Dermoscopy Diagnosis

THE DIAGNOSIS: Angiolymphoid Hyperplasia With Eosinophilia

Angiolymphoid hyperplasia with eosinophilia (ALHE) is a rare, benign, inflammatory vascular proliferation with lymphocytic and eosinophilic infiltration. Bleeding and pruritus associated with ALHE can substantially affect a patient’s quality of life, necessitating correct diagnosis and effective treatment.¹ The etiopathogenesis of ALHE is poorly understood, and it often is attributed to an underlying vascular malformation or local trauma. Vascular proliferation due to hyperestrogenemia could explain why pregnancy is considered a predisposing factor for ALHE.^1,2

Angiolymphoid hyperplasia with eosinophilia typically manifests with solitary or multiple pink to red-brown, dome-shaped papules or nodules occurring most frequently on the head and neck. Lesions may be either asymptomatic or associated with pruritus, pain, and spontaneous bleeding.¹ Dermoscopy is crucial to diagnosis. The most frequent dermoscopic findings include a polymorphic vascular pattern such as dotted and linear irregular vessels over a pink background, white lines, white dots, white structureless areas, and red-purple lacunae.^2,3 Histopathology will demonstrate a vascular proliferation with plump epithelioid endothelial cells showing abundant eosinophilic cytoplasm, accompanied by a variable lymphocytic and eosinophilic inflammatory infiltrate (Figure 1).¹

In our case, dermoscopic-histopathologic correlation suggested that the polymorphic vascular pattern and clods on a pink background corresponded to thin- and thick-walled vessels containing plump endothelial cells and intraluminal erythrocytes within the superficial and deep dermis. White structures could represent underlying fibrosis and altered dermal collagen due to vascular proliferation. The brown pigment network and peripheral brownish pigmentation were most likely secondary to increased melanin and accentuation of the pigment network in the setting of Fitzpatrick skin types IV to V, although pruritic trauma with postinflammatory hyperpigmentation may also have contributed, making dermoscopic-histopathologic correlation challenging.

Surgical excision is considered the primary treatment modality for ALHE, with the lowest recurrence rates.¹ Alternative therapeutic options include intralesional steroids, cryotherapy, sclerotherapy, radiofrequency, pulsed dye laser, and carbon dioxide laser, with varying efficacy reported.¹ Our patient was treated with a combination of a long-pulse Nd:YAG laser (pulse width of 30 ms) to target the vascular component, followed by a single session with an ablative Er:YAG laser. After 4 weeks, healing with good cosmetic results was observed (Figure 2). At 6-month follow-up, there was no recurrence of the lesions.

Kimura disease, often considered the closest differential diagnosis for ALHE, is a rare lymphoproliferative fibroinflammatory condition. Patients present with subcutaneous nodules on the head and neck, often associated with lymphadenopathy. Elevated serum IgE levels and peripheral blood eosinophilia are common.¹ Another consideration in the differential diagnosis is cutaneous bacillary angiomatosis caused by Bartonella species, a vascular proliferative condition that mostly affects individuals with HIV, transplant recipients, and those taking immunosuppressive medications.⁴ Pyogenic granuloma, also known as lobular capillary haemangioma, is another benign vascular proliferation that resembles ALHE. Clinically, it manifests as a solitary, painless, flesh-colored to erythematous papulonodule; however, multiple grouped lesions also can occur. The lesions often are associated with bleeding and erosions.⁵ Epithelioid hemangioendothelioma is a rare vascular tumor most frequently manifesting in the liver, lungs, or bones, and very rarely is limited to skin. Cutaneous epithelioid hemangioendothelioma mimics ALHE and may manifest as a solitary erythematous mass, multiple dome-shaped masses, or dermal nodules.⁶

THE DIAGNOSIS: Angiolymphoid Hyperplasia With Eosinophilia

Angiolymphoid hyperplasia with eosinophilia (ALHE) is a rare, benign, inflammatory vascular proliferation with lymphocytic and eosinophilic infiltration. Bleeding and pruritus associated with ALHE can substantially affect a patient’s quality of life, necessitating correct diagnosis and effective treatment.¹ The etiopathogenesis of ALHE is poorly understood, and it often is attributed to an underlying vascular malformation or local trauma. Vascular proliferation due to hyperestrogenemia could explain why pregnancy is considered a predisposing factor for ALHE.^1,2

