Hepatic steatosis in patients with HIV-Hepatitis C virus coinfection: is it associated with antiretroviral therapy and more advanced hepactic fibrosis?

Verma, Sumita, Goldin, Robert D and Main, Janice (2008) Hepatic steatosis in patients with HIV-Hepatitis C virus coinfection: is it associated with antiretroviral therapy and more advanced hepactic fibrosis? BMC Research Notes, 1 (1). pp. 46-53. ISSN 1756-0500

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Abstract

Background and aims: Patients with HIV and hepatitis C virus (HCV) coinfection are at increased risk of developing hepatic steatosis. The aims of this study were to assess the prevalence of steatosis in a cohort with HIV-HCV coinfection, and to determine an association, if any, between steatosis, antiretroviral therapy (ART), and advanced hepatic fibrosis. Patients and methods: HIV-HCV coinfected patients were retrospectively identified from the HIV clinic. ART was classified as none, nucleoside reverse transcriptase inhibitors (NRTIs) only, highly active antiretroviral therapy (HAART) only, and sequential therapy (initial NRTIs followed by HAART). Fibrosis stage and necroinflammation grade were assessed by the modified HAI (Ishak) scoring method. Steatosis was graded as 0–3. Results: Sixty patients were identified. The overall prevalence of hepatic steatosis was 58%. Those that received HAART only had a lower prevalence of steatosis (41%) compared to those on NRTIs only (70%) or sequential therapy (82%). Independent predictors of hepatic steatosis were absence of HAART only therapy, OR 2.9, p = 0.09, and presence of cirrhosis, OR 4.6, p = 0.044. Forty five percent of the patients had advanced fibrosis (fibrosis stage ≥ 3). NI grade (OR 1.9, p = 0.030), and steatosis grade (OR 3.6, p = 0.045), were independent predictors of advanced fibrosis. Conclusion: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population. HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis. This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.

Item Type: Article
Schools and Departments: Brighton and Sussex Medical School > Clinical and Experimental Medicine
Subjects: R Medicine > RC Internal medicine > RC0109 Infectious and parasitic diseases
Depositing User: Ellen Thomas
Date Deposited: 31 Oct 2012 11:39
Last Modified: 29 Oct 2019 09:45
URI: http://sro.sussex.ac.uk/id/eprint/40374

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