Antiretrovirals
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Post-kala-azar dermal leishmaniasis as an immune reconstitution syndrome: case report A 46-year-old man with AIDS developed post-kala-azar dermal leishmaniasis (PKDL) as an immune reconstitution syndrome during treatment with antiretrovirals [dosages, durations of therapies to reaction onset not stated]. The man was diagnosed with HIV infection in 1986 and started receiving zidovudine. In September 1996, he received zidovudine, lamivudine and indinavir. From 1996 to July 2005, he received multiple antiretroviral regimens including stavudine, nevirapine, nelfinavir, ritonavir, amprenavir, efavirenz and tenofovir* . He was diagnosed with cutaneous Kaposi sarcoma in March 2000. He started receiving didanosine, ritonavir-boosted fosamprenavir, tenofovir and L-870812 or placebo and, in July 2005, he presented with right cervical adenopathy and two papular lesions on his face. Laboratory investigations revealed the following: haemoglobin 9.4 g/dL, platelet count 109 × 103 /µL and a WBC count of 2.140 × 103 /µL, CD4 cell count 71 /µL and viral load 73 200 copies/mL. Physical examination revealed two papular erythematous lesions on his face, and two violaceous lesions, suggestive of Kaposi sarcoma, on his left arm. Biopsies of his facial lesions, a cervical lymph node and bone marrow revealed Leishmania amastigotes. PCR for Leishmania DNA was positive in his peripheral blood, bone marrow aspirate and skin lesion. Molecular typing was consistent with a L. infantum infection. He was diagnosed with Mediterranean visceral leishmaniasis (MVL). The man received IV liposomal amphotericin B with a rapid response. After 2 months, he experienced a relapse of MVL and liposomal amphotericin B was reinitiated. His clinical condition improved. However, throughout the observation period, Leishmania DNAemia was present. Five months after primary MVL diagnosis, he received pentamidine with rapid clearance of Leishmania DNA from peripheral blood. In January 2006, he developed a maculopapular rash on his face, trunk, arms and legs, and monolateral anterior uveitis; his CD4 cell count was 321 /µL and plasma HIV-RNA was undetectable. A high parasite burden in his cutaneous lesions was revealed by histological examination. His aqueous humor was also positive by PCR. A diagnosis of PKDL was made and he received pentamidine. His skin lesions progressively flattened and discoloured with mild persistence of his uveitis and therefore, in March 2006, he received milefosine. At last follow-up (August 2006), his skin lesions and uveitis had completely resolved and regular Leishmania DNA PCR tests on peripheral blood were negative. * It is not clear whether he received tenofovir or tenofovir disoproxil fumarate. Antinori S, et al. Post-kala-azar dermal leishmaniasis as an immune recontitution inflammatory syndrome in a patient with acquired immune deficiency syndrome. British Journal of Dermatology 157: 1032-1036, No. 5, Nov 2007 801091665 Italy
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