Dr. Donna Bilu Martin

Diagnosis: Kaposi’s sarcoma

Kaposi's sarcoma is a vascular neoplasm with four principal clinical variants: HIV/AIDS-related Kaposi's sarcoma, classic Kaposi's sarcoma, African endemic Kaposi's sarcoma, and immunosuppression-associated Kaposi's sarcoma. The etiologic agent in all clinical variants is human herpes virus type 8 (HHV-8). HIV/AIDS-related Kaposi's sarcoma is primarily seen in men who have sex with men.

The four variants of Kaposi's sarcoma can have different clinical presentations. In HIV/AIDS-associated Kaposi's sarcoma, patients may present with a single lesion or with symmetric widespread lesions. Clinically, the lesions can range from faint erythematous macules, to small violaceous papules, to large plaques or ulcerated nodules. The lesions are generally asymptomatic.

Any mucocutaneous surface can be involved. Common body locations include the face (especially the nose), hard palate, trunk, penis, lower legs, and soles. The most common areas of internal involvement are the gastrointestinal system and lymphatics. Histologically, atypical, angular vessels with an associated inflammatory infiltrate containing plasma cells appear in the upper dermis in macular lesions. Nodules and tumors reveal a spindle cell neoplasm pattern. Lesions stain positive for human herpes virus 8 (HHV-8).

Since the introduction of highly active antiretroviral therapy (HAART), the incidence of Kaposi's sarcoma has greatly decreased. HAART is the most effective treatment method, and should be the initial therapy in most patients with mild to moderate disease.

However, some patients with HIV/AIDS-associated Kaposi's sarcoma require further treatment - those who have well-controlled HIV and undetectable viral loads. Other treatments include local destruction (cryotherapy), topical alitretinoin (9-cis-retinoic acid), intralesional interferon or vinblastine, superficial radiotherapy, liposomal doxorubicin, daunorubicin, or paclitaxel.

Diagnosis: Kaposi’s sarcoma

Kaposi's sarcoma is a vascular neoplasm with four principal clinical variants: HIV/AIDS-related Kaposi's sarcoma, classic Kaposi's sarcoma, African endemic Kaposi's sarcoma, and immunosuppression-associated Kaposi's sarcoma. The etiologic agent in all clinical variants is human herpes virus type 8 (HHV-8). HIV/AIDS-related Kaposi's sarcoma is primarily seen in men who have sex with men.

The four variants of Kaposi's sarcoma can have different clinical presentations. In HIV/AIDS-associated Kaposi's sarcoma, patients may present with a single lesion or with symmetric widespread lesions. Clinically, the lesions can range from faint erythematous macules, to small violaceous papules, to large plaques or ulcerated nodules. The lesions are generally asymptomatic.

Any mucocutaneous surface can be involved. Common body locations include the face (especially the nose), hard palate, trunk, penis, lower legs, and soles. The most common areas of internal involvement are the gastrointestinal system and lymphatics. Histologically, atypical, angular vessels with an associated inflammatory infiltrate containing plasma cells appear in the upper dermis in macular lesions. Nodules and tumors reveal a spindle cell neoplasm pattern. Lesions stain positive for human herpes virus 8 (HHV-8).

Since the introduction of highly active antiretroviral therapy (HAART), the incidence of Kaposi's sarcoma has greatly decreased. HAART is the most effective treatment method, and should be the initial therapy in most patients with mild to moderate disease.

However, some patients with HIV/AIDS-associated Kaposi's sarcoma require further treatment - those who have well-controlled HIV and undetectable viral loads. Other treatments include local destruction (cryotherapy), topical alitretinoin (9-cis-retinoic acid), intralesional interferon or vinblastine, superficial radiotherapy, liposomal doxorubicin, daunorubicin, or paclitaxel.

Diagnosis: Kaposi’s sarcoma

Kaposi's sarcoma is a vascular neoplasm with four principal clinical variants: HIV/AIDS-related Kaposi's sarcoma, classic Kaposi's sarcoma, African endemic Kaposi's sarcoma, and immunosuppression-associated Kaposi's sarcoma. The etiologic agent in all clinical variants is human herpes virus type 8 (HHV-8). HIV/AIDS-related Kaposi's sarcoma is primarily seen in men who have sex with men.

The four variants of Kaposi's sarcoma can have different clinical presentations. In HIV/AIDS-associated Kaposi's sarcoma, patients may present with a single lesion or with symmetric widespread lesions. Clinically, the lesions can range from faint erythematous macules, to small violaceous papules, to large plaques or ulcerated nodules. The lesions are generally asymptomatic.

Any mucocutaneous surface can be involved. Common body locations include the face (especially the nose), hard palate, trunk, penis, lower legs, and soles. The most common areas of internal involvement are the gastrointestinal system and lymphatics. Histologically, atypical, angular vessels with an associated inflammatory infiltrate containing plasma cells appear in the upper dermis in macular lesions. Nodules and tumors reveal a spindle cell neoplasm pattern. Lesions stain positive for human herpes virus 8 (HHV-8).

Since the introduction of highly active antiretroviral therapy (HAART), the incidence of Kaposi's sarcoma has greatly decreased. HAART is the most effective treatment method, and should be the initial therapy in most patients with mild to moderate disease.

