January 3, 2012

Influence of interferon-based therapy on liver fibrosis progression in HIV/HCV coinfected patients: A retrospective repeated liver biopsy analysis

Journal of Hepatology
Volume 56, Issue 1 , Pages 49-54, January 2012

Patrick Ingiliz, Marc-Antoine Valantin, Paul Preziosi, Laetitia Finzi, Raluka Pais, Larysa Fedchuk, Stéphanie Dominguez, Christine Katlama, Thierry Poynard, Yves Benhamou

Received 1 October 2010; received in revised form 26 May 2011; accepted 31 May 2011. published online 20 July 2011.

Abstract

Background & Aims

Hepatitis C virus (HCV) coinfection is one of the leading causes of mortality in human immunodeficiency virus-infected patients. The current standard of care leads to cure only in a part of these patients. The course of the disease is determined by the rapidity of liver fibrosis progression (LFP). The influence of interferon on LFP in coinfected patients has yet not been evaluated by comparative liver biopsies.

Methods

We extracted data of patients who had serial liver biopsies from a hospital database. Histopathological findings were compared to factors possibly linked to fibrosis progression. Furthermore, we studied the impact of response to interferon treatment on fibrosis progression.

Results

Hundred and twenty-six patients were included, 68 had received anti-HCV treatment, and 58 had not. The median time between the first and the last biopsy was 4years. Worsened fibrosis was observed in 35 of 58 (60%) untreated patients, and 22 of 50 (44%) patients in the nonresponder/relapser group, and in 5 out of 18 (28%) in the SVR group. Liver fibrosis evolution was significantly better in patients achieving a SVR than in untreated and NR/R patients (p<0.02, odds-ratio [95% CI] for improvement vs. stability vs. worsening=3.16 [1.24–8.07]). This result persisted after adjustment for known predictors of liver fibrosis progression, HBsAg, CD4, and alcohol consumption: adjusted odds ratio=2.89 [1.09–7.68], p=0.03.

Conclusions

HCV treatment can stop fibrosis progression and induce its regression. Nonresponders to treatment may even have a fast fibrosis progression. It remains to be clarified if the same factors that induce nonresponse to treatment may also induce faster fibrosis progression.

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