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White Atrophic Plaques on the Thighs
White Atrophic Plaques on the Thighs
THE DIAGNOSIS: Lichen Sclerosus
Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.
Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.1 The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.1 Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.1
The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.2 Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.
Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.3 The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.
Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.4 The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.
Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.2 Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.
In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.
- De Luca DA, Papara C, Vorobyev A, et al. Lichen sclerosus: the 2023 update. Front Med (Lausanne). 2023;10:1106318. doi:10.3389 /fmed.2023.1106318
- Chovatiya R, Silverberg JI. Pathophysiology of atopic dermatitis and psoriasis: implications for management in children. Children (Basel). 2019;6:108. doi:10.3390/children6100108
- Trayes KP, Savage K, Studdiford JS. Annular lesions: diagnosis and treatment. Am Fam Physician. 2018;98:283-291.
- Ju T, Vander Does A, Mohsin N, et al. Lichen simplex chronicus itch: an update. Acta Derm Venereol. 2022;102:adv00796. doi:10.2340 /actadv.v102.4367
THE DIAGNOSIS: Lichen Sclerosus
Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.
Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.1 The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.1 Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.1
The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.2 Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.
Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.3 The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.
Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.4 The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.
Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.2 Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.
In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.
THE DIAGNOSIS: Lichen Sclerosus
Given the clinical appearance of white atrophic plaques with characteristic wrinkling of the skin, a diagnosis of lichen sclerosus was strongly suspected. At the initial office visit, the patient was prescribed clobetasol 0.05% ointment twice daily for 6 weeks. Histopathology revealed hyperkeratosis, follicular plugging, papillary dermal pallor, and adjacent lymphocytic inflammation, confirming the clinical diagnosis of lichen sclerosus (Figure). The patient then was lost to follow-up.
Lichen sclerosus is a chronic benign dermatologic condition of unknown etiology that is characterized by epidermal atrophy and inflammation and is common in postmenopausal women. It features pale, ivory-colored lesions with partially atrophic skin and a wrinkled cigarette paper appearance.1 The differential for lichen sclerosus is broad, and definitive diagnosis is made via biopsy to rule out potential malignancy and other inflammatory skin diseases.1 Lichen sclerosus is an immune-mediated disorder driven by type 1 T helper cells and regulated by miR-155. There has been an association with extracellular matrix protein 1, a glycoprotein that is found in the dermal-epidermal basement membrane zone, which provides structural integrity to the skin. Autoantibodies against extracellular matrix protein 1 and other antigens in the basement membrane generally are found in anogenital lichen sclerosus; however, their precise roles in the pathogenesis of lichen sclerosus remains unclear.1
The differential diagnoses for lichen sclerosus include psoriasis, tinea corporis, lichen simplex chronicus, and atopic dermatitis. Psoriasis typically manifests as pink plaques with silver scales on the elbows, knees, and scalp in adult patients.2 Our patient’s white plaques may have suggested psoriasis, but the partially atrophic skin with a wrinkled cigarette paper appearance was not compatible with that diagnosis.
Tinea corporis, a superficial fungal infection of the skin, manifests as circular or ovoid lesions with raised erythematous scaly borders, often with central clearing resembling a ring, that can occur anywhere on the body other than the feet, groin, face, scalp, or beard area.3 The fact that our patient previously had tried topical antifungal medications with no relief and that the skin lesions were atrophic rather than ring shaped made the diagnosis of tinea corporis unlikely.
Lichen simplex chronicus is a chronic condition caused by friction or scratching that is characterized by dry, patchy, scaly, and thickened areas of the skin. Typically affecting the head, arms, neck, scalp, and genital region, lichen simplex chronicus manifests with violaceous or hyperpigmented lesions.4 The nonpruritic atrophic plaques on the inner thighs and the presence of white patches on the vaginal area were not indicative of lichen simplex chronicus in our patient.
Atopic dermatitis manifests as pruritic erythematous scaly papules and plaques with secondary excoriation and possible lichenification. In adults, atopic dermatitis commonly appears on flexural surfaces.2 Atopic dermatitis does not manifest with atrophy and skin wrinkling as seen in our patient.
