Solitary Plaque on the Nose

The biopsy revealed hyperkeratosis, hypergranulosis, follicular plugging, vacuolar interface dermatitis with apoptotic bodies, dyskeratotic keratinocytes, pigment incontinence, and melanophages. A perivascular, perifollicular, and periadnexal lymphoplasmacytic inflammatory infiltrate was noted in the superficial and deep dermis (Figure). Based on the characteristic clinical morphology, dermoscopic features, and histopathology, a diagnosis of discoid lupus erythematosus (DLE) was established. The patient was started on mometasone cream 0.1% and tacrolimus ointment 0.1% once daily, with strict recommendations for photoprotection. However, he subsequently was lost to follow-up, and treatment response could not be assessed.

Lupus erythematosus is a multisystemic autoimmune disease with a predilection for skin involvement that is characterized by the production of autoantibodies against nuclear antigens. Discoid lupus erythematosus is the predominant form of the disease, mostly affecting middle-aged women (female-to-male ratio, 4.1:1).¹ Discoid lupus erythematosus usually manifests as well-demarcated, erythematous patches or plaques with partially adherent scales that extend into a patulous follicle. On removal, the scales show horny plugs underneath. This classic finding is known as the carpet tack sign.

As the lesions evolve, they expand with hyperpigmentation at the periphery as well as hypopigmentation, atrophy, scarring, and telangiectasias at the center.² In our patient, the history of discharge and crusting of the lesion and the presence of slight central atrophy—all of which could be attributed to chronic application of topical medications such as corticosteroids, which can cause epidermal thinning, maceration, and secondary crust formation—raised clinical suspicion of cutaneous infections (eg, cutaneous leishmaniasis, lupus vulgaris) and squamous cell carcinoma. The presence of slightly raised margins upon clinical examination brought basal cell carcinoma (BCC) into the differential.

Dermoscopic features commonly seen in DLE reflect the pathologic findings. Follicular plugging and perifollicular white halos correspond to follicular hyperkeratosis and perifollicular fibrosis, respectively (eTable). Disease duration has been shown to alter the dermoscopic appearance of DLE with early active disease showing radially arranged arborizing blood vessels between perifollicular white halos along with follicular red dots, whereas lesions of longer duration display structureless white areas secondary to dermal fibrosis.³ Additionally, background erythema due to neoangiogenesis and dermal inflammation suggests that the disease is in its active state.

On dermoscopy, pigmentation structures such as brown dots, brown lines, and grey-brown dots and globules were seen more prominently in our patient with skin of color, making the underlying erythema more subtle than in patients with lighter skin types. Dotted and linear vessels also were seen in our patient, but not as prominently as typically is seen in lighter skin types.⁴

Lupus vulgaris was ruled out in our patient based on the absence of the typical orange to yellowish-orange background with vessels or any histopathologic evidence of epithelioid granulomas.⁵ Cutaneous leishmaniasis is characterized by polymorphic vascularization, erythema, follicular plugs, yellow-orange structureless areas with scales, and crusts on dermoscopy.⁶ Squamous cell carcinoma tends to show white structureless areas, looped vessels, and central keratin.⁷

Superficial BCC also appears as thin plaques or patches bound by a well-circumscribed, slightly raised, irregular margin. However, on dermoscopy, BCC typically exhibits spoke-wheel areas, arborizing vessels, comma vessels, and concentric structures.⁸

The clinical manifestations of crusting, discharge, and a raised border was atypical, probably owing to the long-term unsupervised application of topical medications, which made the initial diagnosis challenging. Therefore, various differential diagnoses were considered. Dermoscopic evaluation coupled with histology was performed, which ultimately confirmed the diagnosis of DLE.

The biopsy revealed hyperkeratosis, hypergranulosis, follicular plugging, vacuolar interface dermatitis with apoptotic bodies, dyskeratotic keratinocytes, pigment incontinence, and melanophages. A perivascular, perifollicular, and periadnexal lymphoplasmacytic inflammatory infiltrate was noted in the superficial and deep dermis (Figure). Based on the characteristic clinical morphology, dermoscopic features, and histopathology, a diagnosis of discoid lupus erythematosus (DLE) was established. The patient was started on mometasone cream 0.1% and tacrolimus ointment 0.1% once daily, with strict recommendations for photoprotection. However, he subsequently was lost to follow-up, and treatment response could not be assessed.

Lupus erythematosus is a multisystemic autoimmune disease with a predilection for skin involvement that is characterized by the production of autoantibodies against nuclear antigens. Discoid lupus erythematosus is the predominant form of the disease, mostly affecting middle-aged women (female-to-male ratio, 4.1:1).¹ Discoid lupus erythematosus usually manifests as well-demarcated, erythematous patches or plaques with partially adherent scales that extend into a patulous follicle. On removal, the scales show horny plugs underneath. This classic finding is known as the carpet tack sign.

As the lesions evolve, they expand with hyperpigmentation at the periphery as well as hypopigmentation, atrophy, scarring, and telangiectasias at the center.² In our patient, the history of discharge and crusting of the lesion and the presence of slight central atrophy—all of which could be attributed to chronic application of topical medications such as corticosteroids, which can cause epidermal thinning, maceration, and secondary crust formation—raised clinical suspicion of cutaneous infections (eg, cutaneous leishmaniasis, lupus vulgaris) and squamous cell carcinoma. The presence of slightly raised margins upon clinical examination brought basal cell carcinoma (BCC) into the differential.

