Pruritic Papular Eruption Associated with HIV‐Etiopathogenesis Evaluated by Clinical, Immunohistochemical, and Ultrastructural Analysis

Abstract

Pruritic Papular Eruption with Human Immunodeficiency Virus infection (PPE-HIV) is characterized by symmetrically distributed papules with pruritus in the skin of patients suffering advanced HIV infection. Although known since 1985, the etiology of this symptomatic dermatitis is unclear. We set out to characterize the phenotype of the infiltrating cells and the cytokine profile in the lesions, as an attempt to contribute to determining its etiopathogenesis. Clinical data and histological, immunohistochemical, and ultrastructural features of skin biopsies from 20 HIV patients with PPE were studied. The histopathological aspects, cell immunophenotypes, and cytokine expressions in the lesions where quantified and compared to perilesional skin, and to those in the clinically normal skin of HIV patients without PPE-HIV (n=11) and those in normal skin samples from HIV negative individuals (n=10). PPE-HIV occurred mainly in HIV patients with mean CD4+ counts of 124.6 +/- 104 lymphocytes/mm3. Furthermore, their eosinophil counts were significantly increased. The skin lesions were characterized by a predominantly perivascular dermal lymphohistiocytic inflammatory infiltrate. Langerhans cells were normally distributed in the epidermis and seen among the cellular components of dermal infiltrates. The density of CD8+ lymphocytes was elevated and the density of CD4+ cells was reduced in dermal infiltrates. Interleukin 5 was the predominant cytokine in the lesions. Electron microscopic analysis didn't disclose HIV or other infectious agents in the lesions. These results refute the hypothesis of an infectious etiology of PPE-HIV. CD8+ lymphocytes and Langerhans cells seem to have roles in the pathogenesis of PPE-HIV. The increased frequency of IL5 was associated with abundant eosinophils in the lesions, suggesting a type Th2 response in this dermatitis.