itraconazole, and terbinafine. Duration of therapy is typically 4-8 weeks or until all lesions are cleared.3,5
This case and photo were submitted by Mr. Hakimi of University of California San Diego School of Medicine and Dr. Sateesh of San Diego Family Dermatology. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1.“Fitzpatrick’s Dermatology in General Medicine” (New York: McGraw-Hill Medical, 2012).
2. Bonifaz A et al. Gac Med Mex. Sep-Oct 2008;144(5):427-33.
3. Romero FA et al. Transpl Infect Dis. 2011 Aug;13(4):424-3. doi:10.1111/j.1399-3062.2010.00596.x
4. Chou WY, Hsu CJ. Medicine (Baltimore). 2016 Jan;95(2):e2245. doi: 10.1097/MD.0000000000002245.
5. Ilkit M et al. Med Mycol. 2102 Jul;50(5):449-57.
. MG is a dermatophytic folliculitis that classically presents as folliculocentric plaque, in which there are papules, pustules, and nodules, usually found on the lower leg and almost exclusively in adults.1 Wrists are commonly affected as well.
MG is typically caused by mechanical disruption of hair follicles that allows fungi to penetrate deep into dermal tissue.2 Quite often, the source of infection is typically the patient’s skin or nails. Associated risk factors include longstanding fungal infection, shaving or other cutaneous trauma, topical steroids, and immunosuppressive therapy.3,4 Although MG can be caused by other fungal species, it is most often caused by Trichophyton rubrum or Trichophyton tonsurans.1 There are two types of MG, the perifollicular papular form, which is localized and typically occurs in healthy individuals, and the deep subcutaneous plaque or nodular forms that usually occur in immunocompromised individuals.5
MG is an important clinical manifestation to be familiar with because of the increase in the numbers of solid-organ transplants and patients on immunosuppressive therapies. These patients are highly predisposed to opportunistic infections with aggressive clinical courses and will usually require prolonged treatment as relapses are common.3,5
Tissue culture and skin biopsy are often needed to establish the diagnosis. If a topical antifungal has been used, KOH (potassium hydroxide) and culture may be negative. This patient’s tissue culture was positive for T. rubrum. The histopathology revealed hyperkeratosis and acanthosis with focal parakeratosis and a lymphohistiocytic infiltrate in the dermis. On PAS (Periodic acid–Schiff ) stain, PAS-positive hyphae were identified in the keratin layer, confirming a diagnosis of tinea infection.
First line treatment includes systemic antifungals such as griseofulvin, ketoconazole, itraconazole, and terbinafine. Duration of therapy is typically 4-8 weeks or until all lesions are cleared.3,5
This case and photo were submitted by Mr. Hakimi of University of California San Diego School of Medicine and Dr. Sateesh of San Diego Family Dermatology. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1.“Fitzpatrick’s Dermatology in General Medicine” (New York: McGraw-Hill Medical, 2012).
2. Bonifaz A et al. Gac Med Mex. Sep-Oct 2008;144(5):427-33.
3. Romero FA et al. Transpl Infect Dis. 2011 Aug;13(4):424-3. doi:10.1111/j.1399-3062.2010.00596.x
4. Chou WY, Hsu CJ. Medicine (Baltimore). 2016 Jan;95(2):e2245. doi: 10.1097/MD.0000000000002245.
5. Ilkit M et al. Med Mycol. 2102 Jul;50(5):449-57.
. MG is a dermatophytic folliculitis that classically presents as folliculocentric plaque, in which there are papules, pustules, and nodules, usually found on the lower leg and almost exclusively in adults.1 Wrists are commonly affected as well.
MG is typically caused by mechanical disruption of hair follicles that allows fungi to penetrate deep into dermal tissue.2 Quite often, the source of infection is typically the patient’s skin or nails. Associated risk factors include longstanding fungal infection, shaving or other cutaneous trauma, topical steroids, and immunosuppressive therapy.3,4 Although MG can be caused by other fungal species, it is most often caused by Trichophyton rubrum or Trichophyton tonsurans.1 There are two types of MG, the perifollicular papular form, which is localized and typically occurs in healthy individuals, and the deep subcutaneous plaque or nodular forms that usually occur in immunocompromised individuals.5
MG is an important clinical manifestation to be familiar with because of the increase in the numbers of solid-organ transplants and patients on immunosuppressive therapies. These patients are highly predisposed to opportunistic infections with aggressive clinical courses and will usually require prolonged treatment as relapses are common.3,5
Tissue culture and skin biopsy are often needed to establish the diagnosis. If a topical antifungal has been used, KOH (potassium hydroxide) and culture may be negative. This patient’s tissue culture was positive for T. rubrum. The histopathology revealed hyperkeratosis and acanthosis with focal parakeratosis and a lymphohistiocytic infiltrate in the dermis. On PAS (Periodic acid–Schiff ) stain, PAS-positive hyphae were identified in the keratin layer, confirming a diagnosis of tinea infection.
First line treatment includes systemic antifungals such as griseofulvin, ketoconazole, itraconazole, and terbinafine. Duration of therapy is typically 4-8 weeks or until all lesions are cleared.3,5
This case and photo were submitted by Mr. Hakimi of University of California San Diego School of Medicine and Dr. Sateesh of San Diego Family Dermatology. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1.“Fitzpatrick’s Dermatology in General Medicine” (New York: McGraw-Hill Medical, 2012).
2. Bonifaz A et al. Gac Med Mex. Sep-Oct 2008;144(5):427-33.
3. Romero FA et al. Transpl Infect Dis. 2011 Aug;13(4):424-3. doi:10.1111/j.1399-3062.2010.00596.x
4. Chou WY, Hsu CJ. Medicine (Baltimore). 2016 Jan;95(2):e2245. doi: 10.1097/MD.0000000000002245.
5. Ilkit M et al. Med Mycol. 2102 Jul;50(5):449-57.
A 4-year-old with a lesion on her cheek, which grew and became firmer over two months
The patient was diagnosed with idiopathic facial aseptic granuloma (IFAG) based on the clinical findings, as well as the associated history of chalazia and erythematous papules seen in childhood rosacea.
She was treated with several months of azithromycin, sulfur wash, and metronidazole cream with improvement of some of the smaller lesions but no change on the larger nodules. Later she was treated with oral and topical ivermectin with no improvement. Some of the nodules slowly resolved except for the larger lesion on the right cheek. She was later treated with a 6-week course of clarithromycin with partial improvement of the nodule. The lesion resolved after 2 months of stopping clarithromycin.
IFAG is a rare condition seen in prepubescent children. The etiology of this condition is not well understood and is thought to be on the spectrum of childhood rosacea.1 From several recent reports, IFAG usually is seen in children with associated conditions including chalazia, conjunctivitis, blepharitis, and telangiectasias, which can be seen in patients with rosacea. These associated findings suggest the possibility of IFAG being a form of granulomatous rosacea in children.