In the management of lichen sclerosus, the standard treatment is potent topical corticosteroids. Alternatively, topical calcineurin inhibitors can be employed; however, due to the unknown nature of the condition’s underlying cause, targeted treatment is challenging. Our case underscores how lichen sclerosus can be misdiagnosed, highlighting the need for more frequent reporting in the literature to enhance early recognition and reduce delays in patient treatment.
- De Luca DA, Papara C, Vorobyev A, et al. Lichen sclerosus: the 2023 update. Front Med (Lausanne). 2023;10:1106318. doi:10.3389 /fmed.2023.1106318
- Chovatiya R, Silverberg JI. Pathophysiology of atopic dermatitis and psoriasis: implications for management in children. Children (Basel). 2019;6:108. doi:10.3390/children6100108
- Trayes KP, Savage K, Studdiford JS. Annular lesions: diagnosis and treatment. Am Fam Physician. 2018;98:283-291.
- Ju T, Vander Does A, Mohsin N, et al. Lichen simplex chronicus itch: an update. Acta Derm Venereol. 2022;102:adv00796. doi:10.2340 /actadv.v102.4367
- De Luca DA, Papara C, Vorobyev A, et al. Lichen sclerosus: the 2023 update. Front Med (Lausanne). 2023;10:1106318. doi:10.3389 /fmed.2023.1106318
- Chovatiya R, Silverberg JI. Pathophysiology of atopic dermatitis and psoriasis: implications for management in children. Children (Basel). 2019;6:108. doi:10.3390/children6100108
- Trayes KP, Savage K, Studdiford JS. Annular lesions: diagnosis and treatment. Am Fam Physician. 2018;98:283-291.
- Ju T, Vander Does A, Mohsin N, et al. Lichen simplex chronicus itch: an update. Acta Derm Venereol. 2022;102:adv00796. doi:10.2340 /actadv.v102.4367
White Atrophic Plaques on the Thighs
White Atrophic Plaques on the Thighs
A 71-year-old woman presented to the dermatology clinic for evaluation of intense pruritus of the vaginal region and a nonpruritic rash on the inner thighs of 7 months’ duration. Physical examination revealed white atrophic plaques with scaling and a wrinkled appearance on the inner thighs. White atrophic patches also were noted on the vulva. The patient reported that she had tried over-the-counter antifungals with no improvement. A punch biopsy was performed.
Bilateral Brownish-Red Indurated Facial Plaques in an Adult Man
Bilateral Brownish-Red Indurated Facial Plaques in an Adult Man
THE DIAGNOSIS: Granuloma Faciale
Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.1 Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.1 Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.2
Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.1 Oral dapsone is given at a dose of 50 mg to 150 mg once daily.1 Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.1
The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.4 Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.5 The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.6 Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.7
- Al Dhafiri M, Kaliyadan F. Granuloma faciale. StatPearls Publishing. Updated July 4, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK539832/
- Chen A, Harview CL, Rand SE, et al. Refractory granuloma faciale successfully treated with adjunct topical JAK inhibitor. JAAD Case Rep. 2023;33:91-94. doi:10.1016/j.jdcr.2023.01.016
- Dowlati B, Firooz A, Dowlati Y. Granuloma faciale: successful treatment of nine cases with a combination of cryotherapy and intralesional corticosteroid injection. Int J Dermatol. 1997;36:548-551. doi:10.1046 /j.1365-4362.1997.00161.x
- Koritala T, Grubbs H, Crane J. Tumid lupus erythematosus. StatPearls Publishing. Updated June 28, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK482515/
- Caplan A, Rosenbach M, Imadojemu S. Cutaneous sarcoidosis. Semin Respir Crit Care Med. 2020;41:689-699. doi:10.1055/s-0040-1713130
- Singh P, Jain E, Dhingra H, et al. Clinico-pathological spectrum of cutaneous sarcoidosis: an experience from a government institute in North India. Med Pharm Rep. 2020;93:241-245. doi:10.15386 /mpr-1384
- Vaidya T, Badri T. Mycosis fungoides. StatPearls Publishing. Updated July 31, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK519572/
THE DIAGNOSIS: Granuloma Faciale
Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.1 Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.1 Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.2
Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.1 Oral dapsone is given at a dose of 50 mg to 150 mg once daily.1 Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.1
The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.4 Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.5 The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.6 Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.7
THE DIAGNOSIS: Granuloma Faciale
Histology revealed a dense mixed inflammatory cell infiltrate with conspicuous neutrophils and eosinophils in the upper to mid dermis with a narrow uninvolved grenz zone beneath the epidermis (Figures 1 and 2). These findings along with the clinical presentation (Figure 3) were consistent with a diagnosis of granuloma faciale (GF). Most often seen in middle-aged White men, GF is an uncommon localized inflammatory skin condition that often manifests as a single, well-defined, red-to-brown papule, nodule, or plaque on the face or other sun-exposed areas of the skin. Since numerous other skin diseases manifest similarly to GF, biopsy is necessary for definitive diagnosis.1 Histopathology of GF classically shows a mixed inflammatory infiltrate with a narrow band of uninvolved dermis separating it from the epidermis (grenz zone). Dilated follicular plugs and vascular changes frequently are appreciated. Despite its name, GF does not include granulomas and is thought to be similar to leukocytoclastic vasculitis.1 Reports of GF in the literature have shown immunohistochemical staining with the presence of CD4+ lymphocytes that secrete IL-5, a chemotactic agent responsible for attracting eosinophils that contributes to the eosinophilic infiltrate on histology.2
Topical corticosteroids and topical tacrolimus are the first-line treatments for GF. Intralesional corticosteroids also are a treatment option and can be used in combination with cryotherapy.1,3 Additionally, both topical and oral dapsone have been shown to be effective for GF.1 Oral dapsone is given at a dose of 50 mg to 150 mg once daily.1 Clofazimine, typically used as an antileprosy treatment, also has been efficacious in treating GF. Clofazimine has anti-inflammatory and antiproliferative effects on lymphocytes that may attenuate the inflammation underlying GF. It is prescribed at a dose of 300 mg once daily for 3 to 5 months.1
The differential diagnosis for GF is broad and includes tumid lupus erythematosus, Jessner lymphocytic infiltrate (JLI), cutaneous sarcoidosis, and mycosis fungoides. Tumid lupus erythematosus is a subtype of cutaneous lupus erythematosus that rarely is associated with systemic lupus manifestations. Tumid lupus erythematosus manifests as annular, indurated, erythematous plaques, whereas JLI manifests with erythematous papular to nodular lesions without scale on the upper back or face.4 Jessner lymphocytic infiltrate and tumid lupus erythematosus are histopathologically identical, with abundant dermal mucin deposition and a superficial and deep perivascular and periadnexal lymphocytic infiltrate. It is debatable whether JLI is a separate entity or a variant of tumid lupus erythematosus. Sarcoidosis is a granulomatous disease that manifests with a myriad of clinical features. The skin is the second most commonly involved organ.5 The most common morphology is numerous small, firm, nonscaly papules, typically on the face. Histology in cutaneous sarcoidosis will show lymphocyte-poor, noncaseating epithelioid cell granulomas with positive reticulin staining, which were not seen in our patient.6 Lastly, mycosis fungoides is the most common type of cutaneous T-cell lymphoma. It can manifest as patches, plaques, or tumors. The plaque stage may mimic GF as lesions are infiltrative, annular, and raised, with well-defined margins. Histopathology will show intraepidermal lymphocytes out of proportion with spongiosis.7
- Al Dhafiri M, Kaliyadan F. Granuloma faciale. StatPearls Publishing. Updated July 4, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK539832/
- Chen A, Harview CL, Rand SE, et al. Refractory granuloma faciale successfully treated with adjunct topical JAK inhibitor. JAAD Case Rep. 2023;33:91-94. doi:10.1016/j.jdcr.2023.01.016
