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A 95-year-old White male with hypertension presented with itchy patches and bullae on the trunk and extremities
and is associated with various predisposing factors, including HLA genes, comorbidities, aging, and trigger factors such as drugs, trauma, radiation, chemotherapy, and infections. The autoimmune reaction is mediated by a dysregulation of T cells in which IgG and IgE autoantibodies form against hemidesmosomal proteins (BP180 and BP230). These autoantibodies induce neutrophil activation, recruitment, and degradation in the basement membrane of the skin.
Typically, patients present with intense pruritus followed by an urticarial or eczematous eruption. Tense blisters and bullae occur commonly on the trunk and extremities. Drug-associated bullous pemphigoid (DABP) is a common manifestation of the disease with histologic and immunologic features similar to those of the idiopathic version. Eruptions can be triggered by systemic or topical medications, and incidence of these reactions may be related to a genetic predisposition for the disease.
Some research suggests that drug-induced changes to the antigenic properties of the epidermal basement membrane result in an augmented immune response, while others point to structural modification in these zones that stimulate the immune system. Thiol- and phenol-based drugs have been largely implicated in the development of DABP because they are capable of structural modification and disruption of the dermo-epidermal junction in the basement membrane.
DABP often presents with patients taking multiple medications. Some of the most common medications are gliptins, PD-1 inhibitors, diuretics, antibiotics, anti-inflammatory drugs, and ACE-inhibitors, and other cardiovascular drugs. DABP may present with mucosal eruptions unlike its idiopathic counterpart that is mostly contained to the skin.
On this patient, two punch biopsies were taken. Histopathology revealed an eosinophil-rich subepidermal blister with a smooth epidermal undersurface consistent with bullous pemphigoid. Direct immunofluorescence was positive with a deposition of IgG and C3 at the epidermal side of salt split basement membrane zone.
Treatment for BP includes high potency topical and systemic steroids. Tetracyclines and niacinamide have been reported to improve the condition. Treatment is tailored to allow for cutaneous healing and control pruritus, but the physician must be mindful of the patient’s comorbidities and capacity for self-care. Prognosis is often better for DABP as withdrawal of the medication greatly accelerates clearance of the lesions. Worse prognosis is related to increased number of comorbidities and older age. Our patient’s BP is controlled currently with topical steroids and oral doxycycline.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University College of Osteopathic Medicine, Tampa, and Dr. Bilu Martin.
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. Miyamoto D et al. An Bras Dermatol. 2019 Mar-Apr;94(2):133-46.
2. Moro et al. Biomolecules. 2020 Oct 10;10(10):1432.
3. Verheyden M et al. Acta Derm Venereol. 2020 Aug 17;100(15):adv00224.
and is associated with various predisposing factors, including HLA genes, comorbidities, aging, and trigger factors such as drugs, trauma, radiation, chemotherapy, and infections. The autoimmune reaction is mediated by a dysregulation of T cells in which IgG and IgE autoantibodies form against hemidesmosomal proteins (BP180 and BP230). These autoantibodies induce neutrophil activation, recruitment, and degradation in the basement membrane of the skin.
Typically, patients present with intense pruritus followed by an urticarial or eczematous eruption. Tense blisters and bullae occur commonly on the trunk and extremities. Drug-associated bullous pemphigoid (DABP) is a common manifestation of the disease with histologic and immunologic features similar to those of the idiopathic version. Eruptions can be triggered by systemic or topical medications, and incidence of these reactions may be related to a genetic predisposition for the disease.
Some research suggests that drug-induced changes to the antigenic properties of the epidermal basement membrane result in an augmented immune response, while others point to structural modification in these zones that stimulate the immune system. Thiol- and phenol-based drugs have been largely implicated in the development of DABP because they are capable of structural modification and disruption of the dermo-epidermal junction in the basement membrane.
DABP often presents with patients taking multiple medications. Some of the most common medications are gliptins, PD-1 inhibitors, diuretics, antibiotics, anti-inflammatory drugs, and ACE-inhibitors, and other cardiovascular drugs. DABP may present with mucosal eruptions unlike its idiopathic counterpart that is mostly contained to the skin.
On this patient, two punch biopsies were taken. Histopathology revealed an eosinophil-rich subepidermal blister with a smooth epidermal undersurface consistent with bullous pemphigoid. Direct immunofluorescence was positive with a deposition of IgG and C3 at the epidermal side of salt split basement membrane zone.
Treatment for BP includes high potency topical and systemic steroids. Tetracyclines and niacinamide have been reported to improve the condition. Treatment is tailored to allow for cutaneous healing and control pruritus, but the physician must be mindful of the patient’s comorbidities and capacity for self-care. Prognosis is often better for DABP as withdrawal of the medication greatly accelerates clearance of the lesions. Worse prognosis is related to increased number of comorbidities and older age. Our patient’s BP is controlled currently with topical steroids and oral doxycycline.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University College of Osteopathic Medicine, Tampa, and Dr. Bilu Martin.
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. Miyamoto D et al. An Bras Dermatol. 2019 Mar-Apr;94(2):133-46.
2. Moro et al. Biomolecules. 2020 Oct 10;10(10):1432.
3. Verheyden M et al. Acta Derm Venereol. 2020 Aug 17;100(15):adv00224.
and is associated with various predisposing factors, including HLA genes, comorbidities, aging, and trigger factors such as drugs, trauma, radiation, chemotherapy, and infections. The autoimmune reaction is mediated by a dysregulation of T cells in which IgG and IgE autoantibodies form against hemidesmosomal proteins (BP180 and BP230). These autoantibodies induce neutrophil activation, recruitment, and degradation in the basement membrane of the skin.
Typically, patients present with intense pruritus followed by an urticarial or eczematous eruption. Tense blisters and bullae occur commonly on the trunk and extremities. Drug-associated bullous pemphigoid (DABP) is a common manifestation of the disease with histologic and immunologic features similar to those of the idiopathic version. Eruptions can be triggered by systemic or topical medications, and incidence of these reactions may be related to a genetic predisposition for the disease.
Some research suggests that drug-induced changes to the antigenic properties of the epidermal basement membrane result in an augmented immune response, while others point to structural modification in these zones that stimulate the immune system. Thiol- and phenol-based drugs have been largely implicated in the development of DABP because they are capable of structural modification and disruption of the dermo-epidermal junction in the basement membrane.
DABP often presents with patients taking multiple medications. Some of the most common medications are gliptins, PD-1 inhibitors, diuretics, antibiotics, anti-inflammatory drugs, and ACE-inhibitors, and other cardiovascular drugs. DABP may present with mucosal eruptions unlike its idiopathic counterpart that is mostly contained to the skin.