This condition presents in childhood between the ages of 8 months and 13 years. Most of the cases occur in toddlers, and girls appear to be more affected than boys. The lesions appear as pink, rubbery, nontender, nonfluctuant nodules on the cheeks, which can be single or multiple. A large prospective study in 30 children demonstrated that more 70% of the lesions cultured were negative for bacteria. Histologic analysis of some of the lesions showed a chronic dermal lymphohistiocytic granulomatous perifollicular infiltrate with numerous foreign body–type giant cells.2
The differential diagnosis of these lesions should include infectious pyodermas such as mycobacterial infections, cutaneous leishmaniasis, and botryomycosis; deep fungal infections such as sporotrichosis, coccidioidomycosis, and cryptococcosis; childhood nodulocystic acne; pilomatrixoma; epidermoid cyst; vascular tumors or malformations; and leukemia cutis.3
The diagnosis is usually clinical but in atypical cases a skin biopsy with tissue cultures should be performed. The decision to biopsy these lesions will need to be done in a one by one basis, as a biopsy may leave scaring on the area affected.
It has been postulated that a color Doppler ultrasound of the lesion may be a helpful ancillary study. Echographic findings show a well demarcated solid-cystic, hypoechoic dermal lesion, the largest axis of which lies parallel to the skin surface. The lesion lacks calcium deposits. Other findings include increased echogenicity of the underlaying hypodermis. The findings may vary depending on the stage of the lesion.4
The course of the condition may last on average months to years. Some lesions resolve spontaneously and others may respond to courses of oral antibiotics such as clarithromycin, azithromycin, or ivermectin. In our patient, several lesions improved with oral antibiotics, but the larger lesions were more persistent and resolved after a year.
The lesions usually resolve without scarring. In those patients with associated rosacea, maintenance topical treatments may be warranted and also may need follow-up with ophthalmology because they tend to commonly have ocular rosacea as well.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Pediatr Dermatol. 2013 Jan-Feb;30(1):109-11.
2. Br J Dermatol. 2007 Apr;156(4):705-8.
3. Pediatr Dermatol. 2018 Jul;35(4):490-3.
4. Actas Dermosifiliogr. 2019 Oct;110(8):637-41.
The patient was diagnosed with idiopathic facial aseptic granuloma (IFAG) based on the clinical findings, as well as the associated history of chalazia and erythematous papules seen in childhood rosacea.
She was treated with several months of azithromycin, sulfur wash, and metronidazole cream with improvement of some of the smaller lesions but no change on the larger nodules. Later she was treated with oral and topical ivermectin with no improvement. Some of the nodules slowly resolved except for the larger lesion on the right cheek. She was later treated with a 6-week course of clarithromycin with partial improvement of the nodule. The lesion resolved after 2 months of stopping clarithromycin.
IFAG is a rare condition seen in prepubescent children. The etiology of this condition is not well understood and is thought to be on the spectrum of childhood rosacea.1 From several recent reports, IFAG usually is seen in children with associated conditions including chalazia, conjunctivitis, blepharitis, and telangiectasias, which can be seen in patients with rosacea. These associated findings suggest the possibility of IFAG being a form of granulomatous rosacea in children.
This condition presents in childhood between the ages of 8 months and 13 years. Most of the cases occur in toddlers, and girls appear to be more affected than boys. The lesions appear as pink, rubbery, nontender, nonfluctuant nodules on the cheeks, which can be single or multiple. A large prospective study in 30 children demonstrated that more 70% of the lesions cultured were negative for bacteria. Histologic analysis of some of the lesions showed a chronic dermal lymphohistiocytic granulomatous perifollicular infiltrate with numerous foreign body–type giant cells.2
The differential diagnosis of these lesions should include infectious pyodermas such as mycobacterial infections, cutaneous leishmaniasis, and botryomycosis; deep fungal infections such as sporotrichosis, coccidioidomycosis, and cryptococcosis; childhood nodulocystic acne; pilomatrixoma; epidermoid cyst; vascular tumors or malformations; and leukemia cutis.3
The diagnosis is usually clinical but in atypical cases a skin biopsy with tissue cultures should be performed. The decision to biopsy these lesions will need to be done in a one by one basis, as a biopsy may leave scaring on the area affected.
It has been postulated that a color Doppler ultrasound of the lesion may be a helpful ancillary study. Echographic findings show a well demarcated solid-cystic, hypoechoic dermal lesion, the largest axis of which lies parallel to the skin surface. The lesion lacks calcium deposits. Other findings include increased echogenicity of the underlaying hypodermis. The findings may vary depending on the stage of the lesion.4
The course of the condition may last on average months to years. Some lesions resolve spontaneously and others may respond to courses of oral antibiotics such as clarithromycin, azithromycin, or ivermectin. In our patient, several lesions improved with oral antibiotics, but the larger lesions were more persistent and resolved after a year.
The lesions usually resolve without scarring. In those patients with associated rosacea, maintenance topical treatments may be warranted and also may need follow-up with ophthalmology because they tend to commonly have ocular rosacea as well.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Pediatr Dermatol. 2013 Jan-Feb;30(1):109-11.
2. Br J Dermatol. 2007 Apr;156(4):705-8.
3. Pediatr Dermatol. 2018 Jul;35(4):490-3.
4. Actas Dermosifiliogr. 2019 Oct;110(8):637-41.
The patient was diagnosed with idiopathic facial aseptic granuloma (IFAG) based on the clinical findings, as well as the associated history of chalazia and erythematous papules seen in childhood rosacea.
She was treated with several months of azithromycin, sulfur wash, and metronidazole cream with improvement of some of the smaller lesions but no change on the larger nodules. Later she was treated with oral and topical ivermectin with no improvement. Some of the nodules slowly resolved except for the larger lesion on the right cheek. She was later treated with a 6-week course of clarithromycin with partial improvement of the nodule. The lesion resolved after 2 months of stopping clarithromycin.
IFAG is a rare condition seen in prepubescent children. The etiology of this condition is not well understood and is thought to be on the spectrum of childhood rosacea.1 From several recent reports, IFAG usually is seen in children with associated conditions including chalazia, conjunctivitis, blepharitis, and telangiectasias, which can be seen in patients with rosacea. These associated findings suggest the possibility of IFAG being a form of granulomatous rosacea in children.
This condition presents in childhood between the ages of 8 months and 13 years. Most of the cases occur in toddlers, and girls appear to be more affected than boys. The lesions appear as pink, rubbery, nontender, nonfluctuant nodules on the cheeks, which can be single or multiple. A large prospective study in 30 children demonstrated that more 70% of the lesions cultured were negative for bacteria. Histologic analysis of some of the lesions showed a chronic dermal lymphohistiocytic granulomatous perifollicular infiltrate with numerous foreign body–type giant cells.2
The differential diagnosis of these lesions should include infectious pyodermas such as mycobacterial infections, cutaneous leishmaniasis, and botryomycosis; deep fungal infections such as sporotrichosis, coccidioidomycosis, and cryptococcosis; childhood nodulocystic acne; pilomatrixoma; epidermoid cyst; vascular tumors or malformations; and leukemia cutis.3
The diagnosis is usually clinical but in atypical cases a skin biopsy with tissue cultures should be performed. The decision to biopsy these lesions will need to be done in a one by one basis, as a biopsy may leave scaring on the area affected.
