antimony-sodium-gluconate has been researched along with Opportunistic-Infections* in 2 studies
2 other study(ies) available for antimony-sodium-gluconate and Opportunistic-Infections
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Tinea versicolor and visceral leishmaniasis.
Visceral leishmaniasis (VL) is endemic in several areas in the Sudan. The disease is associated with depressed cellular immunity. Tinea versicolor is a normal commensal of the skin which can become pathogenic particularly in patients with depressed cell-mediated immunity. Patients with VL have a high prevalence of tinea versicolor.. One hundred and thirty patients with parasitologic confirmation of VL were screened for tinea versicolor infection. In the suspected cases the diagnosis was made by demonstrating the fungal hyphae and spores in skin scrapings. All patients were treated with sodium stibogluconate.. Of the 130 patients with VL, 10.8% were found to have severe tinea versicolor. The fungal infection developed or became worse with the start of VL. After successful treatment of VL, the tinea lesions disappeared completely or decreased in severity.. Depressed cell-mediated immunity that is a feature of VL is the probable underlying cause for fungal infection. Tinea infection during the course of VL is to be distinguished from lesions of post-kala-azar dermal leishmaniasis. Topics: Adolescent; Adult; Antimony Sodium Gluconate; Child; Diagnosis, Differential; Facial Dermatoses; Female; Follow-Up Studies; Humans; Leishmaniasis, Cutaneous; Leishmaniasis, Visceral; Male; Opportunistic Infections; Remission Induction; Sudan; Time Factors; Tinea Versicolor | 1994 |
Visceral leishmaniasis in an HIV-infected patient: clinical features and response to treatment.
We report the case of 43-year-old homosexual patient with HIV infection and a history of travel to the Far East in whom visceral leishmaniasis was the first infectious complication. Symptoms were fever, malaise, weight loss, hepatosplenomegaly, generalized lymphadenopathy, and oral thrush. Laboratory abnormalities included a slight elevation of liver enzymes, impairment of liver function tests, leukocytopenia, anemia, hypergammaglobulinemia, and markedly depressed CD4(+)-cell counts. Despite initially successful treatment with pentavalent antimony, a relapse of leishmaniasis occurred after 7 months. Eradication of the infection was not achieved. Treatment was continued as a palliative chronic suppressive treatment with fortnightly pentamidine infusions. The clinical course was complicated by legionella pneumonia and the development of rapidly progressing Kaposi's sarcoma. The case is presented in detail, and the influence of HIV infection on the course of leishmaniasis is discussed. Topics: Adult; AIDS Serodiagnosis; Antimony Sodium Gluconate; CD4-CD8 Ratio; HIV Infections; HIV-1; Humans; Leishmaniasis, Visceral; Leukocyte Count; Macrophages; Male; Opportunistic Infections; Pentamidine | 1991 |