Angiolymphoid hyperplasia with eosinophilia typically manifests with solitary or multiple pink to red-brown, dome-shaped papules or nodules occurring most frequently on the head and neck. Lesions may be either asymptomatic or associated with pruritus, pain, and spontaneous bleeding.¹ Dermoscopy is crucial to diagnosis. The most frequent dermoscopic findings include a polymorphic vascular pattern such as dotted and linear irregular vessels over a pink background, white lines, white dots, white structureless areas, and red-purple lacunae.^2,3 Histopathology will demonstrate a vascular proliferation with plump epithelioid endothelial cells showing abundant eosinophilic cytoplasm, accompanied by a variable lymphocytic and eosinophilic inflammatory infiltrate (Figure 1).¹

In our case, dermoscopic-histopathologic correlation suggested that the polymorphic vascular pattern and clods on a pink background corresponded to thin- and thick-walled vessels containing plump endothelial cells and intraluminal erythrocytes within the superficial and deep dermis. White structures could represent underlying fibrosis and altered dermal collagen due to vascular proliferation. The brown pigment network and peripheral brownish pigmentation were most likely secondary to increased melanin and accentuation of the pigment network in the setting of Fitzpatrick skin types IV to V, although pruritic trauma with postinflammatory hyperpigmentation may also have contributed, making dermoscopic-histopathologic correlation challenging.

Surgical excision is considered the primary treatment modality for ALHE, with the lowest recurrence rates.¹ Alternative therapeutic options include intralesional steroids, cryotherapy, sclerotherapy, radiofrequency, pulsed dye laser, and carbon dioxide laser, with varying efficacy reported.¹ Our patient was treated with a combination of a long-pulse Nd:YAG laser (pulse width of 30 ms) to target the vascular component, followed by a single session with an ablative Er:YAG laser. After 4 weeks, healing with good cosmetic results was observed (Figure 2). At 6-month follow-up, there was no recurrence of the lesions.

Kimura disease, often considered the closest differential diagnosis for ALHE, is a rare lymphoproliferative fibroinflammatory condition. Patients present with subcutaneous nodules on the head and neck, often associated with lymphadenopathy. Elevated serum IgE levels and peripheral blood eosinophilia are common.¹ Another consideration in the differential diagnosis is cutaneous bacillary angiomatosis caused by Bartonella species, a vascular proliferative condition that mostly affects individuals with HIV, transplant recipients, and those taking immunosuppressive medications.⁴ Pyogenic granuloma, also known as lobular capillary haemangioma, is another benign vascular proliferation that resembles ALHE. Clinically, it manifests as a solitary, painless, flesh-colored to erythematous papulonodule; however, multiple grouped lesions also can occur. The lesions often are associated with bleeding and erosions.⁵ Epithelioid hemangioendothelioma is a rare vascular tumor most frequently manifesting in the liver, lungs, or bones, and very rarely is limited to skin. Cutaneous epithelioid hemangioendothelioma mimics ALHE and may manifest as a solitary erythematous mass, multiple dome-shaped masses, or dermal nodules.⁶

THE DIAGNOSIS: Angiolymphoid Hyperplasia With Eosinophilia

Angiolymphoid hyperplasia with eosinophilia (ALHE) is a rare, benign, inflammatory vascular proliferation with lymphocytic and eosinophilic infiltration. Bleeding and pruritus associated with ALHE can substantially affect a patient’s quality of life, necessitating correct diagnosis and effective treatment.¹ The etiopathogenesis of ALHE is poorly understood, and it often is attributed to an underlying vascular malformation or local trauma. Vascular proliferation due to hyperestrogenemia could explain why pregnancy is considered a predisposing factor for ALHE.^1,2

Angiolymphoid hyperplasia with eosinophilia typically manifests with solitary or multiple pink to red-brown, dome-shaped papules or nodules occurring most frequently on the head and neck. Lesions may be either asymptomatic or associated with pruritus, pain, and spontaneous bleeding.¹ Dermoscopy is crucial to diagnosis. The most frequent dermoscopic findings include a polymorphic vascular pattern such as dotted and linear irregular vessels over a pink background, white lines, white dots, white structureless areas, and red-purple lacunae.^2,3 Histopathology will demonstrate a vascular proliferation with plump epithelioid endothelial cells showing abundant eosinophilic cytoplasm, accompanied by a variable lymphocytic and eosinophilic inflammatory infiltrate (Figure 1).¹