It has been postulated that a color Doppler ultrasound of the lesion may be a helpful ancillary study. Echographic findings show a well demarcated solid-cystic, hypoechoic dermal lesion, the largest axis of which lies parallel to the skin surface. The lesion lacks calcium deposits. Other findings include increased echogenicity of the underlaying hypodermis. The findings may vary depending on the stage of the lesion.4
The course of the condition may last on average months to years. Some lesions resolve spontaneously and others may respond to courses of oral antibiotics such as clarithromycin, azithromycin, or ivermectin. In our patient, several lesions improved with oral antibiotics, but the larger lesions were more persistent and resolved after a year.
The lesions usually resolve without scarring. In those patients with associated rosacea, maintenance topical treatments may be warranted and also may need follow-up with ophthalmology because they tend to commonly have ocular rosacea as well.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Pediatr Dermatol. 2013 Jan-Feb;30(1):109-11.
2. Br J Dermatol. 2007 Apr;156(4):705-8.
3. Pediatr Dermatol. 2018 Jul;35(4):490-3.
4. Actas Dermosifiliogr. 2019 Oct;110(8):637-41.
A 4-year-old female is brought to our pediatric dermatology clinic for evaluation of a persistent lesion on the cheek.
The mother of the child reports that the lesion started as a small "bug bite" and then started growing and getting firmer for the past 2 months. The girl has developed other smaller red, pimple-like lesions on the cheeks and one of them is starting to increase in size.
She denies any tenderness on the area or any purulent discharge. She has had no fevers, chills, weight loss, nose bleeds, fatigue, or any other symptoms. The mother has not noted any changes on the child's body odor, any rapid growth, or hair on her axillary or pubic area. She was treated with three different courses of oral antibiotics including cephalexin, trimethoprim/sulfamethoxazole, and clindamycin, as well as topical mupirocin, with no improvement.
Her past medical history is significant for several episodes of eyelid cysts that were treated with warm compresses and topical erythromycin ointment. The family history is significant for the father having severe acne as a teenager. She has two cats, she has not traveled, and she has an older sister who has no lesions.
On physical examination she is a lovely 4-year-old female in no acute distress. Her height is on the 70th percentile and weight on the 40th percentile for her age. Her blood pressure is 95/84 with a heart rate of 96. On skin examination she has several pink macules and papules on her bilateral cheeks. On the left cheek there are two pink nodules: One is 1 cm, and the other is 7 mm. The nodules are not tender. There is no warmth, fluctuance, or discharge from the lesions.
She has no cervical lymphadenopathy. She has no axillary or pubic hair. She is Tanner stage I.
Four-year-old boy presents with itchy rash on face, extremities
Contact dermatitis is an eczematous, pruritic eruption caused by direct contact with a substance and an irritant or allergic reaction. While it may not be contagious or life-threatening, contact dermatitis may be tremendously uncomfortable and impactful. Contact dermatitis may occur from exposure to chemicals in soaps, shampoos, cosmetics, metals, plants and topical products, and medications. The hallmark of contact dermatitis is localized eczematous reactions on the portion of the body that has been directly exposed to the reaction-causing substance. – often with oozing and crusting.
Irritant contact dermatitis is the most common type, which occurs when a substance damages the skin’s outer protective layer and does not require prior exposure or sensitization. Allergic contact dermatitis (ACD) can develop after exposure and sensitization, with an external allergen triggering an acute inflammatory response.1 Common causes of ACD include nickel, cobalt, gold, chromium, poison ivy/oak/sumac, cosmetics/personal care products that contain formaldehyde, fragrances, topical medications (anesthetics, antibiotics, corticosteroids), baby wipes, sunscreens, latex materials, protective equipment, soap/cleansers, resins, and acrylics. Among children, nickel sulfate, ammonium persulfate, gold sodium thiosulfate, thimerosal, and toluene-2,5-diamine are the most common sensitizers. Rarely, ACD can be triggered by something that enters the body through foods, flavorings, medicine, or medical or dental procedures (systemic contact dermatitis).
An Id reaction, or autoeczematization, is a generalized acute cutaneous reaction to a variety of stimuli, including infectious and inflammatory skin conditions such as contact dermatitis, stasis dermatitis, or other eczematous dermatitis.3 Id reactions usually are preceded by a preexisting dermatitis. Lesions are, by definition, at a site distant from the primary infection or dermatitis. They often are distributed symmetrically. Papular or papular-vesicular lesions of the extremities and or trunk are common in children.
Our patient had evidence of a localized periocular contact dermatitis reaction that preceded the symmetric papular, eczematous eruption consistent with an id reaction. Our patient was prescribed hydrocortisone 2.5 % ointment for the eyes and triamcinolone 0.1% ointment for the rash on the body, which resulted in significant improvement.
Rosacea is a chronic and relapsing inflammatory skin disorder that primarily involves the central face. Common clinical features include facial erythema, telangiectasias, and inflammatory papules or pustules. Ocular involvement may occur in the presence or absence of cutaneous manifestations. Patients may report the presence of ocular foreign body sensation, burning, photophobia, blurred vision, redness, and tearing. Ocular disease is usually bilateral and is not proportional to the severity of the skin disease.4 Common skin findings are blepharitis, lid margin telangiectasia, tear abnormalities, meibomian gland inflammation, frequent chalazion, bilateral hordeolum, conjunctivitis, and, rarely, corneal ulcers and vascularization. Our patient initially did have bilateral hordeolum in what may seem to be ocular rosacea. However, given the use of a recent topical antibiotic with subsequent eczematous rash of the eyelids and then resulting distant rash on the body 1week later made the rash likely allergic contact dermatitis with id reaction.
Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and in adults. The severity may vary from minimal, asymptomatic scaliness of the scalp (dandruff) to more widespread involvement. It is usually characterized by well-demarcated, erythematous plaques with greasy-looking, yellowish scales distributed on areas rich in sebaceous glands, such as the scalp, the external ear, the center of the face, the upper part of the trunk, and the intertriginous areas.
Psoriasis typically affects the outside of the elbows, knees, or scalp, although it can appear on any location. It tends to go through cycles, flaring for a few weeks or months, then subsiding for a while or going into remission. Ocular involvement is a well known manifestation of psoriasis.5 Psoriatic lesions of the eyelid are rare, even in the erythrodermic variant of the disease. Occasionally, pustular psoriasis may involve the eyelids, with typical psoriatic lesions visible on the skin and lid margin. The reason for the relative sparing of the eyelid skin in patients with psoriasis is unknown. Other manifestations include meibomian gland dysfunction, decreased tear film break-up time, a nonspecific conjunctivitis, and corneal disease secondary to lid disease such as trichiasis.