- Dowlati B, Firooz A, Dowlati Y. Granuloma faciale: successful treatment of nine cases with a combination of cryotherapy and intralesional corticosteroid injection. Int J Dermatol. 1997;36:548-551. doi:10.1046 /j.1365-4362.1997.00161.x
- Koritala T, Grubbs H, Crane J. Tumid lupus erythematosus. StatPearls Publishing. Updated June 28, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK482515/
- Caplan A, Rosenbach M, Imadojemu S. Cutaneous sarcoidosis. Semin Respir Crit Care Med. 2020;41:689-699. doi:10.1055/s-0040-1713130
- Singh P, Jain E, Dhingra H, et al. Clinico-pathological spectrum of cutaneous sarcoidosis: an experience from a government institute in North India. Med Pharm Rep. 2020;93:241-245. doi:10.15386 /mpr-1384
- Vaidya T, Badri T. Mycosis fungoides. StatPearls Publishing. Updated July 31, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK519572/
- Al Dhafiri M, Kaliyadan F. Granuloma faciale. StatPearls Publishing. Updated July 4, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK539832/
- Chen A, Harview CL, Rand SE, et al. Refractory granuloma faciale successfully treated with adjunct topical JAK inhibitor. JAAD Case Rep. 2023;33:91-94. doi:10.1016/j.jdcr.2023.01.016
- Dowlati B, Firooz A, Dowlati Y. Granuloma faciale: successful treatment of nine cases with a combination of cryotherapy and intralesional corticosteroid injection. Int J Dermatol. 1997;36:548-551. doi:10.1046 /j.1365-4362.1997.00161.x
- Koritala T, Grubbs H, Crane J. Tumid lupus erythematosus. StatPearls Publishing. Updated June 28, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK482515/
- Caplan A, Rosenbach M, Imadojemu S. Cutaneous sarcoidosis. Semin Respir Crit Care Med. 2020;41:689-699. doi:10.1055/s-0040-1713130
- Singh P, Jain E, Dhingra H, et al. Clinico-pathological spectrum of cutaneous sarcoidosis: an experience from a government institute in North India. Med Pharm Rep. 2020;93:241-245. doi:10.15386 /mpr-1384
- Vaidya T, Badri T. Mycosis fungoides. StatPearls Publishing. Updated July 31, 2023. Accessed February 18, 2025. https://www.ncbi.nlm.nih.gov/books/NBK519572/
Bilateral Brownish-Red Indurated Facial Plaques in an Adult Man
Bilateral Brownish-Red Indurated Facial Plaques in an Adult Man
A 44-year-old man presented to the dermatology clinic with a facial rash of 2 years’ duration. The patient reported associated pruritus but no systemic symptoms. His medical history was relevant for childhood eczema. He had tried various over-the-counter treatments for the facial rash, including topical hydrocortisone, neomycin/bacitracin/polymyxin antibiotic ointment, moisturizers, and antihistamines, with no success. Physical examination demonstrated symmetric, well-circumscribed, circinate, brownish-red, indurated plaques without scaling on the cheeks. A 4-mm punch biopsy was obtained from a plaque on the left cheek.
Painful Plaque on the Forearm
The Diagnosis: Mycobacterium marinum Infection
A repeat excisional biopsy showed suppurative granulomatous dermatitis with negative stains for infectious organisms; however, tissue culture grew Mycobacterium marinum. The patient had a history of exposure to fish tanks, which are a potential habitat for nontuberculous mycobacteria. These bacteria can enter the body through a minor laceration or cut in the skin, which was likely due to her occupation and pet care activities.1 Her fish tank exposure combined with the cutaneous findings of a long-standing indurated plaque with proximal nodular lymphangitis made M marinum infection the most likely diagnosis.2
Due to the limited specificity and sensitivity of patient symptoms, histologic staining, and direct microscopy, the gold standard for diagnosing acid-fast bacilli is tissue culture. 3 Tissue polymerase chain reaction testing is most useful in identifying the species of mycobacteria when histologic stains identify acid-fast bacilli but repeated tissue cultures are negative.4 With M marinum, a high clinical suspicion is needed to acquire a positive tissue culture because it needs to be grown for several weeks and at a temperature of 30 °C.5 Therefore, the physician should inform the laboratory if there is any suspicion for M marinum to increase the likelihood of obtaining a positive culture.