In our case, dermoscopic-histopathologic correlation suggested that the polymorphic vascular pattern and clods on a pink background corresponded to thin- and thick-walled vessels containing plump endothelial cells and intraluminal erythrocytes within the superficial and deep dermis. White structures could represent underlying fibrosis and altered dermal collagen due to vascular proliferation. The brown pigment network and peripheral brownish pigmentation were most likely secondary to increased melanin and accentuation of the pigment network in the setting of Fitzpatrick skin types IV to V, although pruritic trauma with postinflammatory hyperpigmentation may also have contributed, making dermoscopic-histopathologic correlation challenging.

Surgical excision is considered the primary treatment modality for ALHE, with the lowest recurrence rates.¹ Alternative therapeutic options include intralesional steroids, cryotherapy, sclerotherapy, radiofrequency, pulsed dye laser, and carbon dioxide laser, with varying efficacy reported.¹ Our patient was treated with a combination of a long-pulse Nd:YAG laser (pulse width of 30 ms) to target the vascular component, followed by a single session with an ablative Er:YAG laser. After 4 weeks, healing with good cosmetic results was observed (Figure 2). At 6-month follow-up, there was no recurrence of the lesions.

Kimura disease, often considered the closest differential diagnosis for ALHE, is a rare lymphoproliferative fibroinflammatory condition. Patients present with subcutaneous nodules on the head and neck, often associated with lymphadenopathy. Elevated serum IgE levels and peripheral blood eosinophilia are common.¹ Another consideration in the differential diagnosis is cutaneous bacillary angiomatosis caused by Bartonella species, a vascular proliferative condition that mostly affects individuals with HIV, transplant recipients, and those taking immunosuppressive medications.⁴ Pyogenic granuloma, also known as lobular capillary haemangioma, is another benign vascular proliferation that resembles ALHE. Clinically, it manifests as a solitary, painless, flesh-colored to erythematous papulonodule; however, multiple grouped lesions also can occur. The lesions often are associated with bleeding and erosions.⁵ Epithelioid hemangioendothelioma is a rare vascular tumor most frequently manifesting in the liver, lungs, or bones, and very rarely is limited to skin. Cutaneous epithelioid hemangioendothelioma mimics ALHE and may manifest as a solitary erythematous mass, multiple dome-shaped masses, or dermal nodules.⁶

THE DIAGNOSIS: Pigmented Bowen Disease

Histopathology revealed atypical keratinocytes throughout the entire thickness of a pigmented epidermis extending from the basal layer (Figure). Diffuse epidermal hyperpigmentation and melanophages in the papillary dermis were present. There was no dermal invasion or atypical melanocytic proliferation. On dermoscopy, this lesion had small brown globules, smudging, and an asymmetric nonspecific homogeneous pattern. Based on these features as well as the clinical findings, a diagnosis of pigmented Bowen disease (PBD), a rare subtype of squamous cell carcinoma in situ, was made. Complete removal of the lesion was achieved via the biopsy, and the patient was counselled regarding the malignant but noninvasive nature of the lesion. Appropriate follow-up was recommended to monitor for recurrence.

Our case presentation of PBD on the right upper arm in a female patient with a light skin tone is not classic, as PBD lesions usually manifest as well-demarcated scaly plaques on sun-protected sites in men with darker skin tones who are in the sixth to seventh decades of life.¹

Dermoscopy of PBD in patients with lighter skin tones can present diagnostic challenges because characteristic clustered glomerular vessels may be faint or absent, particularly in small lesions such as this one. In such cases, PBD may instead demonstrate structureless brown pigmentation and irregular globules, patterns that overlap with pigmented actinic keratosis (PAK) and melanoma.³

Our case underscores the importance of maintaining a broad differential when evaluating small pigmented macules and reinforces biopsy as the diagnostic gold standard for PBD when dermoscopic findings are nonspecific.

THE DIAGNOSIS: Pigmented Bowen Disease

Histopathology revealed atypical keratinocytes throughout the entire thickness of a pigmented epidermis extending from the basal layer (Figure). Diffuse epidermal hyperpigmentation and melanophages in the papillary dermis were present. There was no dermal invasion or atypical melanocytic proliferation. On dermoscopy, this lesion had small brown globules, smudging, and an asymmetric nonspecific homogeneous pattern. Based on these features as well as the clinical findings, a diagnosis of pigmented Bowen disease (PBD), a rare subtype of squamous cell carcinoma in situ, was made. Complete removal of the lesion was achieved via the biopsy, and the patient was counselled regarding the malignant but noninvasive nature of the lesion. Appropriate follow-up was recommended to monitor for recurrence.