Gianotti-Crosti syndrome (GCS), also known as papular acrodermatitis, papular acrodermatitis of childhood, and infantile papular acrodermatitis, is a self-limited skin disorder that most often occurs in young children. Viral infections are common GCS precipitating factors . GCS typically manifests as a symmetric, papular eruption, often with larger (3- to 10-mm) flat topped papulovesicles. Classic sites of involvement include the cheeks, buttocks, and extensor surfaces of the forearms and legs. GCS may be pruritic or asymptomatic, and papules typically resolve spontaneously within 2 months. Occasionally, GCS persists for longer periods. The eyelid lesions and localized pattern, with the absence of larger symmetric papules of the buttocks and legs, was not consistent with papular acrodermatitis of childhood.
Dr. Bhatti is a research fellow in pediatric dermatology at Rady Children’s Hospital and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. They had no conflicts of interest to disclose. Email them at pdnews@mdedge.com.
References
1. J Am Acad Dermatol 2016 Jun; 74(6):1043-54.
2. Pediatr Dermatol 2016 Jul; 33(4):399-404.
3. Evans M & Bronson D. (2019) Id Reaction (Autoeczematization). Retrieved from emedicine.medscape.com/article/1049760-overview.
4. Curr Opin Ophthalmol. 2004 Dec;15(6):499-502.
5. Clin Dermatol. Mar-Apr 2016;34(2):146-50.
Contact dermatitis is an eczematous, pruritic eruption caused by direct contact with a substance and an irritant or allergic reaction. While it may not be contagious or life-threatening, contact dermatitis may be tremendously uncomfortable and impactful. Contact dermatitis may occur from exposure to chemicals in soaps, shampoos, cosmetics, metals, plants and topical products, and medications. The hallmark of contact dermatitis is localized eczematous reactions on the portion of the body that has been directly exposed to the reaction-causing substance. – often with oozing and crusting.
Irritant contact dermatitis is the most common type, which occurs when a substance damages the skin’s outer protective layer and does not require prior exposure or sensitization. Allergic contact dermatitis (ACD) can develop after exposure and sensitization, with an external allergen triggering an acute inflammatory response.1 Common causes of ACD include nickel, cobalt, gold, chromium, poison ivy/oak/sumac, cosmetics/personal care products that contain formaldehyde, fragrances, topical medications (anesthetics, antibiotics, corticosteroids), baby wipes, sunscreens, latex materials, protective equipment, soap/cleansers, resins, and acrylics. Among children, nickel sulfate, ammonium persulfate, gold sodium thiosulfate, thimerosal, and toluene-2,5-diamine are the most common sensitizers. Rarely, ACD can be triggered by something that enters the body through foods, flavorings, medicine, or medical or dental procedures (systemic contact dermatitis).
An Id reaction, or autoeczematization, is a generalized acute cutaneous reaction to a variety of stimuli, including infectious and inflammatory skin conditions such as contact dermatitis, stasis dermatitis, or other eczematous dermatitis.3 Id reactions usually are preceded by a preexisting dermatitis. Lesions are, by definition, at a site distant from the primary infection or dermatitis. They often are distributed symmetrically. Papular or papular-vesicular lesions of the extremities and or trunk are common in children.
Our patient had evidence of a localized periocular contact dermatitis reaction that preceded the symmetric papular, eczematous eruption consistent with an id reaction. Our patient was prescribed hydrocortisone 2.5 % ointment for the eyes and triamcinolone 0.1% ointment for the rash on the body, which resulted in significant improvement.
Rosacea is a chronic and relapsing inflammatory skin disorder that primarily involves the central face. Common clinical features include facial erythema, telangiectasias, and inflammatory papules or pustules. Ocular involvement may occur in the presence or absence of cutaneous manifestations. Patients may report the presence of ocular foreign body sensation, burning, photophobia, blurred vision, redness, and tearing. Ocular disease is usually bilateral and is not proportional to the severity of the skin disease.4 Common skin findings are blepharitis, lid margin telangiectasia, tear abnormalities, meibomian gland inflammation, frequent chalazion, bilateral hordeolum, conjunctivitis, and, rarely, corneal ulcers and vascularization. Our patient initially did have bilateral hordeolum in what may seem to be ocular rosacea. However, given the use of a recent topical antibiotic with subsequent eczematous rash of the eyelids and then resulting distant rash on the body 1week later made the rash likely allergic contact dermatitis with id reaction.
Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and in adults. The severity may vary from minimal, asymptomatic scaliness of the scalp (dandruff) to more widespread involvement. It is usually characterized by well-demarcated, erythematous plaques with greasy-looking, yellowish scales distributed on areas rich in sebaceous glands, such as the scalp, the external ear, the center of the face, the upper part of the trunk, and the intertriginous areas.
Psoriasis typically affects the outside of the elbows, knees, or scalp, although it can appear on any location. It tends to go through cycles, flaring for a few weeks or months, then subsiding for a while or going into remission. Ocular involvement is a well known manifestation of psoriasis.5 Psoriatic lesions of the eyelid are rare, even in the erythrodermic variant of the disease. Occasionally, pustular psoriasis may involve the eyelids, with typical psoriatic lesions visible on the skin and lid margin. The reason for the relative sparing of the eyelid skin in patients with psoriasis is unknown. Other manifestations include meibomian gland dysfunction, decreased tear film break-up time, a nonspecific conjunctivitis, and corneal disease secondary to lid disease such as trichiasis.
Gianotti-Crosti syndrome (GCS), also known as papular acrodermatitis, papular acrodermatitis of childhood, and infantile papular acrodermatitis, is a self-limited skin disorder that most often occurs in young children. Viral infections are common GCS precipitating factors . GCS typically manifests as a symmetric, papular eruption, often with larger (3- to 10-mm) flat topped papulovesicles. Classic sites of involvement include the cheeks, buttocks, and extensor surfaces of the forearms and legs. GCS may be pruritic or asymptomatic, and papules typically resolve spontaneously within 2 months. Occasionally, GCS persists for longer periods. The eyelid lesions and localized pattern, with the absence of larger symmetric papules of the buttocks and legs, was not consistent with papular acrodermatitis of childhood.
Dr. Bhatti is a research fellow in pediatric dermatology at Rady Children’s Hospital and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. They had no conflicts of interest to disclose. Email them at pdnews@mdedge.com.
References
1. J Am Acad Dermatol 2016 Jun; 74(6):1043-54.
2. Pediatr Dermatol 2016 Jul; 33(4):399-404.
3. Evans M & Bronson D. (2019) Id Reaction (Autoeczematization). Retrieved from emedicine.medscape.com/article/1049760-overview.