On this patient, two punch biopsies were taken. Histopathology revealed an eosinophil-rich subepidermal blister with a smooth epidermal undersurface consistent with bullous pemphigoid. Direct immunofluorescence was positive with a deposition of IgG and C3 at the epidermal side of salt split basement membrane zone.
Treatment for BP includes high potency topical and systemic steroids. Tetracyclines and niacinamide have been reported to improve the condition. Treatment is tailored to allow for cutaneous healing and control pruritus, but the physician must be mindful of the patient’s comorbidities and capacity for self-care. Prognosis is often better for DABP as withdrawal of the medication greatly accelerates clearance of the lesions. Worse prognosis is related to increased number of comorbidities and older age. Our patient’s BP is controlled currently with topical steroids and oral doxycycline.
This case and photo were submitted by Lucas Shapiro, BS, Nova Southeastern University College of Osteopathic Medicine, Tampa, and Dr. Bilu Martin.
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. Miyamoto D et al. An Bras Dermatol. 2019 Mar-Apr;94(2):133-46.
2. Moro et al. Biomolecules. 2020 Oct 10;10(10):1432.
3. Verheyden M et al. Acta Derm Venereol. 2020 Aug 17;100(15):adv00224.
A 95-year-old White male with hypertension presented with a history of very itchy patches and bullae on the trunk and extremities.
A White female presented with pustules and erythematous macules on the left palm
Psoriasis is an immune-mediated chronic inflammatory disease characterized by well-demarcated, scaly, erythematous plaques. Those who present with the condition often have a family history, which supports recent research uncovering various genes implicated in its pathogenesis. The disease is also associated with other systemic complications, most notably cardiovascular disease.
This condition is found in a small percentage of patients with psoriasis and presentation varies from hyperkeratotic plaques to pustular lesions. The pustular form is known as palmoplantar pustulosis and is within the spectrum of palmoplantar psoriasis.
Psoriasis is typically a clinical diagnosis and its severity can be measured using the Psoriasis Area and Severity Index. If biopsy is performed, the histology demonstrates parakeratosis, orthokeratosis, loss of the stratum granulosum, and dilated vasculature with an inflammatory cell infiltrate. The keratinocytes present with abnormal differentiation and hyperplasia, and the presence of foci of neutrophils known as “Munro’s microabscesses” in the stratum corneum serve as the hallmark of histological diagnosis. However, it is important to note that appearance can vary based on the stage of the lesion and the subtype of psoriasis present.
Palmoplantar psoriasis can be especially limiting and difficult to treat because of its distribution. Topical steroids, topical vitamin D analogues, and narrow band ultraviolet light therapy can be effective for less severe cases. Methotrexate, biologic treatments, and apremilast can be used for more extensive disease.
This patient is HLA-B27 positive and has uveitis. The presence of the HLA-B27 allele has been associated with inflammatory bowel disease, uveitis, psoriatic arthritis, and reactive arthritis. It has also been reported to be associated with pustular psoriasis. She responded well to topical steroids and vitamin D analogues.
This case and photo were submitted by Mr. Shapiro at Nova Southeastern University College of Osteopathic Medicine, Davie, Fla., and Dr. Bilu Martin.
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. Psoriasis: Overview and Diagnosis, in “Evidence-Based Psoriasis. Updates in Clinical Dermatology.” (Cham, Switzerland: Springer International, 2018).
2. Merola JF et al. Dermatol Ther. 2018 May;31(3):e12589.
3. Chung J et al. J Am Acad Dermatol. 2014 Oct;71(4):623-32.
Psoriasis is an immune-mediated chronic inflammatory disease characterized by well-demarcated, scaly, erythematous plaques. Those who present with the condition often have a family history, which supports recent research uncovering various genes implicated in its pathogenesis. The disease is also associated with other systemic complications, most notably cardiovascular disease.
This condition is found in a small percentage of patients with psoriasis and presentation varies from hyperkeratotic plaques to pustular lesions. The pustular form is known as palmoplantar pustulosis and is within the spectrum of palmoplantar psoriasis.
Psoriasis is typically a clinical diagnosis and its severity can be measured using the Psoriasis Area and Severity Index. If biopsy is performed, the histology demonstrates parakeratosis, orthokeratosis, loss of the stratum granulosum, and dilated vasculature with an inflammatory cell infiltrate. The keratinocytes present with abnormal differentiation and hyperplasia, and the presence of foci of neutrophils known as “Munro’s microabscesses” in the stratum corneum serve as the hallmark of histological diagnosis. However, it is important to note that appearance can vary based on the stage of the lesion and the subtype of psoriasis present.
Palmoplantar psoriasis can be especially limiting and difficult to treat because of its distribution. Topical steroids, topical vitamin D analogues, and narrow band ultraviolet light therapy can be effective for less severe cases. Methotrexate, biologic treatments, and apremilast can be used for more extensive disease.
This patient is HLA-B27 positive and has uveitis. The presence of the HLA-B27 allele has been associated with inflammatory bowel disease, uveitis, psoriatic arthritis, and reactive arthritis. It has also been reported to be associated with pustular psoriasis. She responded well to topical steroids and vitamin D analogues.
This case and photo were submitted by Mr. Shapiro at Nova Southeastern University College of Osteopathic Medicine, Davie, Fla., and Dr. Bilu Martin.
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. Psoriasis: Overview and Diagnosis, in “Evidence-Based Psoriasis. Updates in Clinical Dermatology.” (Cham, Switzerland: Springer International, 2018).
2. Merola JF et al. Dermatol Ther. 2018 May;31(3):e12589.
3. Chung J et al. J Am Acad Dermatol. 2014 Oct;71(4):623-32.
Psoriasis is an immune-mediated chronic inflammatory disease characterized by well-demarcated, scaly, erythematous plaques. Those who present with the condition often have a family history, which supports recent research uncovering various genes implicated in its pathogenesis. The disease is also associated with other systemic complications, most notably cardiovascular disease.
This condition is found in a small percentage of patients with psoriasis and presentation varies from hyperkeratotic plaques to pustular lesions. The pustular form is known as palmoplantar pustulosis and is within the spectrum of palmoplantar psoriasis.
Psoriasis is typically a clinical diagnosis and its severity can be measured using the Psoriasis Area and Severity Index. If biopsy is performed, the histology demonstrates parakeratosis, orthokeratosis, loss of the stratum granulosum, and dilated vasculature with an inflammatory cell infiltrate. The keratinocytes present with abnormal differentiation and hyperplasia, and the presence of foci of neutrophils known as “Munro’s microabscesses” in the stratum corneum serve as the hallmark of histological diagnosis. However, it is important to note that appearance can vary based on the stage of the lesion and the subtype of psoriasis present.