The differential diagnosis for M marinum infection includes other skin diseases that can cause nodular lymphangitis (also known as sporotrichoid spread) such as sporotrichosis, leishmaniasis, and certain bacterial and fungal infections. Although cat scratch disease, which is caused by Bartonella henselae, can appear similar to M marinum on histopathology, it clinically manifests with a single papulovesicular lesion at the site of inoculation that then forms a central eschar and resolves within a few weeks. Cat scratch disease typically causes painful lymphadenopathy, but it does not cause nodular lymphangitis or sporotrichoid spread.6 Sporotrichosis can have a similar clinical and histologic manifestation to M marinum infection, but the patient history typically includes exposure to Sporothrix schenckii through gardening or other contact with thorns, plants, or soil.2 Cutaneous sarcoidosis can have a similar clinical appearance to M marinum infection, but nodular lymphangitis does not occur and histopathology would demonstrate noncaseating epithelioid cell granulomas.7 Lastly, although vegetative pyoderma gangrenosum can have some of the same histologic findings as M marinum, it typically also demonstrates sinus tract formation, which was not present in our case. Additionally, vegetative pyoderma gangrenosum manifests with a verrucous and pustular plaque that would not have lymphocutaneous spread.8
Treatment of cutaneous M marinum infection is guided by antibiotic susceptibility testing. One regimen is clarithromycin (500 mg twice daily9) plus ethambutol. 10 Treatment often entails a multidrug combination due to the high rates of antibiotic resistance. Other antibiotics that potentially can be used include rifampin, trimethoprim-sulfamethoxazole, minocycline, and quinolones. The treatment duration typically is more than 3 months, and therapy is continued for 4 to 6 weeks after the skin lesions resolve.11 Excision of the lesion is reserved for patients with M marinum infection that fails to respond to antibiotic therapy.5
- Wayne LG, Sramek HA. Agents of newly recognized or infrequently encountered mycobacterial diseases. Clin Microbiol Rev. 1992;5:1-25. doi:10.1128/CMR.5.1.1
- Tobin EH, Jih WW. Sporotrichoid lymphocutaneous infections: etiology, diagnosis and therapy. Am Fam Physician. 2001;63:326-332.
- van Ingen J. Diagnosis of nontuberculous mycobacterial infections. Semin Respir Crit Care Med. 2013;34:103-109. doi:10.1055/s-0033-1333569
- Williamson H, Phillips R, Sarfo S, et al. Genetic diversity of PCR-positive, culture-negative and culture-positive Mycobacterium ulcerans isolated from Buruli ulcer patients in Ghana. PLoS One. 2014;9:E88007. doi:10.1371/journal.pone.0088007
- Aubry A, Mougari F, Reibel F, et al. Mycobacterium marinum. Microbiol Spectr. 2017;5. doi:10.1128/microbiolspec.TNMI7-0038-2016
- Baranowski K, Huang B. Cat scratch disease. StatPearls [Internet]. Updated June 12, 2023. Accessed July 15, 2024. https://www.ncbi.nlm .nih.gov/books/NBK482139/
- Sanchez M, Haimovic A, Prystowsky S. Sarcoidosis. Dermatol Clin. 2015;33:389-416. doi:10.1016/j.det.2015.03.006
- Borg Grech S, Vella Baldacchino A, Corso R, et al. Superficial granulomatous pyoderma successfully treated with intravenous immunoglobulin. Eur J Case Rep Intern Med. 2021;8:002656. doi:10.12890/2021_002656
- Krooks J, Weatherall A, Markowitz S. Complete resolution of Mycobacterium marinum infection with clarithromycin and ethambutol: a case report and a review of the literature. J Clin Aesthet Dermatol. 2018;11:48-51.