4. Curr Opin Ophthalmol. 2004 Dec;15(6):499-502.
5. Clin Dermatol. Mar-Apr 2016;34(2):146-50.
Contact dermatitis is an eczematous, pruritic eruption caused by direct contact with a substance and an irritant or allergic reaction. While it may not be contagious or life-threatening, contact dermatitis may be tremendously uncomfortable and impactful. Contact dermatitis may occur from exposure to chemicals in soaps, shampoos, cosmetics, metals, plants and topical products, and medications. The hallmark of contact dermatitis is localized eczematous reactions on the portion of the body that has been directly exposed to the reaction-causing substance. – often with oozing and crusting.
Irritant contact dermatitis is the most common type, which occurs when a substance damages the skin’s outer protective layer and does not require prior exposure or sensitization. Allergic contact dermatitis (ACD) can develop after exposure and sensitization, with an external allergen triggering an acute inflammatory response.1 Common causes of ACD include nickel, cobalt, gold, chromium, poison ivy/oak/sumac, cosmetics/personal care products that contain formaldehyde, fragrances, topical medications (anesthetics, antibiotics, corticosteroids), baby wipes, sunscreens, latex materials, protective equipment, soap/cleansers, resins, and acrylics. Among children, nickel sulfate, ammonium persulfate, gold sodium thiosulfate, thimerosal, and toluene-2,5-diamine are the most common sensitizers. Rarely, ACD can be triggered by something that enters the body through foods, flavorings, medicine, or medical or dental procedures (systemic contact dermatitis).
An Id reaction, or autoeczematization, is a generalized acute cutaneous reaction to a variety of stimuli, including infectious and inflammatory skin conditions such as contact dermatitis, stasis dermatitis, or other eczematous dermatitis.3 Id reactions usually are preceded by a preexisting dermatitis. Lesions are, by definition, at a site distant from the primary infection or dermatitis. They often are distributed symmetrically. Papular or papular-vesicular lesions of the extremities and or trunk are common in children.
Our patient had evidence of a localized periocular contact dermatitis reaction that preceded the symmetric papular, eczematous eruption consistent with an id reaction. Our patient was prescribed hydrocortisone 2.5 % ointment for the eyes and triamcinolone 0.1% ointment for the rash on the body, which resulted in significant improvement.
Rosacea is a chronic and relapsing inflammatory skin disorder that primarily involves the central face. Common clinical features include facial erythema, telangiectasias, and inflammatory papules or pustules. Ocular involvement may occur in the presence or absence of cutaneous manifestations. Patients may report the presence of ocular foreign body sensation, burning, photophobia, blurred vision, redness, and tearing. Ocular disease is usually bilateral and is not proportional to the severity of the skin disease.4 Common skin findings are blepharitis, lid margin telangiectasia, tear abnormalities, meibomian gland inflammation, frequent chalazion, bilateral hordeolum, conjunctivitis, and, rarely, corneal ulcers and vascularization. Our patient initially did have bilateral hordeolum in what may seem to be ocular rosacea. However, given the use of a recent topical antibiotic with subsequent eczematous rash of the eyelids and then resulting distant rash on the body 1week later made the rash likely allergic contact dermatitis with id reaction.
Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and in adults. The severity may vary from minimal, asymptomatic scaliness of the scalp (dandruff) to more widespread involvement. It is usually characterized by well-demarcated, erythematous plaques with greasy-looking, yellowish scales distributed on areas rich in sebaceous glands, such as the scalp, the external ear, the center of the face, the upper part of the trunk, and the intertriginous areas.
Psoriasis typically affects the outside of the elbows, knees, or scalp, although it can appear on any location. It tends to go through cycles, flaring for a few weeks or months, then subsiding for a while or going into remission. Ocular involvement is a well known manifestation of psoriasis.5 Psoriatic lesions of the eyelid are rare, even in the erythrodermic variant of the disease. Occasionally, pustular psoriasis may involve the eyelids, with typical psoriatic lesions visible on the skin and lid margin. The reason for the relative sparing of the eyelid skin in patients with psoriasis is unknown. Other manifestations include meibomian gland dysfunction, decreased tear film break-up time, a nonspecific conjunctivitis, and corneal disease secondary to lid disease such as trichiasis.
Gianotti-Crosti syndrome (GCS), also known as papular acrodermatitis, papular acrodermatitis of childhood, and infantile papular acrodermatitis, is a self-limited skin disorder that most often occurs in young children. Viral infections are common GCS precipitating factors . GCS typically manifests as a symmetric, papular eruption, often with larger (3- to 10-mm) flat topped papulovesicles. Classic sites of involvement include the cheeks, buttocks, and extensor surfaces of the forearms and legs. GCS may be pruritic or asymptomatic, and papules typically resolve spontaneously within 2 months. Occasionally, GCS persists for longer periods. The eyelid lesions and localized pattern, with the absence of larger symmetric papules of the buttocks and legs, was not consistent with papular acrodermatitis of childhood.
Dr. Bhatti is a research fellow in pediatric dermatology at Rady Children’s Hospital and the University of California, San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children’s Hospital–San Diego. He is vice chair of the department of dermatology and professor of dermatology and pediatrics at the University of California, San Diego. They had no conflicts of interest to disclose. Email them at pdnews@mdedge.com.
References
1. J Am Acad Dermatol 2016 Jun; 74(6):1043-54.
2. Pediatr Dermatol 2016 Jul; 33(4):399-404.
3. Evans M & Bronson D. (2019) Id Reaction (Autoeczematization). Retrieved from emedicine.medscape.com/article/1049760-overview.
4. Curr Opin Ophthalmol. 2004 Dec;15(6):499-502.
5. Clin Dermatol. Mar-Apr 2016;34(2):146-50.
A 4-year-old healthy male with no significant prior medical history presents for evaluation of "itchy bumps" on the face and extremities of 2 weeks' duration.
The child was well until around 2 and a half weeks ago when he presented for evaluation of two lesions on the lower eyelids, diagnosed as hordeolum (a stye). He was prescribed ofloxacin ophthalmic solution.
One week later he developed bilateral itchy red eyes with red, thickened areas on the upper lids, followed several days later by pruritic papules on the ears, wrists, elbows, knees, and ankles. His mother used Vaseline for the eyelids for 1 week with no improvement. Physical exam at the dermatologist's office showed mild erythema, induration, and lichenification of the upper eyelids, and bilateral periocular eczematous patches with overlying scale. Subtle papules were evident on the elbows and feet.