Palmoplantar psoriasis can be especially limiting and difficult to treat because of its distribution. Topical steroids, topical vitamin D analogues, and narrow band ultraviolet light therapy can be effective for less severe cases. Methotrexate, biologic treatments, and apremilast can be used for more extensive disease.
This patient is HLA-B27 positive and has uveitis. The presence of the HLA-B27 allele has been associated with inflammatory bowel disease, uveitis, psoriatic arthritis, and reactive arthritis. It has also been reported to be associated with pustular psoriasis. She responded well to topical steroids and vitamin D analogues.
This case and photo were submitted by Mr. Shapiro at Nova Southeastern University College of Osteopathic Medicine, Davie, Fla., and Dr. Bilu Martin.
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. Psoriasis: Overview and Diagnosis, in “Evidence-Based Psoriasis. Updates in Clinical Dermatology.” (Cham, Switzerland: Springer International, 2018).
2. Merola JF et al. Dermatol Ther. 2018 May;31(3):e12589.
3. Chung J et al. J Am Acad Dermatol. 2014 Oct;71(4):623-32.
A healthy White male presented with a rash consisting of erythematous to purpuric macules
Vasculitis is a process in which blood vessels become inflamed and necrotic. Classic small vessel vasculitis reveals a leukocytoclastic vasculitis and most commonly presents as palpable purpura. .” A form of EIV has been described in the literature as “Disney dermatitis.” It is often seen in healthy adults after a long day of walking at the parks. Other forms of exercise, such as jogging, hiking, or swimming, may also cause the condition.
Clinically, EIV affects the lower legs and presents as purpuric macules. Edema may be present. Lesions may be asymptomatic or may present with pruritus or burning. Diagnosis is often made clinically. Skin biopsies for H&E and DIF (direct immunofluorescence) can help distinguish the type of vasculitis that is present. Laboratory tests may be needed to exclude other causes of vasculitis. Episodes may be recurrent.
Henoch-Schönlein purpura (HSP), also called anaphylactoid purpura, is a subtype of small-vessel vasculitis where IgA immunoglobulin is deposited in the vessel walls. It is the most common form of vasculitis is children (usually ages 4-8). In addition to skin, organs such as joints, kidneys, and intestines can be involved. Schamberg’s disease, or capillaritis, is also called pigmented purpura. In this benign condition, leakage from capillaries results in erythematous to brown patches on the lower extremities. A true vasculitis is not seen. The brown discoloration is due to hemosiderin deposition. Cryoglobulinemia is a rare condition in which abnormal immunoglobulin complexes deposit in tissues and vessels. Leukocytoclastic vasculitis is present in small vessels. Palpable purpura and livedo may be seen clinically, and systemic symptoms may be present.
Treatment of EIV is largely supportive as lesions will resolve on their own over 3-4 weeks. Postinflammatory hyperpigmentation may result. Temporary cessation of exercise and compression stockings can help speed up the resolution of lesions. Systemic medications used in the treatment of severe vasculitis, such as systemic steroids, dapsone, and colchicine, are not needed in EIV.
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.
Vasculitis is a process in which blood vessels become inflamed and necrotic. Classic small vessel vasculitis reveals a leukocytoclastic vasculitis and most commonly presents as palpable purpura. .” A form of EIV has been described in the literature as “Disney dermatitis.” It is often seen in healthy adults after a long day of walking at the parks. Other forms of exercise, such as jogging, hiking, or swimming, may also cause the condition.
Clinically, EIV affects the lower legs and presents as purpuric macules. Edema may be present. Lesions may be asymptomatic or may present with pruritus or burning. Diagnosis is often made clinically. Skin biopsies for H&E and DIF (direct immunofluorescence) can help distinguish the type of vasculitis that is present. Laboratory tests may be needed to exclude other causes of vasculitis. Episodes may be recurrent.
Henoch-Schönlein purpura (HSP), also called anaphylactoid purpura, is a subtype of small-vessel vasculitis where IgA immunoglobulin is deposited in the vessel walls. It is the most common form of vasculitis is children (usually ages 4-8). In addition to skin, organs such as joints, kidneys, and intestines can be involved. Schamberg’s disease, or capillaritis, is also called pigmented purpura. In this benign condition, leakage from capillaries results in erythematous to brown patches on the lower extremities. A true vasculitis is not seen. The brown discoloration is due to hemosiderin deposition. Cryoglobulinemia is a rare condition in which abnormal immunoglobulin complexes deposit in tissues and vessels. Leukocytoclastic vasculitis is present in small vessels. Palpable purpura and livedo may be seen clinically, and systemic symptoms may be present.
Treatment of EIV is largely supportive as lesions will resolve on their own over 3-4 weeks. Postinflammatory hyperpigmentation may result. Temporary cessation of exercise and compression stockings can help speed up the resolution of lesions. Systemic medications used in the treatment of severe vasculitis, such as systemic steroids, dapsone, and colchicine, are not needed in EIV.
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.
Vasculitis is a process in which blood vessels become inflamed and necrotic. Classic small vessel vasculitis reveals a leukocytoclastic vasculitis and most commonly presents as palpable purpura. .” A form of EIV has been described in the literature as “Disney dermatitis.” It is often seen in healthy adults after a long day of walking at the parks. Other forms of exercise, such as jogging, hiking, or swimming, may also cause the condition.
Clinically, EIV affects the lower legs and presents as purpuric macules. Edema may be present. Lesions may be asymptomatic or may present with pruritus or burning. Diagnosis is often made clinically. Skin biopsies for H&E and DIF (direct immunofluorescence) can help distinguish the type of vasculitis that is present. Laboratory tests may be needed to exclude other causes of vasculitis. Episodes may be recurrent.
Henoch-Schönlein purpura (HSP), also called anaphylactoid purpura, is a subtype of small-vessel vasculitis where IgA immunoglobulin is deposited in the vessel walls. It is the most common form of vasculitis is children (usually ages 4-8). In addition to skin, organs such as joints, kidneys, and intestines can be involved. Schamberg’s disease, or capillaritis, is also called pigmented purpura. In this benign condition, leakage from capillaries results in erythematous to brown patches on the lower extremities. A true vasculitis is not seen. The brown discoloration is due to hemosiderin deposition. Cryoglobulinemia is a rare condition in which abnormal immunoglobulin complexes deposit in tissues and vessels. Leukocytoclastic vasculitis is present in small vessels. Palpable purpura and livedo may be seen clinically, and systemic symptoms may be present.
Treatment of EIV is largely supportive as lesions will resolve on their own over 3-4 weeks. Postinflammatory hyperpigmentation may result. Temporary cessation of exercise and compression stockings can help speed up the resolution of lesions. Systemic medications used in the treatment of severe vasculitis, such as systemic steroids, dapsone, and colchicine, are not needed in EIV.
