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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

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



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


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.


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.


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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