PubMed · 1760267
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1991-11-29. Update on AIDS.. https://pubmed.ncbi.nlm.nih.gov/1760267/
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Post-kala-azar dermal leishmaniasis (PKDL) is rarely reported in South America. In spite of the fact that there are many reports about the association of visceral leishmaniasis and AIDS, PKDL is very uncommon in HIV-positive patients, and so far only four cases have been documented in the literature. We present another case with unusual clinicopathological aspects. The patient, a 28-year-old male, from Salvador, Bahia (an endemic area) presented with clinical manifestations of visceral leishmaniasis three years after the diagnosis of AIDS. During treatment for visceral leishmaniasis he developed disseminated miliary papules. Microscopically, the skin biopsy showed a "saw-tooth" pattern with a lichenoid mononuclear infiltrate simulating lichen planus. The histopathological diagnosis was achieved through the finding of amastigotes. The authors discuss the clinicopathological aspects of this case based on a review of the specific literature.
The functional and phenotypic maturation of myeloid dendritic cells (DCs), circulating and monocyte-derived, from subjects at different stages of HIV-1 infection was evaluated. The results showed that the capacity of circulating DCs was significantly impaired in subjects with CD4+ T cell counts of <200/microL, correlated with the potential of CD40 ligand expression on CD4+ T cells (R = 0.84; P = 0.002), and improved with successful antiretroviral therapy. However, the function and phenotype of monocyte-derived DCs generated by in vitro culture from subjects at any stage of HIV-1 infection were similar to those in uninfected healthy subjects. Our findings suggest that although the potential of myeloid DC precursors to achieve full maturation is preserved in subjects with late-stage HIV-1 infection, in vivo maturation of myeloid DCs was impaired in these subjects, which may be due to decreased potential of CD40 ligand expression on CD4+ T cells. That myeloid DCs fail to achieve full maturation in vivo in late-stage HIV-1 infection may contribute to the failure to induce effective cellular immunity against HIV-1 and opportunistic pathogens.