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.
A Hispanic male presented with a 3-month history of a spreading, itchy rash
, more often on exposed skin. In the United States, Trichophyton rubrum, T. mentagrophytes, and Microsporum canis are the most common causal organisms. People can become infected from contact with other people, animals, or soil. Variants of tinea corporis include tinea imbricata (caused by T. concentricum), bullous tinea corporis, tinea gladiatorum (seen in wrestlers), tinea incognito (atypical tinea resulting from topical steroid use), and Majocchi’s granuloma. Widespread tinea may be secondary to underlying immunodeficiency such as HIV/AIDS or treatment with topical or oral steroids.
The typical presentation of tinea corporis is scaly erythematous or hypopigmented annular patches with a raised border and central clearing. In tinea imbricata, which is more commonly seen in southeast Asia, India, and Central America, concentric circles and serpiginous plaques are present. Majocchi’s granuloma has a deeper involvement of fungus in the hair follicles, presenting with papules and pustules at the periphery of the patches. Lesions of tinea incognito may lack a scaly border and can be more widespread.
Diagnosis can be confirmed with a skin scraping and potassium hydroxide (KOH) staining, which will reveal septate and branching hyphae. Biopsy is often helpful, especially in tinea incognito. Classically, a “sandwich sign” is seen: hyphae between orthokeratosis and compact hyperkeratosis or parakeratosis. In this patient, a biopsy from the left hip revealed dermatophytosis, with PAS positive for organisms.
Localized lesions respond to topical antifungal creams such as azoles or topical terbinafine. More extensive tinea will often require a systemic antifungal with griseofulvin, terbinafine, itraconazole, or fluconazole. This patient responded to topical ketoconazole cream and oral terbinafine. A workup for underlying immunodeficiency was negative.
Dr. Bilu Martin provided this case and photo.
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.
, more often on exposed skin. In the United States, Trichophyton rubrum, T. mentagrophytes, and Microsporum canis are the most common causal organisms. People can become infected from contact with other people, animals, or soil. Variants of tinea corporis include tinea imbricata (caused by T. concentricum), bullous tinea corporis, tinea gladiatorum (seen in wrestlers), tinea incognito (atypical tinea resulting from topical steroid use), and Majocchi’s granuloma. Widespread tinea may be secondary to underlying immunodeficiency such as HIV/AIDS or treatment with topical or oral steroids.
The typical presentation of tinea corporis is scaly erythematous or hypopigmented annular patches with a raised border and central clearing. In tinea imbricata, which is more commonly seen in southeast Asia, India, and Central America, concentric circles and serpiginous plaques are present. Majocchi’s granuloma has a deeper involvement of fungus in the hair follicles, presenting with papules and pustules at the periphery of the patches. Lesions of tinea incognito may lack a scaly border and can be more widespread.
Diagnosis can be confirmed with a skin scraping and potassium hydroxide (KOH) staining, which will reveal septate and branching hyphae. Biopsy is often helpful, especially in tinea incognito. Classically, a “sandwich sign” is seen: hyphae between orthokeratosis and compact hyperkeratosis or parakeratosis. In this patient, a biopsy from the left hip revealed dermatophytosis, with PAS positive for organisms.
Localized lesions respond to topical antifungal creams such as azoles or topical terbinafine. More extensive tinea will often require a systemic antifungal with griseofulvin, terbinafine, itraconazole, or fluconazole. This patient responded to topical ketoconazole cream and oral terbinafine. A workup for underlying immunodeficiency was negative.
Dr. Bilu Martin provided this case and photo.
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.
, more often on exposed skin. In the United States, Trichophyton rubrum, T. mentagrophytes, and Microsporum canis are the most common causal organisms. People can become infected from contact with other people, animals, or soil. Variants of tinea corporis include tinea imbricata (caused by T. concentricum), bullous tinea corporis, tinea gladiatorum (seen in wrestlers), tinea incognito (atypical tinea resulting from topical steroid use), and Majocchi’s granuloma. Widespread tinea may be secondary to underlying immunodeficiency such as HIV/AIDS or treatment with topical or oral steroids.
The typical presentation of tinea corporis is scaly erythematous or hypopigmented annular patches with a raised border and central clearing. In tinea imbricata, which is more commonly seen in southeast Asia, India, and Central America, concentric circles and serpiginous plaques are present. Majocchi’s granuloma has a deeper involvement of fungus in the hair follicles, presenting with papules and pustules at the periphery of the patches. Lesions of tinea incognito may lack a scaly border and can be more widespread.
Diagnosis can be confirmed with a skin scraping and potassium hydroxide (KOH) staining, which will reveal septate and branching hyphae. Biopsy is often helpful, especially in tinea incognito. Classically, a “sandwich sign” is seen: hyphae between orthokeratosis and compact hyperkeratosis or parakeratosis. In this patient, a biopsy from the left hip revealed dermatophytosis, with PAS positive for organisms.
Localized lesions respond to topical antifungal creams such as azoles or topical terbinafine. More extensive tinea will often require a systemic antifungal with griseofulvin, terbinafine, itraconazole, or fluconazole. This patient responded to topical ketoconazole cream and oral terbinafine. A workup for underlying immunodeficiency was negative.
Dr. Bilu Martin provided this case and photo.
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.
A 64-year-old woman presents with a history of asymptomatic erythematous grouped papules on the right breast
. Recurrences may occur. Rarely, lymph nodes, the gastrointestinal system, lung, bone and bone marrow may be involved as extracutaneous sites.
Primary cutaneous B-cell lymphomas account for approximately 25% of all cutaneous lymphomas. Clinically, patients present with either solitary or multiple papules or plaques, typically on the upper extremities or trunk.
Histopathology is vital for the correct diagnosis. In this patient, the histologic report was written as follows: “The findings are those of a well-differentiated but atypical diffuse mixed small lymphocytic infiltrate representing a mixture of T-cells and B-cells. The minor component of the infiltrate is of T-cell lineage, whereby the cells do not show any phenotypic abnormalities. The background cell population is interpreted as reactive. However, the dominant cell population is in fact of B-cell lineage. It is extensively highlighted by CD20. Only a minor component of the B cell infiltrate appeared to be in the context of representing germinal centers as characterized by small foci of centrocytic and centroblastic infiltration highlighted by BCL6 and CD10. The overwhelming B-cell component is a non–germinal center small B cell that does demonstrate BCL2 positivity and significant immunoreactivity for CD23. This small lymphocytic infiltrate obscures the germinal centers. There are only a few plasma cells; they do not show light chain restriction.”