A 72-year-old with an acute, pruritic, bullous eruption involving his right pretibial extremity
Localized bullous pemphigoid
with a predilection in the elderly population.1
Localized variants of bullous pemphigoid (BP) are rare and have been reported to arise at sites of mechanical trauma, prior radiation, lymphedema, surgical scars, burns, fistulas, and ostomies.1-3 Although the mechanism remains unclear, the Koebner phenomenon is thought to induce dysregulation of immunologic and vascular factors in sites of mechanical shear and trauma in susceptible individuals.3
Localized BP is an important entity for the dermatologist to be familiar with, as the diagnosis is often delayed. The localized, well-defined skin lesions frequently mimic contact dermatitis. In fact, previous reports have shown the most likely misdiagnosis of localized BP is acute allergic contact dermatitis, stasis dermatitis, and eczematous dermatitis.4,5
In this patient, histopathologic examination of a biopsy revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed strong linear IgG and C3 deposits at the basal membrane level. Serum level of autoantibody to BP180 antigen was elevated. Bacterial culture was positive for Staphylococcus aureus. These findings were suggestive of unilateral, localized BP with superimposed bacterial infection. Initial treatment with an extended course of doxycycline 200 mg twice daily, topical triamcinolone 0.1% ointment twice daily with compression therapy, and leg elevation led to clinical improvement with healing of previous lesions on the leg. At follow-up 3 weeks later, the patient had continued to develop new bullous lesions on the trunk and upper thighs. He was subsequently started on systemic immunosuppressive therapy for generalized bullous pemphigoid.
Importantly, localized BP generally follows a more benign disease course, although long-term follow-up is recommended for monitoring given the potential risk of developing the generalized form of BP of approximately 15%.3 Topical corticosteroids and oral antibiotics are recommended as the first-line therapy in these patients, with an escalated systemic therapy if needed for disease progression.3,5
Our case represents an important differential diagnosis to consider when evaluating an acute localized bullous eruption in an elderly patient.
Dr. Cusick and Dr. Dolohanty are with the department of dermatology, University of Rochester (N.Y.), and provided the case and photo. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Kohroh K et al. J Dermatol. 2007 Jul;34(7):482-5.
2. Nguyen T et al. Dermatology 2014;229(2):88-96.
3. Sen BB et al. Indian J Dermatol Venereol Leprol. 2013;79(4):554.
4. Salomon RJ et al. Arch Dermatol. 1987 Mar;123(3):389-92.
5. Tran JT, Mutasim DF. Int J Dermatol. 2005 Nov;44(11):942-5.
Localized bullous pemphigoid
with a predilection in the elderly population.1
Localized variants of bullous pemphigoid (BP) are rare and have been reported to arise at sites of mechanical trauma, prior radiation, lymphedema, surgical scars, burns, fistulas, and ostomies.1-3 Although the mechanism remains unclear, the Koebner phenomenon is thought to induce dysregulation of immunologic and vascular factors in sites of mechanical shear and trauma in susceptible individuals.3
Localized BP is an important entity for the dermatologist to be familiar with, as the diagnosis is often delayed. The localized, well-defined skin lesions frequently mimic contact dermatitis. In fact, previous reports have shown the most likely misdiagnosis of localized BP is acute allergic contact dermatitis, stasis dermatitis, and eczematous dermatitis.4,5
In this patient, histopathologic examination of a biopsy revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed strong linear IgG and C3 deposits at the basal membrane level. Serum level of autoantibody to BP180 antigen was elevated. Bacterial culture was positive for Staphylococcus aureus. These findings were suggestive of unilateral, localized BP with superimposed bacterial infection. Initial treatment with an extended course of doxycycline 200 mg twice daily, topical triamcinolone 0.1% ointment twice daily with compression therapy, and leg elevation led to clinical improvement with healing of previous lesions on the leg. At follow-up 3 weeks later, the patient had continued to develop new bullous lesions on the trunk and upper thighs. He was subsequently started on systemic immunosuppressive therapy for generalized bullous pemphigoid.
Importantly, localized BP generally follows a more benign disease course, although long-term follow-up is recommended for monitoring given the potential risk of developing the generalized form of BP of approximately 15%.3 Topical corticosteroids and oral antibiotics are recommended as the first-line therapy in these patients, with an escalated systemic therapy if needed for disease progression.3,5
Our case represents an important differential diagnosis to consider when evaluating an acute localized bullous eruption in an elderly patient.
Dr. Cusick and Dr. Dolohanty are with the department of dermatology, University of Rochester (N.Y.), and provided the case and photo. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Kohroh K et al. J Dermatol. 2007 Jul;34(7):482-5.
2. Nguyen T et al. Dermatology 2014;229(2):88-96.
3. Sen BB et al. Indian J Dermatol Venereol Leprol. 2013;79(4):554.
4. Salomon RJ et al. Arch Dermatol. 1987 Mar;123(3):389-92.
5. Tran JT, Mutasim DF. Int J Dermatol. 2005 Nov;44(11):942-5.
Localized bullous pemphigoid
with a predilection in the elderly population.1
Localized variants of bullous pemphigoid (BP) are rare and have been reported to arise at sites of mechanical trauma, prior radiation, lymphedema, surgical scars, burns, fistulas, and ostomies.1-3 Although the mechanism remains unclear, the Koebner phenomenon is thought to induce dysregulation of immunologic and vascular factors in sites of mechanical shear and trauma in susceptible individuals.3
Localized BP is an important entity for the dermatologist to be familiar with, as the diagnosis is often delayed. The localized, well-defined skin lesions frequently mimic contact dermatitis. In fact, previous reports have shown the most likely misdiagnosis of localized BP is acute allergic contact dermatitis, stasis dermatitis, and eczematous dermatitis.4,5
In this patient, histopathologic examination of a biopsy revealed a subepidermal blister with numerous eosinophils. Direct immunofluorescence study of perilesional skin showed strong linear IgG and C3 deposits at the basal membrane level. Serum level of autoantibody to BP180 antigen was elevated. Bacterial culture was positive for Staphylococcus aureus. These findings were suggestive of unilateral, localized BP with superimposed bacterial infection. Initial treatment with an extended course of doxycycline 200 mg twice daily, topical triamcinolone 0.1% ointment twice daily with compression therapy, and leg elevation led to clinical improvement with healing of previous lesions on the leg. At follow-up 3 weeks later, the patient had continued to develop new bullous lesions on the trunk and upper thighs. He was subsequently started on systemic immunosuppressive therapy for generalized bullous pemphigoid.
Importantly, localized BP generally follows a more benign disease course, although long-term follow-up is recommended for monitoring given the potential risk of developing the generalized form of BP of approximately 15%.3 Topical corticosteroids and oral antibiotics are recommended as the first-line therapy in these patients, with an escalated systemic therapy if needed for disease progression.3,5
Our case represents an important differential diagnosis to consider when evaluating an acute localized bullous eruption in an elderly patient.
Dr. Cusick and Dr. Dolohanty are with the department of dermatology, University of Rochester (N.Y.), and provided the case and photo. Donna Bilu Martin, MD, edited the column.
