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AIDS. 2019 Jan 14. doi: 10.1097/QAD.0000000000002138. [Epub ahead of print]

Progression of liver fibrosis following acute hepatitis C virus infection in HIV-positive MSM.

Author information

1
Department of Infectious Diseases, Research and Prevention, Public Health Service of Amsterdam.
2
Division of Infectious Diseases, Amsterdam Infection and Immunity Institute.
3
both authors contributed equally to this manuscript.
4
Department of Global Health, Amsterdam Public Health Research Institute, Amsterdam UMC, University of Amsterdam.
5
Amsterdam Institute for Global Health and Development, Amsterdam, The Netherlands.
6
INSERM, Institut Pierre Louis d'Epidémiologie et de Santé Publique, Sorbonne Université, Paris, France.
7
Stichting HIV Monitoring, Amsterdam, The Netherlands.

Abstract

BACKGROUND:

Whether continued, accelerated liver fibrosis progression occurs following acute hepatitis C virus infection (AHCVI) in HIV-positive MSM is unknown.

DESIGN AND METHODS:

HIV-positive MSM from the AIDS Therapy Evaluation in the Netherlands and MSM Observational Study for Acute Infection with Hepatitis C-cohorts with primary AHCVI and at least one fibrosis-4 (FIB-4) measurement less than 2 years before and 1 year after estimated AHCVI were included. Mixed-effect linear models were used to evaluate (time-updated) determinants of FIB-4 levels over time. Determinants of transitioning to and from FIB-4 of 1.45 or less and more than 1.45 were examined using multistate Markov models.

RESULTS:

Of 313 MSM, median FIB-4 measurements per individual was 12 (interquartile range  = 8-18) and median follow-up following AHCVI was 3.5 years (interquartile range = 1.9-5.6). FIB-4 measurements averaged at 1.00 [95% confidence interval (CI) = 0.95-1.05] before AHCVI, 1.31 (95% CI = 1.25-1.38) during the first year of AHCVI and 1.10 (95% CI = 1.05-1.15) more than 1 year after AHCVI. Mean FIB-4 more than 1 year after AHCVI was higher for chronically infected patients compared with those successfully treated (P = 0.007). Overall FIB-4 scores were significantly higher with older age, lower CD4 cell count, longer duration from HIV-diagnosis or AHCVI, and nonresponse to HCV-treatment. At the end of follow-up, 60 (19.2%) and eight MSM (2.6%) had FIB-4 between 1.45-3.25 and at least 3.25, respectively. Older age, lower CD4-cell count and detectable HIV-RNA were significantly associated with higher rates of progression to FIB-4 more than 1.45, whereas older age, longer duration from HIV-diagnosis and nonresponse to HCV-treatment were significantly associated with lower rates of regression to FIB-4 of 1.45 or less.

CONCLUSION:

In this population of HIV-positive MSM, FIB-4 scores were higher during the first year of AHCVI, but FIB-4 at least 3.25 was uncommon by the end of follow-up. Well controlled HIV-infection appears to attenuate FIB-4 progression.

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