Maida, Ivana Rita and Babudieri, Sergio and Selva, Cinzia and D'Offizi, Gianpiero and Fenu, Luisa and Solinas, Maria Giuliana and Narciso, Pasqualino and Mura, Maria Stella Anna and Núñez, Marina (2006) Liver enzyme elevation in hepatitis C virus (HCV)-HIV-coinfected patients prior to and after initiating HAART: role of HCV genotypes. Aids Research and Human Retroviruses, Vol. 22 (2), p. 139-143. eISSN 1931-8405. Article.
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Transaminase elevation is frequently seen in hepatitis C virus (HCV)–HIV-coinfected patients receiving antiretroviral therapy (ART), representing an increase in the immune response against HCV and being one of the mechanisms proposed to be involved. There is a report claiming that HCV genotype 3 is an independent risk factor. Our objectives were to assess the incidence of liver toxicity in an HIV–HCV-coinfected population with relatively preserved cellular immunity, and the role of HCV genotypes in the elevation of liver enzymes, both at baseline and after initiating ART. All HIV+ patients with positive anti-HCV serology and CD4+ cell counts above 100/mm3 who began triple ART were identified, and their HCV-RNA levels and HCV genotype were determined. Liver enzymes were determined at baseline and bimonthly during follow-up. Of anti-HCV patients 147 were included, 128 (87.1%) of whom had detectable plasma HCV-RNA. HCV-1 and HCV-4 genotypes were found to confer an increased probability of having at baseline transaminases within normal limits over the other genotypes. Severe transaminase elevations (grades 3 and 4) occurred in 5/124 patients (4.0%), all with high pre-HAART ALT and positive HCV-RNA levels. Multivariate analysis showed that patients with genotype HCV-3 had a 3.27 times higher risk of developing HAART-related transaminase elevations of any grade. In conclusion, subjects with the HCV-1 genotype more often had transaminases within normal limits at baseline. The incidence of severe transaminase elevation after initiating ART was very low (4%) in this HIV+ population with relatively preserved cellular immunity. HCV genotype 3 was identified as a risk factor for the development of transaminase elevation of any grade.
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