Dr. Bilu Martin is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at mdedge.com/dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
References
1. Kohroh K et al. J Dermatol. 2007 Jul;34(7):482-5.
2. Nguyen T et al. Dermatology 2014;229(2):88-96.
3. Sen BB et al. Indian J Dermatol Venereol Leprol. 2013;79(4):554.
4. Salomon RJ et al. Arch Dermatol. 1987 Mar;123(3):389-92.
5. Tran JT, Mutasim DF. Int J Dermatol. 2005 Nov;44(11):942-5.
What presents as deep erythematous papules, pustules, and may form an annular or circular plaque?
Scrapings of the child’s rash were analyzed with potassium hydroxide (KOH) under microscopy which revealed multiple septate hyphae.
She was diagnosed with Majocchi’s granuloma. The fungal culture was positive for Trichophyton rubrum.
Majocchi’s granuloma (MG) is cutaneous mycosis in which the fungal infection goes deeper into the hair follicle causing granulomatous folliculitis and perifolliculitis.1 It was first described by Domenico Majocchi in 1883, and he named the condition “granuloma tricofitico.”2
It is commonly caused by T. rubrum but also can be caused by T. mentagrophytes, T. tonsurans, T. verrucosum, Microsporum canis, and Epidermophyton floccosum.2,3 Patients at risk for developing this infection include those previously treated with topical corticosteroids, immunosuppressed patients, patients with areas under occlusion, and those with areas traumatized by shaving. This infection is most commonly seen in the lower extremities, but can happen anywhere in the body. The lesions present as deep erythematous papules, pustules, and may form an annular or circular plaque as seen on our patient.
A KOH test of skin scrapings and hair extractions often can reveal fungal hyphae. Identification of the pathogen can be performed with culture or polymerase chain reaction of skin samples. If the diagnosis is uncertain or the KOH is negative, a skin biopsy can be performed. Histopathologic examination reveals perifollicular granulomas with associated dermal abscesses. Giant cells may be observed. MG is associated with chronic inflammation with lymphocytes, macrophages, epithelioid cells, and scattered multinucleated giant cells.2,3
The differential diagnosis for these lesions in children includes other granulomatous conditions such as granulomatous rosacea, sarcoidosis, and granuloma faciale, as well as bacterial or atypical mycobacterial infections, cutaneous leishmaniasis, and eosinophilic pustular folliculitis.
Treatment of MG requires systemic treatment with griseofulvin, itraconazole, or terbinafine for at least 4-8 weeks or until all the lesions have resolved. Our patient was treated with 6 weeks of high-dose griseofulvin with resolution of her lesions.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Dermatol Online J. 2018 Dec 15;24(12):13030/qt89k4t6wj.
2. Med Mycol. 2012 Jul;50(5):449-57.
3. Clin Microbiol Rev. 2011 Apr;24(2):247-80.
Scrapings of the child’s rash were analyzed with potassium hydroxide (KOH) under microscopy which revealed multiple septate hyphae.
She was diagnosed with Majocchi’s granuloma. The fungal culture was positive for Trichophyton rubrum.
Majocchi’s granuloma (MG) is cutaneous mycosis in which the fungal infection goes deeper into the hair follicle causing granulomatous folliculitis and perifolliculitis.1 It was first described by Domenico Majocchi in 1883, and he named the condition “granuloma tricofitico.”2
It is commonly caused by T. rubrum but also can be caused by T. mentagrophytes, T. tonsurans, T. verrucosum, Microsporum canis, and Epidermophyton floccosum.2,3 Patients at risk for developing this infection include those previously treated with topical corticosteroids, immunosuppressed patients, patients with areas under occlusion, and those with areas traumatized by shaving. This infection is most commonly seen in the lower extremities, but can happen anywhere in the body. The lesions present as deep erythematous papules, pustules, and may form an annular or circular plaque as seen on our patient.
A KOH test of skin scrapings and hair extractions often can reveal fungal hyphae. Identification of the pathogen can be performed with culture or polymerase chain reaction of skin samples. If the diagnosis is uncertain or the KOH is negative, a skin biopsy can be performed. Histopathologic examination reveals perifollicular granulomas with associated dermal abscesses. Giant cells may be observed. MG is associated with chronic inflammation with lymphocytes, macrophages, epithelioid cells, and scattered multinucleated giant cells.2,3
The differential diagnosis for these lesions in children includes other granulomatous conditions such as granulomatous rosacea, sarcoidosis, and granuloma faciale, as well as bacterial or atypical mycobacterial infections, cutaneous leishmaniasis, and eosinophilic pustular folliculitis.
Treatment of MG requires systemic treatment with griseofulvin, itraconazole, or terbinafine for at least 4-8 weeks or until all the lesions have resolved. Our patient was treated with 6 weeks of high-dose griseofulvin with resolution of her lesions.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Dermatol Online J. 2018 Dec 15;24(12):13030/qt89k4t6wj.
2. Med Mycol. 2012 Jul;50(5):449-57.
3. Clin Microbiol Rev. 2011 Apr;24(2):247-80.
Scrapings of the child’s rash were analyzed with potassium hydroxide (KOH) under microscopy which revealed multiple septate hyphae.
She was diagnosed with Majocchi’s granuloma. The fungal culture was positive for Trichophyton rubrum.
Majocchi’s granuloma (MG) is cutaneous mycosis in which the fungal infection goes deeper into the hair follicle causing granulomatous folliculitis and perifolliculitis.1 It was first described by Domenico Majocchi in 1883, and he named the condition “granuloma tricofitico.”2
It is commonly caused by T. rubrum but also can be caused by T. mentagrophytes, T. tonsurans, T. verrucosum, Microsporum canis, and Epidermophyton floccosum.2,3 Patients at risk for developing this infection include those previously treated with topical corticosteroids, immunosuppressed patients, patients with areas under occlusion, and those with areas traumatized by shaving. This infection is most commonly seen in the lower extremities, but can happen anywhere in the body. The lesions present as deep erythematous papules, pustules, and may form an annular or circular plaque as seen on our patient.
A KOH test of skin scrapings and hair extractions often can reveal fungal hyphae. Identification of the pathogen can be performed with culture or polymerase chain reaction of skin samples. If the diagnosis is uncertain or the KOH is negative, a skin biopsy can be performed. Histopathologic examination reveals perifollicular granulomas with associated dermal abscesses. Giant cells may be observed. MG is associated with chronic inflammation with lymphocytes, macrophages, epithelioid cells, and scattered multinucleated giant cells.2,3
The differential diagnosis for these lesions in children includes other granulomatous conditions such as granulomatous rosacea, sarcoidosis, and granuloma faciale, as well as bacterial or atypical mycobacterial infections, cutaneous leishmaniasis, and eosinophilic pustular folliculitis.
Treatment of MG requires systemic treatment with griseofulvin, itraconazole, or terbinafine for at least 4-8 weeks or until all the lesions have resolved. Our patient was treated with 6 weeks of high-dose griseofulvin with resolution of her lesions.
Dr. Matiz is a pediatric dermatologist at Southern California Permanente Medical Group, San Diego. She said she had no relevant financial disclosures. Email her at pdnews@mdedge.com.
