Hepatic steatosis in HIV/HCV co-infected patients: Correlates, efficacy and outcomes of anti-HCV therapy: A paired liver biopsy study☆
Background/Aims
Hepatic steatosis is caused by the complex interaction of host and viral factors, such as metabolic syndrome (MS), alcoholism and HCV genotype, and in HIV–HCV co-infected patients, antiretroviral therapy may also play a role. A large population of patients from the AIDS Pegasys Ribavirin International Co-infection Trial (APRICOT) had paired liver biopsies interpreted and graded for steatosis along with lipid measurements and anthropometric data.
Methods
We analyzed these patients to determine the prevalence of steatosis, baseline factors associated with steatosis, effect of steatosis in HCV therapy efficacy and the impact of anti-HCV treatment on steatosis.
Results
A total of 65/283 (23%) patients with paired biopsies were positive for steatosis. Patients with steatosis were significantly more likely to have HCV genotype 3, bridging fibrosis/cirrhosis, higher HCV RNA levels, increased triglycerides and lower cholesterol levels. The only different body measurement was neck circumference which was greater in patients with steatosis and significantly decreased from baseline during the study. Hip circumference was predictive of steatosis at baseline.
Conclusions
Factors associated to the metabolic syndrome are important in co-infected patients. Treatment outcome affected steatosis in that viral eradication reduced steatosis in genotype 3 patients, but altogether steatosis did not affect efficacy of treatment in any genotype.
Abbreviations: HCV, hepatitis C virus, HIV, human immunodeficiency virus, BMI, body mass index, ART, antiretroviral therapy, Peg-IFN, pegylated interferon, SVR, sustained virological response, HAI, histological activity index, ITT, intent-to-treat
Keywords: HCV/HIV, Steatosis, Efficacy of therapy
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☆ The authors who have taken part in the research of this paper declared that they have a relationship with the manufacturers of the drug involved and Dr. J. DePamphilis is employed by Roche Nutley, NJ, USA. They received funding from Roche for the conduct of the original APRICOT trial. This study was supported by a grant from Roche, Basel, Switzerland. Roche provided statistical analysis and initial editorial assistance for the preparation of this manuscript.
PII: S0168-8278(08)00066-4
doi:10.1016/j.jhep.2008.01.015
© 2008 European Association for the Study of the Liver. Published by Elsevier Inc. All rights reserved.