- Medel-Plaza M., Esteban J. Current treatment options for Mycobacterium marinum cutaneous infections. Expert Opin Pharmacother. 2023;24:1113-1123. doi:10.1080/14656566.2023.2211258
- Tirado-Sánchez A, Bonifaz A. Nodular lymphangitis (sporotrichoid lymphocutaneous infections): clues to differential diagnosis. J Fungi (Basel). 2018;4:56. doi:10.3390/jof4020056
The Diagnosis: Mycobacterium marinum Infection
A repeat excisional biopsy showed suppurative granulomatous dermatitis with negative stains for infectious organisms; however, tissue culture grew Mycobacterium marinum. The patient had a history of exposure to fish tanks, which are a potential habitat for nontuberculous mycobacteria. These bacteria can enter the body through a minor laceration or cut in the skin, which was likely due to her occupation and pet care activities.1 Her fish tank exposure combined with the cutaneous findings of a long-standing indurated plaque with proximal nodular lymphangitis made M marinum infection the most likely diagnosis.2
Due to the limited specificity and sensitivity of patient symptoms, histologic staining, and direct microscopy, the gold standard for diagnosing acid-fast bacilli is tissue culture. 3 Tissue polymerase chain reaction testing is most useful in identifying the species of mycobacteria when histologic stains identify acid-fast bacilli but repeated tissue cultures are negative.4 With M marinum, a high clinical suspicion is needed to acquire a positive tissue culture because it needs to be grown for several weeks and at a temperature of 30 °C.5 Therefore, the physician should inform the laboratory if there is any suspicion for M marinum to increase the likelihood of obtaining a positive culture.
The differential diagnosis for M marinum infection includes other skin diseases that can cause nodular lymphangitis (also known as sporotrichoid spread) such as sporotrichosis, leishmaniasis, and certain bacterial and fungal infections. Although cat scratch disease, which is caused by Bartonella henselae, can appear similar to M marinum on histopathology, it clinically manifests with a single papulovesicular lesion at the site of inoculation that then forms a central eschar and resolves within a few weeks. Cat scratch disease typically causes painful lymphadenopathy, but it does not cause nodular lymphangitis or sporotrichoid spread.6 Sporotrichosis can have a similar clinical and histologic manifestation to M marinum infection, but the patient history typically includes exposure to Sporothrix schenckii through gardening or other contact with thorns, plants, or soil.2 Cutaneous sarcoidosis can have a similar clinical appearance to M marinum infection, but nodular lymphangitis does not occur and histopathology would demonstrate noncaseating epithelioid cell granulomas.7 Lastly, although vegetative pyoderma gangrenosum can have some of the same histologic findings as M marinum, it typically also demonstrates sinus tract formation, which was not present in our case. Additionally, vegetative pyoderma gangrenosum manifests with a verrucous and pustular plaque that would not have lymphocutaneous spread.8
Treatment of cutaneous M marinum infection is guided by antibiotic susceptibility testing. One regimen is clarithromycin (500 mg twice daily9) plus ethambutol. 10 Treatment often entails a multidrug combination due to the high rates of antibiotic resistance. Other antibiotics that potentially can be used include rifampin, trimethoprim-sulfamethoxazole, minocycline, and quinolones. The treatment duration typically is more than 3 months, and therapy is continued for 4 to 6 weeks after the skin lesions resolve.11 Excision of the lesion is reserved for patients with M marinum infection that fails to respond to antibiotic therapy.5
The Diagnosis: Mycobacterium marinum Infection
A repeat excisional biopsy showed suppurative granulomatous dermatitis with negative stains for infectious organisms; however, tissue culture grew Mycobacterium marinum. The patient had a history of exposure to fish tanks, which are a potential habitat for nontuberculous mycobacteria. These bacteria can enter the body through a minor laceration or cut in the skin, which was likely due to her occupation and pet care activities.1 Her fish tank exposure combined with the cutaneous findings of a long-standing indurated plaque with proximal nodular lymphangitis made M marinum infection the most likely diagnosis.2
Due to the limited specificity and sensitivity of patient symptoms, histologic staining, and direct microscopy, the gold standard for diagnosing acid-fast bacilli is tissue culture. 3 Tissue polymerase chain reaction testing is most useful in identifying the species of mycobacteria when histologic stains identify acid-fast bacilli but repeated tissue cultures are negative.4 With M marinum, a high clinical suspicion is needed to acquire a positive tissue culture because it needs to be grown for several weeks and at a temperature of 30 °C.5 Therefore, the physician should inform the laboratory if there is any suspicion for M marinum to increase the likelihood of obtaining a positive culture.