The pathologist remarked that “this type of morphology of a diffuse small B-cell lymphocytic infiltrate that is without any evidence of light chain restriction amidst plasma cells, whereby the B cell component is dominant over the T-cell component would in fact be consistent with a unique variant of marginal zone lymphoma derived from a naive mantle zone.”
PCMZL has an excellent prognosis. When limited to the skin, local radiation or excision are effective treatments. Intravenous rituximab has been used to treat multifocal PCMZL. This patient was found to have no extracutaneous involvement and was treated with radiation.
This case and photo were submitted by Dr. Bilu Martin.
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
Virmani P et al. JAAD Case Rep. 2017 Jun 14;3(4):269-72.
Magro CM and Olson LC. Ann Diagn Pathol. 2018 Jun;34:116-21.
. Recurrences may occur. Rarely, lymph nodes, the gastrointestinal system, lung, bone and bone marrow may be involved as extracutaneous sites.
Primary cutaneous B-cell lymphomas account for approximately 25% of all cutaneous lymphomas. Clinically, patients present with either solitary or multiple papules or plaques, typically on the upper extremities or trunk.
Histopathology is vital for the correct diagnosis. In this patient, the histologic report was written as follows: “The findings are those of a well-differentiated but atypical diffuse mixed small lymphocytic infiltrate representing a mixture of T-cells and B-cells. The minor component of the infiltrate is of T-cell lineage, whereby the cells do not show any phenotypic abnormalities. The background cell population is interpreted as reactive. However, the dominant cell population is in fact of B-cell lineage. It is extensively highlighted by CD20. Only a minor component of the B cell infiltrate appeared to be in the context of representing germinal centers as characterized by small foci of centrocytic and centroblastic infiltration highlighted by BCL6 and CD10. The overwhelming B-cell component is a non–germinal center small B cell that does demonstrate BCL2 positivity and significant immunoreactivity for CD23. This small lymphocytic infiltrate obscures the germinal centers. There are only a few plasma cells; they do not show light chain restriction.”
The pathologist remarked that “this type of morphology of a diffuse small B-cell lymphocytic infiltrate that is without any evidence of light chain restriction amidst plasma cells, whereby the B cell component is dominant over the T-cell component would in fact be consistent with a unique variant of marginal zone lymphoma derived from a naive mantle zone.”
PCMZL has an excellent prognosis. When limited to the skin, local radiation or excision are effective treatments. Intravenous rituximab has been used to treat multifocal PCMZL. This patient was found to have no extracutaneous involvement and was treated with radiation.
This case and photo were submitted by Dr. Bilu Martin.
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
Virmani P et al. JAAD Case Rep. 2017 Jun 14;3(4):269-72.
Magro CM and Olson LC. Ann Diagn Pathol. 2018 Jun;34:116-21.
. Recurrences may occur. Rarely, lymph nodes, the gastrointestinal system, lung, bone and bone marrow may be involved as extracutaneous sites.
Primary cutaneous B-cell lymphomas account for approximately 25% of all cutaneous lymphomas. Clinically, patients present with either solitary or multiple papules or plaques, typically on the upper extremities or trunk.
Histopathology is vital for the correct diagnosis. In this patient, the histologic report was written as follows: “The findings are those of a well-differentiated but atypical diffuse mixed small lymphocytic infiltrate representing a mixture of T-cells and B-cells. The minor component of the infiltrate is of T-cell lineage, whereby the cells do not show any phenotypic abnormalities. The background cell population is interpreted as reactive. However, the dominant cell population is in fact of B-cell lineage. It is extensively highlighted by CD20. Only a minor component of the B cell infiltrate appeared to be in the context of representing germinal centers as characterized by small foci of centrocytic and centroblastic infiltration highlighted by BCL6 and CD10. The overwhelming B-cell component is a non–germinal center small B cell that does demonstrate BCL2 positivity and significant immunoreactivity for CD23. This small lymphocytic infiltrate obscures the germinal centers. There are only a few plasma cells; they do not show light chain restriction.”
The pathologist remarked that “this type of morphology of a diffuse small B-cell lymphocytic infiltrate that is without any evidence of light chain restriction amidst plasma cells, whereby the B cell component is dominant over the T-cell component would in fact be consistent with a unique variant of marginal zone lymphoma derived from a naive mantle zone.”
PCMZL has an excellent prognosis. When limited to the skin, local radiation or excision are effective treatments. Intravenous rituximab has been used to treat multifocal PCMZL. This patient was found to have no extracutaneous involvement and was treated with radiation.
This case and photo were submitted by Dr. Bilu Martin.
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
Virmani P et al. JAAD Case Rep. 2017 Jun 14;3(4):269-72.
Magro CM and Olson LC. Ann Diagn Pathol. 2018 Jun;34:116-21.
75-year-old White male presenting with progressive pruritus and a worsening rash
, although it can also be contracted through contaminated bedding and clothing. It can affect all races and ages.
Patients typically present with extremely pruritic, symmetric papules and excoriations. In nodular scabies, nodules and large papules are seen on exam. Thin lines in the skin called burrows may be present, especially in the webs between fingers. Female mites create burrows as they tunnel through the epidermis and lay eggs. The wrists, areola, waistline, and groin may all be involved, creating an imaginary circle between the areas described as the “circle of Hebra.” Penile and scrotal lesions are common in men.
Patients usually experience worse pruritus at night, which disturbs sleep. Crusted scabies is a severe form of scabies more often seen in those with immunocompromised immune systems. Clinically, thick crusted and scaly patches are present that are teeming with mites.
Diagnosis can be confirmed by performing a scabies prep, during which a burrow is scraped with a surgical blade. A drop of mineral oil is placed on the skin cells. The mite, ova, and feces can be visualized under the microscope. Wrists and hands usually have the highest yield for finding the parasites.
Topical treatments include permethrin 5% cream, lindane, benzyl benzoate, and crotamiton, and should be applied as two treatments a week apart. In the United States, permethrin is most commonly used. Ivermectin pills are used off label and are very effective and may be repeated for 1-2 weeks. All household contacts should be treated. Patients may still have pruritus for 2-4 weeks following treatment.
In this patient, a scabies prep was performed prior to performing repeat skin biopsies. Microscopic examination revealed ova, one mite, and feces. Treatment was initiated with ivermectin and permethrin.
Photos and case were submitted by Susannah Berke, MD, and Damon McClain, MD, Three Rivers Dermatology, Coraopolis, Pa.; and Dr. Bilu Martin.
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.
, although it can also be contracted through contaminated bedding and clothing. It can affect all races and ages.