Our case presentation of PBD on the right upper arm in a female patient with a light skin tone is not classic, as PBD lesions usually manifest as well-demarcated scaly plaques on sun-protected sites in men with darker skin tones who are in the sixth to seventh decades of life.¹

Dermoscopy of PBD in patients with lighter skin tones can present diagnostic challenges because characteristic clustered glomerular vessels may be faint or absent, particularly in small lesions such as this one. In such cases, PBD may instead demonstrate structureless brown pigmentation and irregular globules, patterns that overlap with pigmented actinic keratosis (PAK) and melanoma.³

Our case underscores the importance of maintaining a broad differential when evaluating small pigmented macules and reinforces biopsy as the diagnostic gold standard for PBD when dermoscopic findings are nonspecific.

THE DIAGNOSIS: Pigmented Bowen Disease

Histopathology revealed atypical keratinocytes throughout the entire thickness of a pigmented epidermis extending from the basal layer (Figure). Diffuse epidermal hyperpigmentation and melanophages in the papillary dermis were present. There was no dermal invasion or atypical melanocytic proliferation. On dermoscopy, this lesion had small brown globules, smudging, and an asymmetric nonspecific homogeneous pattern. Based on these features as well as the clinical findings, a diagnosis of pigmented Bowen disease (PBD), a rare subtype of squamous cell carcinoma in situ, was made. Complete removal of the lesion was achieved via the biopsy, and the patient was counselled regarding the malignant but noninvasive nature of the lesion. Appropriate follow-up was recommended to monitor for recurrence.

Our case presentation of PBD on the right upper arm in a female patient with a light skin tone is not classic, as PBD lesions usually manifest as well-demarcated scaly plaques on sun-protected sites in men with darker skin tones who are in the sixth to seventh decades of life.¹

Dermoscopy of PBD in patients with lighter skin tones can present diagnostic challenges because characteristic clustered glomerular vessels may be faint or absent, particularly in small lesions such as this one. In such cases, PBD may instead demonstrate structureless brown pigmentation and irregular globules, patterns that overlap with pigmented actinic keratosis (PAK) and melanoma.³

Our case underscores the importance of maintaining a broad differential when evaluating small pigmented macules and reinforces biopsy as the diagnostic gold standard for PBD when dermoscopic findings are nonspecific.

THE DIAGNOSIS: Seborrheic Keratosis

Histopathology revealed epidermal hyperplasia and hyperkeratosis with no notation of atypical melanocytic activity (Figure). There were no Kamino bodies, junctional nesting, or cytologic atypia. Based on these features as well as the clinical and dermoscopic findings, a diagnosis of an inflamed seborrheic keratosis (SK) was made. No further treatment was required following the shave biopsy, and the patient was reassured regarding the benign nature of the lesion.

Seborrheic keratoses are benign epidermal growths that can manifest on any area of the skin except the palms and soles. They present clinically as tan, yellow, gray, brown, or black with a smooth, waxy, or verrucous surface. They range from 1 mm to several centimeters in diameter. Although SKs traditionally manifest more frequently in individuals with lighter skin tones, pigmented variants, such as dermatosis papulosa nigra, have been reported to occur more commonly and at younger ages in patients with skin of color.¹

Dermoscopy of SK in patients with skin of color can present diagnostic challenges, as these lesions may display atypical pigmented patterns that overlap with melanocytic lesions, including Spitz nevi, particularly when starburstlike or globular structures are present.² What sets inflamed SKs apart from other SKs is the lack of a heavily keratinized surface on both clinical and dermoscopic evaluation. Common histopathologic diagnostic criteria for Spitz nevi include Kamino bodies, uniform nuclear enlargement, and spindled or epithelioid nevus cells, which were not noted in our patient.³ Therefore, in presentations such as this, histopathology remains the gold standard for diagnosis.