The differential diagnosis for M marinum infection includes other skin diseases that can cause nodular lymphangitis (also known as sporotrichoid spread) such as sporotrichosis, leishmaniasis, and certain bacterial and fungal infections. Although cat scratch disease, which is caused by Bartonella henselae, can appear similar to M marinum on histopathology, it clinically manifests with a single papulovesicular lesion at the site of inoculation that then forms a central eschar and resolves within a few weeks. Cat scratch disease typically causes painful lymphadenopathy, but it does not cause nodular lymphangitis or sporotrichoid spread.6 Sporotrichosis can have a similar clinical and histologic manifestation to M marinum infection, but the patient history typically includes exposure to Sporothrix schenckii through gardening or other contact with thorns, plants, or soil.2 Cutaneous sarcoidosis can have a similar clinical appearance to M marinum infection, but nodular lymphangitis does not occur and histopathology would demonstrate noncaseating epithelioid cell granulomas.7 Lastly, although vegetative pyoderma gangrenosum can have some of the same histologic findings as M marinum, it typically also demonstrates sinus tract formation, which was not present in our case. Additionally, vegetative pyoderma gangrenosum manifests with a verrucous and pustular plaque that would not have lymphocutaneous spread.8
Treatment of cutaneous M marinum infection is guided by antibiotic susceptibility testing. One regimen is clarithromycin (500 mg twice daily9) plus ethambutol. 10 Treatment often entails a multidrug combination due to the high rates of antibiotic resistance. Other antibiotics that potentially can be used include rifampin, trimethoprim-sulfamethoxazole, minocycline, and quinolones. The treatment duration typically is more than 3 months, and therapy is continued for 4 to 6 weeks after the skin lesions resolve.11 Excision of the lesion is reserved for patients with M marinum infection that fails to respond to antibiotic therapy.5
- Wayne LG, Sramek HA. Agents of newly recognized or infrequently encountered mycobacterial diseases. Clin Microbiol Rev. 1992;5:1-25. doi:10.1128/CMR.5.1.1
- Tobin EH, Jih WW. Sporotrichoid lymphocutaneous infections: etiology, diagnosis and therapy. Am Fam Physician. 2001;63:326-332.
- van Ingen J. Diagnosis of nontuberculous mycobacterial infections. Semin Respir Crit Care Med. 2013;34:103-109. doi:10.1055/s-0033-1333569
- Williamson H, Phillips R, Sarfo S, et al. Genetic diversity of PCR-positive, culture-negative and culture-positive Mycobacterium ulcerans isolated from Buruli ulcer patients in Ghana. PLoS One. 2014;9:E88007. doi:10.1371/journal.pone.0088007
- Aubry A, Mougari F, Reibel F, et al. Mycobacterium marinum. Microbiol Spectr. 2017;5. doi:10.1128/microbiolspec.TNMI7-0038-2016
- Baranowski K, Huang B. Cat scratch disease. StatPearls [Internet]. Updated June 12, 2023. Accessed July 15, 2024. https://www.ncbi.nlm .nih.gov/books/NBK482139/
- Sanchez M, Haimovic A, Prystowsky S. Sarcoidosis. Dermatol Clin. 2015;33:389-416. doi:10.1016/j.det.2015.03.006
- Borg Grech S, Vella Baldacchino A, Corso R, et al. Superficial granulomatous pyoderma successfully treated with intravenous immunoglobulin. Eur J Case Rep Intern Med. 2021;8:002656. doi:10.12890/2021_002656
- Krooks J, Weatherall A, Markowitz S. Complete resolution of Mycobacterium marinum infection with clarithromycin and ethambutol: a case report and a review of the literature. J Clin Aesthet Dermatol. 2018;11:48-51.