Patients typically present with extremely pruritic, symmetric papules and excoriations. In nodular scabies, nodules and large papules are seen on exam. Thin lines in the skin called burrows may be present, especially in the webs between fingers. Female mites create burrows as they tunnel through the epidermis and lay eggs. The wrists, areola, waistline, and groin may all be involved, creating an imaginary circle between the areas described as the “circle of Hebra.” Penile and scrotal lesions are common in men.
Patients usually experience worse pruritus at night, which disturbs sleep. Crusted scabies is a severe form of scabies more often seen in those with immunocompromised immune systems. Clinically, thick crusted and scaly patches are present that are teeming with mites.
Diagnosis can be confirmed by performing a scabies prep, during which a burrow is scraped with a surgical blade. A drop of mineral oil is placed on the skin cells. The mite, ova, and feces can be visualized under the microscope. Wrists and hands usually have the highest yield for finding the parasites.
Topical treatments include permethrin 5% cream, lindane, benzyl benzoate, and crotamiton, and should be applied as two treatments a week apart. In the United States, permethrin is most commonly used. Ivermectin pills are used off label and are very effective and may be repeated for 1-2 weeks. All household contacts should be treated. Patients may still have pruritus for 2-4 weeks following treatment.
In this patient, a scabies prep was performed prior to performing repeat skin biopsies. Microscopic examination revealed ova, one mite, and feces. Treatment was initiated with ivermectin and permethrin.
Photos and case were submitted by Susannah Berke, MD, and Damon McClain, MD, Three Rivers Dermatology, Coraopolis, Pa.; and Dr. Bilu Martin.
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.
, although it can also be contracted through contaminated bedding and clothing. It can affect all races and ages.
Patients typically present with extremely pruritic, symmetric papules and excoriations. In nodular scabies, nodules and large papules are seen on exam. Thin lines in the skin called burrows may be present, especially in the webs between fingers. Female mites create burrows as they tunnel through the epidermis and lay eggs. The wrists, areola, waistline, and groin may all be involved, creating an imaginary circle between the areas described as the “circle of Hebra.” Penile and scrotal lesions are common in men.
Patients usually experience worse pruritus at night, which disturbs sleep. Crusted scabies is a severe form of scabies more often seen in those with immunocompromised immune systems. Clinically, thick crusted and scaly patches are present that are teeming with mites.
Diagnosis can be confirmed by performing a scabies prep, during which a burrow is scraped with a surgical blade. A drop of mineral oil is placed on the skin cells. The mite, ova, and feces can be visualized under the microscope. Wrists and hands usually have the highest yield for finding the parasites.
Topical treatments include permethrin 5% cream, lindane, benzyl benzoate, and crotamiton, and should be applied as two treatments a week apart. In the United States, permethrin is most commonly used. Ivermectin pills are used off label and are very effective and may be repeated for 1-2 weeks. All household contacts should be treated. Patients may still have pruritus for 2-4 weeks following treatment.
In this patient, a scabies prep was performed prior to performing repeat skin biopsies. Microscopic examination revealed ova, one mite, and feces. Treatment was initiated with ivermectin and permethrin.
Photos and case were submitted by Susannah Berke, MD, and Damon McClain, MD, Three Rivers Dermatology, Coraopolis, Pa.; and Dr. Bilu Martin.
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.
A 22-year-old presented with erythematous papules on her fingers and toes
than men. Clinically, distal extremities such as toes, fingertips and heels, as well as the rims of the ears or nose develop erythematous to purple plaques. Lesions may be painful or pruritic. Over time, lesions may develop atrophy and resemble those of discoid lupus. While the pathogenesis is unknown, exposure to cold or wet environments can precipitate lesions.
Histopathology reveals a deep and superficial lymphocytic infiltrate with perieccrine involvement and fibrin deposition in vessels. Dermal edema is often present. Direct immunofluorescence shows an interface dermatitis positive for IgM, IgA, and C3.
The Mayo Clinic developed diagnostic criteria for diagnosing chilblains lupus. Two major criteria are acral skin lesions induced by cold exposure and evidence of lupus erythematosus in skin lesions (histopathologically or by direct immunofluorescence). Three minor criteria are the coexistence of systemic lupus erythematosus or discoid lupus erythematosus, response to antilupus treatment, and negative cryoglobulin and cold agglutinin studies.
Chilblains, or perniosis, has a similar clinical presentation to chilblain lupus erythematosus. However, serologic evidence of lupus, such as a positive antinuclear antibody (ANA), will be absent. Lupus pernio (Besnier-Tenneson syndrome) is a form of sarcoidosis that tends to favor the nose. These lesions are not precipitated by cold. It can be differentiated on histology. “COVID toes” is an entity described during the coronavirus pandemic, during which dermatologists noted pernio-like lesions in patients testing positive for coronavirus.
The patient’s labs revealed a positive ANA at 1:320 in a nucleolar speckled pattern, elevated double-stranded DNA, low C3 and C4 levels, elevated cardiolipin IgM Ab, and elevated sedimentation rate. COVID-19 antigen testing and COVID-19 antibodies were negative. A serum protein electrophoresis was negative. Cryoglobulins were negative.
Treatment includes protection from cold. Smoking cessation should be discussed. Topical steroids and topical calcineurin inhibitors are first-line treatments for mild disease. Antimalarials, such as hydroxychloroquine can be helpful. Systemic calcium channel blockers, systemic steroids, mycophenolate mofetil, and tacrolimus have all been reported as treatments. This patient responded well to hydroxychloroquine and topical steroids with full resolution of lesions.
This case was submitted by Dr. Bilu Martin.
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
Su WP et al. Cutis. 1994 Dec;54(6):395-9.
Werth V and Newman S. Chilblain lupus (SLE pernio). Dermatology Advisor. 2017.
than men. Clinically, distal extremities such as toes, fingertips and heels, as well as the rims of the ears or nose develop erythematous to purple plaques. Lesions may be painful or pruritic. Over time, lesions may develop atrophy and resemble those of discoid lupus. While the pathogenesis is unknown, exposure to cold or wet environments can precipitate lesions.
Histopathology reveals a deep and superficial lymphocytic infiltrate with perieccrine involvement and fibrin deposition in vessels. Dermal edema is often present. Direct immunofluorescence shows an interface dermatitis positive for IgM, IgA, and C3.
The Mayo Clinic developed diagnostic criteria for diagnosing chilblains lupus. Two major criteria are acral skin lesions induced by cold exposure and evidence of lupus erythematosus in skin lesions (histopathologically or by direct immunofluorescence). Three minor criteria are the coexistence of systemic lupus erythematosus or discoid lupus erythematosus, response to antilupus treatment, and negative cryoglobulin and cold agglutinin studies.