The differential diagnosis in this case included benign nevus, dysplastic nevus, melanoma, and Spitz nevus. Benign nevi typically demonstrate uniform pigmentation and symmetric dermoscopic patterns. Dysplastic nevi may show architectural disorder and cytologic atypia but lack invasive features.³ Melanoma often exhibits asymmetry, atypical network patterns, and irregular pigmentation.⁴ Spitz nevi characteristically demonstrate large epithelioid or spindle cells with Kamino bodies on histopathology, which were absent in our patient.

THE DIAGNOSIS: Seborrheic Keratosis

Histopathology revealed epidermal hyperplasia and hyperkeratosis with no notation of atypical melanocytic activity (Figure). There were no Kamino bodies, junctional nesting, or cytologic atypia. Based on these features as well as the clinical and dermoscopic findings, a diagnosis of an inflamed seborrheic keratosis (SK) was made. No further treatment was required following the shave biopsy, and the patient was reassured regarding the benign nature of the lesion.

Seborrheic keratoses are benign epidermal growths that can manifest on any area of the skin except the palms and soles. They present clinically as tan, yellow, gray, brown, or black with a smooth, waxy, or verrucous surface. They range from 1 mm to several centimeters in diameter. Although SKs traditionally manifest more frequently in individuals with lighter skin tones, pigmented variants, such as dermatosis papulosa nigra, have been reported to occur more commonly and at younger ages in patients with skin of color.¹

Dermoscopy of SK in patients with skin of color can present diagnostic challenges, as these lesions may display atypical pigmented patterns that overlap with melanocytic lesions, including Spitz nevi, particularly when starburstlike or globular structures are present.² What sets inflamed SKs apart from other SKs is the lack of a heavily keratinized surface on both clinical and dermoscopic evaluation. Common histopathologic diagnostic criteria for Spitz nevi include Kamino bodies, uniform nuclear enlargement, and spindled or epithelioid nevus cells, which were not noted in our patient.³ Therefore, in presentations such as this, histopathology remains the gold standard for diagnosis.

The differential diagnosis in this case included benign nevus, dysplastic nevus, melanoma, and Spitz nevus. Benign nevi typically demonstrate uniform pigmentation and symmetric dermoscopic patterns. Dysplastic nevi may show architectural disorder and cytologic atypia but lack invasive features.³ Melanoma often exhibits asymmetry, atypical network patterns, and irregular pigmentation.⁴ Spitz nevi characteristically demonstrate large epithelioid or spindle cells with Kamino bodies on histopathology, which were absent in our patient.

THE DIAGNOSIS: Seborrheic Keratosis

Histopathology revealed epidermal hyperplasia and hyperkeratosis with no notation of atypical melanocytic activity (Figure). There were no Kamino bodies, junctional nesting, or cytologic atypia. Based on these features as well as the clinical and dermoscopic findings, a diagnosis of an inflamed seborrheic keratosis (SK) was made. No further treatment was required following the shave biopsy, and the patient was reassured regarding the benign nature of the lesion.

Seborrheic keratoses are benign epidermal growths that can manifest on any area of the skin except the palms and soles. They present clinically as tan, yellow, gray, brown, or black with a smooth, waxy, or verrucous surface. They range from 1 mm to several centimeters in diameter. Although SKs traditionally manifest more frequently in individuals with lighter skin tones, pigmented variants, such as dermatosis papulosa nigra, have been reported to occur more commonly and at younger ages in patients with skin of color.¹

Dermoscopy of SK in patients with skin of color can present diagnostic challenges, as these lesions may display atypical pigmented patterns that overlap with melanocytic lesions, including Spitz nevi, particularly when starburstlike or globular structures are present.² What sets inflamed SKs apart from other SKs is the lack of a heavily keratinized surface on both clinical and dermoscopic evaluation. Common histopathologic diagnostic criteria for Spitz nevi include Kamino bodies, uniform nuclear enlargement, and spindled or epithelioid nevus cells, which were not noted in our patient.³ Therefore, in presentations such as this, histopathology remains the gold standard for diagnosis.

The differential diagnosis in this case included benign nevus, dysplastic nevus, melanoma, and Spitz nevus. Benign nevi typically demonstrate uniform pigmentation and symmetric dermoscopic patterns. Dysplastic nevi may show architectural disorder and cytologic atypia but lack invasive features.³ Melanoma often exhibits asymmetry, atypical network patterns, and irregular pigmentation.⁴ Spitz nevi characteristically demonstrate large epithelioid or spindle cells with Kamino bodies on histopathology, which were absent in our patient.

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.