- Medel-Plaza M., Esteban J. Current treatment options for Mycobacterium marinum cutaneous infections. Expert Opin Pharmacother. 2023;24:1113-1123. doi:10.1080/14656566.2023.2211258
- Tirado-Sánchez A, Bonifaz A. Nodular lymphangitis (sporotrichoid lymphocutaneous infections): clues to differential diagnosis. J Fungi (Basel). 2018;4:56. doi:10.3390/jof4020056
- Wayne LG, Sramek HA. Agents of newly recognized or infrequently encountered mycobacterial diseases. Clin Microbiol Rev. 1992;5:1-25. doi:10.1128/CMR.5.1.1
- Tobin EH, Jih WW. Sporotrichoid lymphocutaneous infections: etiology, diagnosis and therapy. Am Fam Physician. 2001;63:326-332.
- van Ingen J. Diagnosis of nontuberculous mycobacterial infections. Semin Respir Crit Care Med. 2013;34:103-109. doi:10.1055/s-0033-1333569
- Williamson H, Phillips R, Sarfo S, et al. Genetic diversity of PCR-positive, culture-negative and culture-positive Mycobacterium ulcerans isolated from Buruli ulcer patients in Ghana. PLoS One. 2014;9:E88007. doi:10.1371/journal.pone.0088007
- Aubry A, Mougari F, Reibel F, et al. Mycobacterium marinum. Microbiol Spectr. 2017;5. doi:10.1128/microbiolspec.TNMI7-0038-2016
- Baranowski K, Huang B. Cat scratch disease. StatPearls [Internet]. Updated June 12, 2023. Accessed July 15, 2024. https://www.ncbi.nlm .nih.gov/books/NBK482139/
- Sanchez M, Haimovic A, Prystowsky S. Sarcoidosis. Dermatol Clin. 2015;33:389-416. doi:10.1016/j.det.2015.03.006
- Borg Grech S, Vella Baldacchino A, Corso R, et al. Superficial granulomatous pyoderma successfully treated with intravenous immunoglobulin. Eur J Case Rep Intern Med. 2021;8:002656. doi:10.12890/2021_002656
- Krooks J, Weatherall A, Markowitz S. Complete resolution of Mycobacterium marinum infection with clarithromycin and ethambutol: a case report and a review of the literature. J Clin Aesthet Dermatol. 2018;11:48-51.
- Medel-Plaza M., Esteban J. Current treatment options for Mycobacterium marinum cutaneous infections. Expert Opin Pharmacother. 2023;24:1113-1123. doi:10.1080/14656566.2023.2211258
- Tirado-Sánchez A, Bonifaz A. Nodular lymphangitis (sporotrichoid lymphocutaneous infections): clues to differential diagnosis. J Fungi (Basel). 2018;4:56. doi:10.3390/jof4020056
A 30-year-old woman presented to the dermatology clinic with lesions on the right forearm of 2 years’ duration. Her medical history was unremarkable. She reported working as a chef and caring for multiple pets in her home, including 3 cats, 6 fish tanks, 3 dogs, and 3 lizards. Physical examination revealed a painful, indurated, red-violaceous plaque on the right forearm with satellite pink nodules that had been slowly migrating proximally up the forearm. An outside excisional biopsy performed 1 year prior had shown suppurative granulomatous dermatitis with negative stains for infectious organisms and negative tissue cultures. At that time, the patient was diagnosed with ruptured folliculitis; however, a subsequent lack of clinical improvement prompted her to seek a second opinion at our clinic.