References
1. Dermatol Online J. 2018 Dec 15;24(12):13030/qt89k4t6wj.
2. Med Mycol. 2012 Jul;50(5):449-57.
3. Clin Microbiol Rev. 2011 Apr;24(2):247-80.
A 3-year-old girl with a known history of eczema presented to our dermatology clinic for evaluation of a persistent rash for about a year on the right cheek.
The mother reported she was treating the lesions with hydrocortisone cream 2.5% as instructed previously for her eczema. Initially the rash got partially better but then started getting worse again. The area was itchy.
The child was later seen in the emergency department, where she was recommended to treat the area with a combination cream of terbinafine 1% and betamethasone dipropionate 0.05%. The mother applied this cream as instructed for 3 weeks with some improvement of the lesions on the cheek.
A few weeks later, pimples started coming back. The mother tried the medication again but this time it was not helpful and the rash continued to expand.
The mother reported having a rash on her hand months back, which she successfully treated with the combination cream provided at the emergency department. They have no pets at home.
The child has a little sister who also has mild eczema.
She goes to day care and dances ballet.
Flat-topped papules on the neck, arms, and trunk
that typically occur on the trunk, extremities, or genitalia of children and young adults. However, it can affect people of all ages and all areas of skin. Lichen nitidus lesions may emerge in areas of trauma, often in a linear arrangement, called the Koebner phenomenon. It is not thought to be associated with any systemic disease. Nail involvement may be present. Oral lesions are not commonly seen. The diagnosis of LN is often a clinical one.
Histopathology for this patient showed a focally dense lymphohistiocytic infiltrate with multinucleate giant cells in the papillary dermis, associated with overlying epidermal atrophy and adjacent elongated rete ridges surrounding the infiltrate in a characteristic “ball and claw” pattern. These findings were consistent with a diagnosis of lichen nitidus.
The differential diagnosis includes lichen planus (LP). In LP, lesions tend to be larger and more violaceous. They tend to favor wrists, lower extremities, and genitalia. Oral and nail involvement are common. Histologically, a band-like lichenoid infiltrate in the dermis is present. Granulomatous inflammation and giant cells are absent. Direct immunofluorescence is positive for globular deposits of IgG, IgA, IgM and/or complement at the dermal-epidermal junction.
A hepatitis panel was drawn for this patient and was negative. Treatment for lichen nitidus is only needed if symptomatic because lesions will generally resolve spontaneously. Lesions may take months or years to resolve. For significant pruritus, topical corticosteroids or antihistamines may be used. Topical emollients are recommended. Topical tacrolimus has been reported to improve lesions. Oral steroids and light therapy have been reported to improve generalized lichen nitidus not responding to topical treatments.
The case and these photos were submitted byMs. Swartz of Nova Southeastern University, Ft. Lauderdale, Fla.; Dr. Chen and Dr. Walder of Bay Harbor Islands, Fla.; and Dr. Winslow of Pompano Beach, Fla. Donna Bilu Martin, MD, editor of this column, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
that typically occur on the trunk, extremities, or genitalia of children and young adults. However, it can affect people of all ages and all areas of skin. Lichen nitidus lesions may emerge in areas of trauma, often in a linear arrangement, called the Koebner phenomenon. It is not thought to be associated with any systemic disease. Nail involvement may be present. Oral lesions are not commonly seen. The diagnosis of LN is often a clinical one.
Histopathology for this patient showed a focally dense lymphohistiocytic infiltrate with multinucleate giant cells in the papillary dermis, associated with overlying epidermal atrophy and adjacent elongated rete ridges surrounding the infiltrate in a characteristic “ball and claw” pattern. These findings were consistent with a diagnosis of lichen nitidus.
The differential diagnosis includes lichen planus (LP). In LP, lesions tend to be larger and more violaceous. They tend to favor wrists, lower extremities, and genitalia. Oral and nail involvement are common. Histologically, a band-like lichenoid infiltrate in the dermis is present. Granulomatous inflammation and giant cells are absent. Direct immunofluorescence is positive for globular deposits of IgG, IgA, IgM and/or complement at the dermal-epidermal junction.
A hepatitis panel was drawn for this patient and was negative. Treatment for lichen nitidus is only needed if symptomatic because lesions will generally resolve spontaneously. Lesions may take months or years to resolve. For significant pruritus, topical corticosteroids or antihistamines may be used. Topical emollients are recommended. Topical tacrolimus has been reported to improve lesions. Oral steroids and light therapy have been reported to improve generalized lichen nitidus not responding to topical treatments.
The case and these photos were submitted byMs. Swartz of Nova Southeastern University, Ft. Lauderdale, Fla.; Dr. Chen and Dr. Walder of Bay Harbor Islands, Fla.; and Dr. Winslow of Pompano Beach, Fla. Donna Bilu Martin, MD, editor of this column, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
that typically occur on the trunk, extremities, or genitalia of children and young adults. However, it can affect people of all ages and all areas of skin. Lichen nitidus lesions may emerge in areas of trauma, often in a linear arrangement, called the Koebner phenomenon. It is not thought to be associated with any systemic disease. Nail involvement may be present. Oral lesions are not commonly seen. The diagnosis of LN is often a clinical one.
Histopathology for this patient showed a focally dense lymphohistiocytic infiltrate with multinucleate giant cells in the papillary dermis, associated with overlying epidermal atrophy and adjacent elongated rete ridges surrounding the infiltrate in a characteristic “ball and claw” pattern. These findings were consistent with a diagnosis of lichen nitidus.
The differential diagnosis includes lichen planus (LP). In LP, lesions tend to be larger and more violaceous. They tend to favor wrists, lower extremities, and genitalia. Oral and nail involvement are common. Histologically, a band-like lichenoid infiltrate in the dermis is present. Granulomatous inflammation and giant cells are absent. Direct immunofluorescence is positive for globular deposits of IgG, IgA, IgM and/or complement at the dermal-epidermal junction.
A hepatitis panel was drawn for this patient and was negative. Treatment for lichen nitidus is only needed if symptomatic because lesions will generally resolve spontaneously. Lesions may take months or years to resolve. For significant pruritus, topical corticosteroids or antihistamines may be used. Topical emollients are recommended. Topical tacrolimus has been reported to improve lesions. Oral steroids and light therapy have been reported to improve generalized lichen nitidus not responding to topical treatments.
The case and these photos were submitted byMs. Swartz of Nova Southeastern University, Ft. Lauderdale, Fla.; Dr. Chen and Dr. Walder of Bay Harbor Islands, Fla.; and Dr. Winslow of Pompano Beach, Fla. Donna Bilu Martin, MD, editor of this column, is a board-certified dermatologist in private practice at Premier Dermatology, MD, in Aventura, Fla. More diagnostic cases are available at MDedge.com/Dermatology. To submit a case for possible publication, send an email to dermnews@mdedge.com.