However, some patients with HIV/AIDS-associated Kaposi's sarcoma require further treatment - those who have well-controlled HIV and undetectable viral loads. Other treatments include local destruction (cryotherapy), topical alitretinoin (9-cis-retinoic acid), intralesional interferon or vinblastine, superficial radiotherapy, liposomal doxorubicin, daunorubicin, or paclitaxel.

Diagnosis: Granuloma annulare

Granuloma annulare (GA) is a self-limited cutaneous disorder predominantly seen in women that affects children and adults. The cause is unknown. Inciting factors can include herpes zoster infection, sun exposure, medications, and trauma.

Several clinical variants exist. Localized GA is the most common form, often presenting in the first three decades of life as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. Generalized GA accounts for 15% of reported cases and presents in the fourth to seventh decades of life as multiple asymptomatic or pruritic skin-colored or erythematous papules and plaques on the trunk and extremities. Subcutaneous GA is more common in children and presents as multiple painless nodules on the scalp or extremities. Patch GA can be localized or generalized. Perforating GA presents as asymptomatic erythematous papules that evolve into yellow, umbilicated papules with a clear-to-white discharge.

Histopathologically, an interstitial or palisading pattern is seen with a dermal lymphohistiocytic infiltrate, degenerated collagen, and mucin deposition (visualized with alcian blue or colloidal iron stains). The interstitial pattern presents in the majority of cases.

Diagnosis of GA is predominantly clinically based. When the diagnosis is questionable or the presentation is atypical, biopsy is useful. Granuloma annulare is often self-limiting and resolves within 2 years, although recurrence is possible. First-line therapy for localized GA includes high-potency topical corticosteroids or intralesional corticosteroids. Other treatments include cryotherapy, phototherapy, and topical tacrolimus. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, hydroxychloroquine, isotretinion, and dapsone also have been reported as treatments in the literature.

Diagnosis: Granuloma annulare

Granuloma annulare (GA) is a self-limited cutaneous disorder predominantly seen in women that affects children and adults. The cause is unknown. Inciting factors can include herpes zoster infection, sun exposure, medications, and trauma.

Several clinical variants exist. Localized GA is the most common form, often presenting in the first three decades of life as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. Generalized GA accounts for 15% of reported cases and presents in the fourth to seventh decades of life as multiple asymptomatic or pruritic skin-colored or erythematous papules and plaques on the trunk and extremities. Subcutaneous GA is more common in children and presents as multiple painless nodules on the scalp or extremities. Patch GA can be localized or generalized. Perforating GA presents as asymptomatic erythematous papules that evolve into yellow, umbilicated papules with a clear-to-white discharge.

Histopathologically, an interstitial or palisading pattern is seen with a dermal lymphohistiocytic infiltrate, degenerated collagen, and mucin deposition (visualized with alcian blue or colloidal iron stains). The interstitial pattern presents in the majority of cases.

Diagnosis of GA is predominantly clinically based. When the diagnosis is questionable or the presentation is atypical, biopsy is useful. Granuloma annulare is often self-limiting and resolves within 2 years, although recurrence is possible. First-line therapy for localized GA includes high-potency topical corticosteroids or intralesional corticosteroids. Other treatments include cryotherapy, phototherapy, and topical tacrolimus. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, hydroxychloroquine, isotretinion, and dapsone also have been reported as treatments in the literature.

Diagnosis: Granuloma annulare

Granuloma annulare (GA) is a self-limited cutaneous disorder predominantly seen in women that affects children and adults. The cause is unknown. Inciting factors can include herpes zoster infection, sun exposure, medications, and trauma.

Several clinical variants exist. Localized GA is the most common form, often presenting in the first three decades of life as an asymptomatic, erythematous, annular plaque with a firm border and central clearing localized to the wrists, ankles, and dorsal hands or feet. Generalized GA accounts for 15% of reported cases and presents in the fourth to seventh decades of life as multiple asymptomatic or pruritic skin-colored or erythematous papules and plaques on the trunk and extremities. Subcutaneous GA is more common in children and presents as multiple painless nodules on the scalp or extremities. Patch GA can be localized or generalized. Perforating GA presents as asymptomatic erythematous papules that evolve into yellow, umbilicated papules with a clear-to-white discharge.

Histopathologically, an interstitial or palisading pattern is seen with a dermal lymphohistiocytic infiltrate, degenerated collagen, and mucin deposition (visualized with alcian blue or colloidal iron stains). The interstitial pattern presents in the majority of cases.

Diagnosis of GA is predominantly clinically based. When the diagnosis is questionable or the presentation is atypical, biopsy is useful. Granuloma annulare is often self-limiting and resolves within 2 years, although recurrence is possible. First-line therapy for localized GA includes high-potency topical corticosteroids or intralesional corticosteroids. Other treatments include cryotherapy, phototherapy, and topical tacrolimus. For generalized GA, topical or intralesional corticosteroids may be used for select lesions. Topical calcineurin inhibitors, light therapy, hydroxychloroquine, isotretinion, and dapsone also have been reported as treatments in the literature.