Chilblains, or perniosis, has a similar clinical presentation to chilblain lupus erythematosus. However, serologic evidence of lupus, such as a positive antinuclear antibody (ANA), will be absent. Lupus pernio (Besnier-Tenneson syndrome) is a form of sarcoidosis that tends to favor the nose. These lesions are not precipitated by cold. It can be differentiated on histology. “COVID toes” is an entity described during the coronavirus pandemic, during which dermatologists noted pernio-like lesions in patients testing positive for coronavirus.
The patient’s labs revealed a positive ANA at 1:320 in a nucleolar speckled pattern, elevated double-stranded DNA, low C3 and C4 levels, elevated cardiolipin IgM Ab, and elevated sedimentation rate. COVID-19 antigen testing and COVID-19 antibodies were negative. A serum protein electrophoresis was negative. Cryoglobulins were negative.
Treatment includes protection from cold. Smoking cessation should be discussed. Topical steroids and topical calcineurin inhibitors are first-line treatments for mild disease. Antimalarials, such as hydroxychloroquine can be helpful. Systemic calcium channel blockers, systemic steroids, mycophenolate mofetil, and tacrolimus have all been reported as treatments. This patient responded well to hydroxychloroquine and topical steroids with full resolution of lesions.
This case was submitted by Dr. Bilu Martin.
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
Su WP et al. Cutis. 1994 Dec;54(6):395-9.
Werth V and Newman S. Chilblain lupus (SLE pernio). Dermatology Advisor. 2017.
than men. Clinically, distal extremities such as toes, fingertips and heels, as well as the rims of the ears or nose develop erythematous to purple plaques. Lesions may be painful or pruritic. Over time, lesions may develop atrophy and resemble those of discoid lupus. While the pathogenesis is unknown, exposure to cold or wet environments can precipitate lesions.
Histopathology reveals a deep and superficial lymphocytic infiltrate with perieccrine involvement and fibrin deposition in vessels. Dermal edema is often present. Direct immunofluorescence shows an interface dermatitis positive for IgM, IgA, and C3.
The Mayo Clinic developed diagnostic criteria for diagnosing chilblains lupus. Two major criteria are acral skin lesions induced by cold exposure and evidence of lupus erythematosus in skin lesions (histopathologically or by direct immunofluorescence). Three minor criteria are the coexistence of systemic lupus erythematosus or discoid lupus erythematosus, response to antilupus treatment, and negative cryoglobulin and cold agglutinin studies.
Chilblains, or perniosis, has a similar clinical presentation to chilblain lupus erythematosus. However, serologic evidence of lupus, such as a positive antinuclear antibody (ANA), will be absent. Lupus pernio (Besnier-Tenneson syndrome) is a form of sarcoidosis that tends to favor the nose. These lesions are not precipitated by cold. It can be differentiated on histology. “COVID toes” is an entity described during the coronavirus pandemic, during which dermatologists noted pernio-like lesions in patients testing positive for coronavirus.
The patient’s labs revealed a positive ANA at 1:320 in a nucleolar speckled pattern, elevated double-stranded DNA, low C3 and C4 levels, elevated cardiolipin IgM Ab, and elevated sedimentation rate. COVID-19 antigen testing and COVID-19 antibodies were negative. A serum protein electrophoresis was negative. Cryoglobulins were negative.
Treatment includes protection from cold. Smoking cessation should be discussed. Topical steroids and topical calcineurin inhibitors are first-line treatments for mild disease. Antimalarials, such as hydroxychloroquine can be helpful. Systemic calcium channel blockers, systemic steroids, mycophenolate mofetil, and tacrolimus have all been reported as treatments. This patient responded well to hydroxychloroquine and topical steroids with full resolution of lesions.
This case was submitted by Dr. Bilu Martin.
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
Su WP et al. Cutis. 1994 Dec;54(6):395-9.
Werth V and Newman S. Chilblain lupus (SLE pernio). Dermatology Advisor. 2017.
The patient denied any arthralgias, alopecia, oral ulcers, or photosensitivity. She denied any recent illness.
A 73-year-old White male presented with 2 days of a very pruritic rash
Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.
Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.
In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.
Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.
This case and photo were submitted by Dr. Bilu Martin.
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. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).
2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).
Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.
Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.
In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.
Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.
This case and photo were submitted by Dr. Bilu Martin.
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. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).
2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).
Reactions can occur anytime from within the first 2 weeks of treatment up to 10 days after the treatment has been discontinued. If a drug is rechallenged, eruptions may occur sooner. Pruritus is commonly seen. Clinically, erythematous papules and macules present symmetrically on the trunk and upper extremities and then become more generalized. A low-grade fever may be present.
Antibiotics are the most common causes of exanthematous drug eruptions. Penicillins and trimethoprim-sulfamethoxazole are common offenders. Cephalosporins, anticonvulsants, and allopurinol may also induce a reaction. As this condition is diagnosed clinically, skin biopsy is often not necessary. Histology is nonspecific and shows a mild perivascular lymphocytic infiltrate and few epidermal necrotic keratinocytes.
In drug reaction with eosinophilia and systemic symptoms (DRESS), symptoms present 2-6 weeks after the offending medication has been started. The cutaneous rash appears similar to an exanthematous drug eruption; however, lesions will also present on the face, and facial edema may occur. Fever is often present. Laboratory findings include a marked peripheral blood hypereosinophilia. Elevated liver function tests may be seen. Viruses such as Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus 6, and parvovirus B19 have a similar clinical appearance to an exanthematous drug eruption. A mild eosinophilia, as seen in a drug eruption, helps to distinguish between a drug eruption and viral exanthem. In Stevens-Johnson Syndrome, mucosal membranes are involved and skin is often painful or appears dusky.
Treatment of exanthematous drug eruptions is largely supportive. Discontinuing the drug will help speed resolution and topical steroids may alleviate pruritus.
This case and photo were submitted by Dr. Bilu Martin.
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. Bolognia J et al. “Dermatology” (St. Louis: Mosby/Elsevier, 2008).
2. James W et al. “Andrews’ Diseases of the Skin,” 13th ed. (Philadelphia: Saunders Elsevier, 2006).
A 70-year-old man presents with firm papules on his hand and fingers
, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.
GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.1
Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.
Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.
This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.
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 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.
, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.
GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.1
Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.
Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.
This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.
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 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.
, although women are more often affected than men. GA most commonly appears in the first 3 decades of life. Although the etiology is not known, GA may represent a delayed hypersensitivity reaction. A link between GA and diabetes mellitus, autoimmune thyroiditis, dyslipidemia, and rarely, malignancy may exist.
