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Despite numerous drug interactions that occur with human immunodeficiency virus-1 protease inhibitors, there are relatively few drug reactions. We present two patients receiving saquinavir who developed fixed drug reactions. Both reactions cleared while patients received a therapeutic dose of the medication, and in one patient a flare was seen when the patient later stopped and then restarted the medication. Although fixed drug reactions are relatively inconsequential, it is important to know that these eruptions may clear when the patient is given uninterrupted therapy of a human immunodeficiency virus-1 protease inhibitor, with only post-inflammatory hyperpigmentation.

Organisms with little pathogenic potential in immunocompetent hosts may produce disease in HIV-1 + patients. We describe three HIV-1 + patients in late disease who presented with pruritic papules with central ulceration over the face and arms. In all the patients the eruptions had been present for months, and the patients did not develop sepsis. Biopsy specimens in all the patients showed large Gram-positive cocci, forming tetrads. Colony morphology, catalase positivity and coagulase negativity, and resistance to nitrofurantoin were used to separate micrococci from staphylococci. Micrococcus species are usually considered normal inhabitants of the skin; however, in patients with HIV-1 disease, Micrococcus species can produce localized cutaneous infections.

CD30 is a member of the tumour necrosis factor/nerve growth factor receptor superfamily, which is expressed on CD4+ and CD8+ T-cell clones which produce T helper (Th) 2-type cytokines. It has been proposed that disease progression in HIV-1 is associated with Th1 to Th2 cytokine switching. In 70 cutaneous biopsies from HIV-1 positive patients in different stages of disease, we performed a battery of immunohistochemical stains. These included antibodies to CD3, UCHL-1, OPD-4, L-26, KP-1 and CD30 (Ki-1). In addition, we used a similar battery of stains on cutaneous biopsies of HIV-1 negative patients with inflammatory dermatoses which are established as Th1 or Th2 dominant, e.g. polar leprosy. CD30+ cells were rarely present in early stages of HIV-1 disease, but commonly present in later stages of disease. However, there were cases of late HIV-1 disease which did not contain CD30+ cells. Increased numbers of CD30+ cells were more commonly seen in later stages of HIV-1 disease. However, the expression of CD30 appeared to be better in predicting other established Th2 cutaneous infiltrates in HIV-1 negative patients than in predicting a Th2 cutaneous cytokine pattern in advanced HIV-1 disease.

Background: One important factor in understanding the pathogenesis of human immune deficiency virus (HIV) disease is documenting the patterns of immune dysregulation present in HIV-positive patients. The cells which home to skin are mainly certain subsets of T cells and, as opposed to the peripheral blood, where circulating factors may inhibit terminal phenotypic differentiation, the cutaneous environment potentiates differentiation during cutaneous eruptions., Objective: The authors' aim was to characterize the inflammatory dermatoses in biopsy specimens from HIV-positive patients with immunohistochemical stains for lymphoid markers, activation markers, and adhesion molecules and to determine if there was any correlation with the type of dermatosis and the HIV-disease stage., Methods: Lymphoid and activation markers as well as adhesion molecules were studied on cutaneous biopsy specimens from 96 inflammatory dermatoses in HIV-positive patients. The dermatoses included psoriasiform dermatoses with and without a lichenoid component, perivascular lymphoid dermatoses, perivascular and periadnexal inflammatory dermatoses, spongiotic dermatoses, granulomatous dermatoses, and neutrophilic dermatoses with and without vasculitis., Results: Although there was a decrease in CD4/CD8 ratios in the cutaneous inflammatory dermatoses with progression of the disease, the ratios of CD4/CD8 cells were far higher than those in the peripheral blood. There were also increasing numbers of CD23+ cells and increased E-Selectin expression on endothelial cells from the early stages of disease, with no consistent pattern of ICAM-1 expression on epithelial cells with disease progression., Conclusions: The expression of lymphoid markers, activation markers, and adhesion molecules in the skin with progression of HIV disease, is consistent with a T helper (Th)1 to Th0/Th2 cytokine pattern of immune dysregulation. This cytokine pattern may be modified by the cytopathic effects of HIV on lymphoid and dendritic populations and by effects of other concurrent infections. Significant numbers of CD4+ T cells in skin infiltrates, with low peripheral CD4 T-cell counts, suggest that the cutaneous T-cell populations may be distinctive.

Xanthomas may be associated with benign or malignant lymphoproliferative diseases, often with associated hypergammaglobulinema. In human immunodeficiency virus type 1 (HIV-1) disease, there is a high lymphoproliferative rate despite the immunodeficiency and increased cell death. We report three HIV-1-positive patients with facial papular xanthomatosis eruptions associated with hypergammaglobulinema, and an immunoglobulin A (IgA) gammopathy. Histopathologic features include lipid-laden macrophages, extracellular nuclear dust with phagocytosized nuclear debris, and hyalinization with areas of hyaline necrosis of collagen fibers. These distinctive papular xanthomas may be a marker of HIV-1 disease and of a pattern of immunodysregulation, immunodeficiency, and lymphoid proliferation seen in HIV-1 disease.

Background: Pruritus in HIV-1+ patients is common and increases with disease progression. The causes of pruritus are numerous including xerosis, drug and photoeruptions, follicular and papular eruptions as well as infestations and infections by a wide range of organisms. One other possible factor contributing to pruritus is the pattern of immune dysregulation. With advancing HIV-1 disease there is Th1 to Th2 cytokine switching., Methods: After some positive results with prostaglandin inhibitors, we undertook a study in which we randomly placed patients on four different forms of therapy for their pruritus. The therapies included hydroxyzine with or without doxepin at night, pentoxifylline, indomethacin and topical moisturization with medium-strength topical steroids. All patients were evaluated for both subjective relief as well as side effects., Results: Patients placed on indomethacin obtained relief more consistently and more completely. Patients on pentoxifylline had the fewest side effects of all oral therapies. Patients on antihistamines with or without doxepin had the highest incidence of side effects, although more of these patients reported a greater degree of relief than patients on pentoxifylline. All patients on oral therapy overall had greater relief than patients using topical steroids., Conclusion: The systemic therapies which may modulate the pattern of immune dysregulation seen in HIV-1 disease may be beneficial in the pruritus seen in late-stage patients.