Regression of liver stiffness after sustained hepatitis C... : AIDS (original) (raw)

CLINICAL SCIENCE

Regression of liver stiffness after sustained hepatitis C virus (HCV) virological responses among HIV/HCV-coinfected patients

*The members of the writing committee and ‘The ANRS CO13 HEPAVIH Cohort’ have been included under the ‘Acknowledgements’ section along with their institutional/organizational details.

Correspondence to Professor Dominique Salmon, MD, PhD, Department of Medicine, Infectious Diseases Federation, Cochin Hospital, Paris Descartes University, 27, rue du Faubourg Saint Jacques, 75679 Paris cedex 14, France. Tel: +33(0)1 58 41 21 34; fax: +33(0) 1 58 41 20 80; e-mail: [email protected]

Received 5 March, 2015

Revised 23 April, 2015

Accepted 19 June, 2015

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Abstract

Objective:

We assessed the impact of a sustained virological response (SVR) on liver stiffness among HIV/hepatitis C virus (HCV)-coinfected patients enrolled in the ANRS CO13 HEPAVIH cohort.

Methods:

We studied HIV/HCV-coinfected patients who received at least one dose of any anti-HCV treatment and who had documented SVR status, a pretreatment FibroScan value of at least 7.1 kPa, and at least one posttreatment FibroScan value. The time required to achieve at least a 30% decrease in liver stiffness was analyzed by constructing Kaplan–Meier curves and using Cox proportional hazards models.

Results:

Among 98 patients treated for HCV infection with either pegylated interferon along with ribavirin (n = 89) or protease inhibitor-based triple therapy (n = 9), 53 patients (54%) had an SVR. Median follow-up was 44.6 (interquartile range: 28.8–58.9) months. The probability of achieving a 30% decrease in FibroScan values was 51% [95% confidence interval (CI): 39–66] in patients with an SVR and 21% in nonresponders (95% CI: 11–36) at 1 year, and 74% (61–86) and 28% (17–44) at 2 years, respectively. In the subgroup of 35 cirrhotic patients (pretreatment liver stiffness ≥12.5 kPa), 14 of 18 patients with an SVR and three of 17 nonresponders had a fibrosis score below 12.5 kPa at the last follow-up examination. Multivariable analysis showed that SVR was independently associated with a ≥30% reduction in liver stiffness, both in the overall study group (hazard ratio: 5.77; 95% CI: 2.00–16.62; P = 0.0012) and in cirrhotic patients (hazard ratio: 8.21; 95% CI: 2.15–31.34; P = 0.0021). Robustness analyses using FIB4 values showed similar results.

Conclusion:

SVR is significantly associated with improvement in liver stiffness in HIV/HCV-coinfected patients, including those with cirrhosis.