GA is most commonly localized, presenting as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. This form is the type most often seen in children. Generalized GA is far less common and presents later in life as multiple asymptomatic or pruritic papules and plaques on the trunk and extremities. Less common variants include subcutaneous GA, patch GA, atypical GA, and perforating GA. Perforating GA occurs on the dorsal hands and presents as (umbilicated) papules, and seems consistent with this patient’s clinical presentation. Histologically, transepidermal elimination of collagen is typically seen in perforating GA.1
Histology in this patient’s biopsy revealed a granulomatous dermatitis consistent with granuloma annulare. A palisaded arrangement of histiocytic cells surrounding altered collagen with increased dermal mucin was seen. There was associated perivascular mononuclear inflammatory infiltrates. The overlying epidermis was unremarkable.
Granuloma annulare often spontaneously resolves without sequelae. In some cases, atrophy may result. Lesions may also recur. Localized GA is often treated with high-potency topical corticosteroids or intralesional corticosteroids. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, cryotherapy, imiquimod, hydroxychloroquine, isotretinoin, and dapsone have also been reported in the literature as possible treatments.
This case and photo were provided by Dr. Berke, of Three Rivers Dermatology, Pittsburgh, and Dr. Bilu Martin.
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 Alves J, Barreiros H, Bartolo E. Healthcare (Basel). 2014 Sep 4;2(3):338-45.
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
3. “Andrews’ Diseases of the Skin,” 13th ed. James W et al. Philadelphia: Saunders Elsevier, 2006.
An 80-year-old female developed a painful purulent nodule a day after gardening
. There are more than 100 species of dematiaceous fungi that can cause phaeohyphomycosis, including Alternaria, Exophiala, Phialophora, Wangiella, Bipolaris, Curvularia, and Exserohilum.1,2 The causative fungi are found in plants and soil, so they are commonly seen after activities such as gardening or walking barefoot. Trauma, such as a splinter, typically incites the infection. Infections can present with superficial, cutaneous and subcutaneous involvement.
Sporotrichosis, also called Rose gardener’s disease, is a mycosis caused by Sporothrix schenckii. A typical presentation is when a gardener gets pricked by a rose thorn. Classically, a pustule will develop at the site of inoculation, with additional lesions forming along the path of lymphatic drainage (called a “sporotrichoid” pattern) weeks later. Atypical mycobacterial infections, mainly Mycobacterium marinum, may also present in this way. Histopathology and tissue cultures help to differentiate the two.
An incision and drainage with pathology was performed in the office. Upon opening the nodule, a large wood splinter was extracted. Both the foreign body and a punch biopsy of skin were sent in for examination. Pathology revealed polarizable foreign material in association with suppurative inflammation and dematiaceous fungi. PAS (Periodic-acid Schiff) and GMS (Grocott methenamine silver) stain highlighted fungal forms. Cultures were negative.
Local disease may be treated with excision alone. Oral antifungals, such as itraconazole, fluconazole, or ketoconazole may be used, although may require long treatment courses for months. Amphotericin B and flucytosine may be required in systemic cases. Almost all cases of disseminated disease occur in immunocompromised patients. Our patient’s hand resolved after removal of the causative thorn.
This case and these photos were submitted by Dr. Bilu Martin.
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. Kradin R. Diagnostic Pathology of Infectious Disease, 1st edition (Saunders, Feb. 2, 2010).
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
. There are more than 100 species of dematiaceous fungi that can cause phaeohyphomycosis, including Alternaria, Exophiala, Phialophora, Wangiella, Bipolaris, Curvularia, and Exserohilum.1,2 The causative fungi are found in plants and soil, so they are commonly seen after activities such as gardening or walking barefoot. Trauma, such as a splinter, typically incites the infection. Infections can present with superficial, cutaneous and subcutaneous involvement.
Sporotrichosis, also called Rose gardener’s disease, is a mycosis caused by Sporothrix schenckii. A typical presentation is when a gardener gets pricked by a rose thorn. Classically, a pustule will develop at the site of inoculation, with additional lesions forming along the path of lymphatic drainage (called a “sporotrichoid” pattern) weeks later. Atypical mycobacterial infections, mainly Mycobacterium marinum, may also present in this way. Histopathology and tissue cultures help to differentiate the two.
An incision and drainage with pathology was performed in the office. Upon opening the nodule, a large wood splinter was extracted. Both the foreign body and a punch biopsy of skin were sent in for examination. Pathology revealed polarizable foreign material in association with suppurative inflammation and dematiaceous fungi. PAS (Periodic-acid Schiff) and GMS (Grocott methenamine silver) stain highlighted fungal forms. Cultures were negative.
Local disease may be treated with excision alone. Oral antifungals, such as itraconazole, fluconazole, or ketoconazole may be used, although may require long treatment courses for months. Amphotericin B and flucytosine may be required in systemic cases. Almost all cases of disseminated disease occur in immunocompromised patients. Our patient’s hand resolved after removal of the causative thorn.
This case and these photos were submitted by Dr. Bilu Martin.
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. Kradin R. Diagnostic Pathology of Infectious Disease, 1st edition (Saunders, Feb. 2, 2010).
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
. There are more than 100 species of dematiaceous fungi that can cause phaeohyphomycosis, including Alternaria, Exophiala, Phialophora, Wangiella, Bipolaris, Curvularia, and Exserohilum.1,2 The causative fungi are found in plants and soil, so they are commonly seen after activities such as gardening or walking barefoot. Trauma, such as a splinter, typically incites the infection. Infections can present with superficial, cutaneous and subcutaneous involvement.
Sporotrichosis, also called Rose gardener’s disease, is a mycosis caused by Sporothrix schenckii. A typical presentation is when a gardener gets pricked by a rose thorn. Classically, a pustule will develop at the site of inoculation, with additional lesions forming along the path of lymphatic drainage (called a “sporotrichoid” pattern) weeks later. Atypical mycobacterial infections, mainly Mycobacterium marinum, may also present in this way. Histopathology and tissue cultures help to differentiate the two.
An incision and drainage with pathology was performed in the office. Upon opening the nodule, a large wood splinter was extracted. Both the foreign body and a punch biopsy of skin were sent in for examination. Pathology revealed polarizable foreign material in association with suppurative inflammation and dematiaceous fungi. PAS (Periodic-acid Schiff) and GMS (Grocott methenamine silver) stain highlighted fungal forms. Cultures were negative.
Local disease may be treated with excision alone. Oral antifungals, such as itraconazole, fluconazole, or ketoconazole may be used, although may require long treatment courses for months. Amphotericin B and flucytosine may be required in systemic cases. Almost all cases of disseminated disease occur in immunocompromised patients. Our patient’s hand resolved after removal of the causative thorn.
This case and these photos were submitted by Dr. Bilu Martin.
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. Kradin R. Diagnostic Pathology of Infectious Disease, 1st edition (Saunders, Feb. 2, 2010).
2. Bolognia J et al. Dermatology (St. Louis: Mosby/Elsevier, 2008).