Dermoscopic features commonly seen in DLE reflect the pathologic findings. Follicular plugging and perifollicular white halos correspond to follicular hyperkeratosis and perifollicular fibrosis, respectively (eTable). Disease duration has been shown to alter the dermoscopic appearance of DLE with early active disease showing radially arranged arborizing blood vessels between perifollicular white halos along with follicular red dots, whereas lesions of longer duration display structureless white areas secondary to dermal fibrosis.³ Additionally, background erythema due to neoangiogenesis and dermal inflammation suggests that the disease is in its active state.

On dermoscopy, pigmentation structures such as brown dots, brown lines, and grey-brown dots and globules were seen more prominently in our patient with skin of color, making the underlying erythema more subtle than in patients with lighter skin types. Dotted and linear vessels also were seen in our patient, but not as prominently as typically is seen in lighter skin types.⁴

Lupus vulgaris was ruled out in our patient based on the absence of the typical orange to yellowish-orange background with vessels or any histopathologic evidence of epithelioid granulomas.⁵ Cutaneous leishmaniasis is characterized by polymorphic vascularization, erythema, follicular plugs, yellow-orange structureless areas with scales, and crusts on dermoscopy.⁶ Squamous cell carcinoma tends to show white structureless areas, looped vessels, and central keratin.⁷

Superficial BCC also appears as thin plaques or patches bound by a well-circumscribed, slightly raised, irregular margin. However, on dermoscopy, BCC typically exhibits spoke-wheel areas, arborizing vessels, comma vessels, and concentric structures.⁸

The clinical manifestations of crusting, discharge, and a raised border was atypical, probably owing to the long-term unsupervised application of topical medications, which made the initial diagnosis challenging. Therefore, various differential diagnoses were considered. Dermoscopic evaluation coupled with histology was performed, which ultimately confirmed the diagnosis of DLE.

The biopsy revealed hyperkeratosis, hypergranulosis, follicular plugging, vacuolar interface dermatitis with apoptotic bodies, dyskeratotic keratinocytes, pigment incontinence, and melanophages. A perivascular, perifollicular, and periadnexal lymphoplasmacytic inflammatory infiltrate was noted in the superficial and deep dermis (Figure). Based on the characteristic clinical morphology, dermoscopic features, and histopathology, a diagnosis of discoid lupus erythematosus (DLE) was established. The patient was started on mometasone cream 0.1% and tacrolimus ointment 0.1% once daily, with strict recommendations for photoprotection. However, he subsequently was lost to follow-up, and treatment response could not be assessed.

Lupus erythematosus is a multisystemic autoimmune disease with a predilection for skin involvement that is characterized by the production of autoantibodies against nuclear antigens. Discoid lupus erythematosus is the predominant form of the disease, mostly affecting middle-aged women (female-to-male ratio, 4.1:1).¹ Discoid lupus erythematosus usually manifests as well-demarcated, erythematous patches or plaques with partially adherent scales that extend into a patulous follicle. On removal, the scales show horny plugs underneath. This classic finding is known as the carpet tack sign.

As the lesions evolve, they expand with hyperpigmentation at the periphery as well as hypopigmentation, atrophy, scarring, and telangiectasias at the center.² In our patient, the history of discharge and crusting of the lesion and the presence of slight central atrophy—all of which could be attributed to chronic application of topical medications such as corticosteroids, which can cause epidermal thinning, maceration, and secondary crust formation—raised clinical suspicion of cutaneous infections (eg, cutaneous leishmaniasis, lupus vulgaris) and squamous cell carcinoma. The presence of slightly raised margins upon clinical examination brought basal cell carcinoma (BCC) into the differential.

Dermoscopic features commonly seen in DLE reflect the pathologic findings. Follicular plugging and perifollicular white halos correspond to follicular hyperkeratosis and perifollicular fibrosis, respectively (eTable). Disease duration has been shown to alter the dermoscopic appearance of DLE with early active disease showing radially arranged arborizing blood vessels between perifollicular white halos along with follicular red dots, whereas lesions of longer duration display structureless white areas secondary to dermal fibrosis.³ Additionally, background erythema due to neoangiogenesis and dermal inflammation suggests that the disease is in its active state.

On dermoscopy, pigmentation structures such as brown dots, brown lines, and grey-brown dots and globules were seen more prominently in our patient with skin of color, making the underlying erythema more subtle than in patients with lighter skin types. Dotted and linear vessels also were seen in our patient, but not as prominently as typically is seen in lighter skin types.⁴

Lupus vulgaris was ruled out in our patient based on the absence of the typical orange to yellowish-orange background with vessels or any histopathologic evidence of epithelioid granulomas.⁵ Cutaneous leishmaniasis is characterized by polymorphic vascularization, erythema, follicular plugs, yellow-orange structureless areas with scales, and crusts on dermoscopy.⁶ Squamous cell carcinoma tends to show white structureless areas, looped vessels, and central keratin.⁷

Superficial BCC also appears as thin plaques or patches bound by a well-circumscribed, slightly raised, irregular margin. However, on dermoscopy, BCC typically exhibits spoke-wheel areas, arborizing vessels, comma vessels, and concentric structures.⁸

The clinical manifestations of crusting, discharge, and a raised border was atypical, probably owing to the long-term unsupervised application of topical medications, which made the initial diagnosis challenging. Therefore, various differential diagnoses were considered. Dermoscopic evaluation coupled with histology was performed, which ultimately confirmed the diagnosis of DLE.