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Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV

BACKGROUND: 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. We aimed to compar...

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Autores principales: Odolini, Silvia, Amadasi, Silvia, Cerini, Carlo, Giralda, Mariarosaria, Nasta, Paola, Castelli, Francesco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160898/
https://www.ncbi.nlm.nih.gov/pubmed/25236496
http://dx.doi.org/10.1186/1471-2334-14-S5-S4
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author Odolini, Silvia
Amadasi, Silvia
Cerini, Carlo
Giralda, Mariarosaria
Nasta, Paola
Castelli, Francesco
author_facet Odolini, Silvia
Amadasi, Silvia
Cerini, Carlo
Giralda, Mariarosaria
Nasta, Paola
Castelli, Francesco
author_sort Odolini, Silvia
collection PubMed
description BACKGROUND: 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. We aimed to compare SVR rates of these two populations. METHODS: We 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. RESULTS: 461 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 ANALYSIS: At 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/mm(3 )[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 ANALYSIS: Only 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]. CONCLUSIONS: Higher 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.
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spelling pubmed-41608982014-09-25 Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV Odolini, Silvia Amadasi, Silvia Cerini, Carlo Giralda, Mariarosaria Nasta, Paola Castelli, Francesco BMC Infect Dis Research Article BACKGROUND: 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. We aimed to compare SVR rates of these two populations. METHODS: We 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. RESULTS: 461 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 ANALYSIS: At 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/mm(3 )[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 ANALYSIS: Only 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]. CONCLUSIONS: Higher 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. BioMed Central 2014-09-05 /pmc/articles/PMC4160898/ /pubmed/25236496 http://dx.doi.org/10.1186/1471-2334-14-S5-S4 Text en Copyright © 2014 Odolini et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Odolini, Silvia
Amadasi, Silvia
Cerini, Carlo
Giralda, Mariarosaria
Nasta, Paola
Castelli, Francesco
Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title_full Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title_fullStr Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title_full_unstemmed Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title_short Sustained virological response to peginterferon therapy in patients infected with HCV (genotypes 2 and 3), with or without HIV
title_sort sustained virological response to peginterferon therapy in patients infected with hcv (genotypes 2 and 3), with or without hiv
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160898/
https://www.ncbi.nlm.nih.gov/pubmed/25236496
http://dx.doi.org/10.1186/1471-2334-14-S5-S4
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