Abstract

BackgroundHIV infection leads to a faster progression of liver disease in subjects infected with HCV, as compared with HCV mono-infected patients. Previous reports suggest that sustained virological response (SVR) rates are lower in HIV/HCV coinfection than in HCV monoinfection. We aimed to compare SVR rates of these two populations.MethodsWe retrospectively analyzed clinical, biochemical and virological data of HCV and HIV/HCV infected patients with HCV genotypes 2 and 3 who started anti-HCV treatment between March 2004 and November 2012, at a single large center. Intention-to-treat (ITT) and per-protocol (PP) analysis were performed. Univariate and multivariate logistic regression analyses were performed to assess predictors of SVR.Results461 patients were analyzed: 307 (66.6%) males, 76 (16.5%) infected with HIV. Several differences at baseline between HCV monoinfected and HIV/HCV coinfected patients were observed. HCV monoinfected group was characterized by higher prevalence of genotype 2 (53% vs 5.3%), higher baseline HCV viral load (50% vs 35%), shorter mean duration of treatment (19 vs 41 weeks), more frequent use of peginterferon alfa-2a (84.5% vs 69.7%), lower prevalence of cirrhosis (6% vs 31.6%). Globally, SVR was achieved by 353 (76.6%) patients and 321 (83.8%) in the PP analysis. No statistically relevant differences were found in SVR rates between the two groups, either in ITT [78.2% (n = 301/385) vs 68.4% (n = 52/76), p =0.066, respectively] than in PP analysis [83.6% (n = 276/330) vs 84.9% (n = 45/53), p = 0.8].ITT analysisAt univariate and multivariate analysis, baseline HCV-RNA >500.000 IU/ml [OR 0.4 (0.24-0.66), p = 0.0004], use of peginterferon alfa-2b [OR 0.5 (0.27-0.93) p = 0.033], platelets count <130.000/mm3 [OR 0.45 (0.2-0.99), p = 0.045], interruption of peginterferon therapy [OR 0.2 (0.1-0.4), p<0.0001], interruption of ribavirin treatment [OR 0.34 (0.17-0.69), p = 0.0026] were related with lower rate of SVR.PP analysisOnly HCV-RNA >500.000 IU/ml and interruption of ribavirin were related to lower probability to achieve SVR at both univariate and multivariate analysis [OR 0.41 (0.23-0.75), p = 0.004; OR 0.24 (0.1-0.5), p = 0.0004, respectively].ConclusionsHigher baseline viral loads and interruption of peginterferon and/or ribavirin were associated with a poor outcome of anti-HCV treatment while HIV infection was not related to major or minor probability to achieve SVR.

Highlights

  • human immunodeficiency virus (HIV) infection leads to a faster progression of liver disease in subjects infected with Hepatitis C virus (HCV), as compared with HCV mono-infected patients

  • Hepatitis C virus (HCV) infection is highly prevalent (2040%) in subjects infected with the human immunodeficiency virus (HIV) because of common transmission pathways [1]

  • The rate of sustained virological response (SVR) in HCV monoinfected patients varies between 46-55% for genotypes 1 or 4 and 76-88% for genotypes 2 or 3 [10,11] while in HIV/HCV coinfected subjects it varies between 14-38% for genotypes 1 or 4 and 43-73% for genotypes 2 or 3 [6,7,8,9]

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Summary

Introduction

HIV infection leads to a faster progression of liver disease in subjects infected with HCV, as compared with HCV mono-infected patients. Previous reports suggest that sustained virological response (SVR) rates are lower in HIV/HCV coinfection than in HCV monoinfection. HIV/HCV coinfected subjects have higher HCV viral load, faster progression to cirrhosis, higher incidence of liver decompensation and liver related deaths when compared to HCV monoinfected patients [2,3]. A shortened duration of treatment (12-16 weeks) can be considered in patients with HCV genotypes 2 or 3, low baseline HCV-RNA levels and mild fibrosis, who achieved undetectable HCV-RNA at week 4 of treatment (rapid virological response, or RVR). Sustained virological response (SVR) is rather defined as an undetectable HCV-RNA level (

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