Author information
1Department of Medicine, Emory University, Atlanta, Georgia, USA.
2Department of Medicine, University of California San Francisco, San Francisco, California, USA.
3Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA.
4Department of Epidemiology and Biostatistics, University at Albany, State University of New York, Rensselaer, New York, USA.
5Department of Medicine, Stroger Hospital, Cook County Health, Chicago, Illinois, USA.
6Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
7Department of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA.
8Department of Obstetrics and Gynecology, State University of New York Downstate Health Sciences University, Brooklyn, New York, USA.
9Department of Medicine, Georgetown University Medical Center, Washington, District of Columbia, USA.
10Institute for Liver and Digestive Health, Division of Medicine, University College London, London, United Kingdom.
11Department of Pediatrics, University of Southern California, Los Angeles, California, USA.
12Infectious Disease Section, Department of Veterans Affairs Medical Center, San Francisco, California, USA.
Abstract
Background: The trajectory of liver fibrosis is not well understood in the contemporary era of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) therapy.
Methods: We assessed the Enhanced Liver Fibrosis (ELF) score, aspartate transaminase-to-platelet ratio index (APRI) and Fibrosis-4 (FIB-4) in 116 women with HIV/HCV coinfection over a 4-year period. Random-effects linear regression models examined the rate of fibrosis change 1-2 years before starting HCV treatment, within 1 year before starting (peri-HCV treatment), within 1 year after and 1-2 years post-HCV treatment in unadjusted and adjusted models including age, race, and changes from pretreatment of factors that might affect fibrosis (eg, alcohol, integrase strand inhibitor [INSTI] use, waist circumference, CD4 count).
Results: INSTI use nearly doubled from pre- to peri-HCV treatment. In unadjusted analysis, there was a 3.3% rate of rise in ELF pre-HCV treatment, 2.2% and 3.6% rate of decline during the peri- and 1-year post-HCV treatment period, respectively, followed by a 0.3% rise. Similar findings were observed for APRI and FIB-4. There was little effect on the estimated fibrosis trajectories after adjustment.
Conclusions: The apparent lack of decline in biomarkers of liver fibrosis beyond 1 year after HCV cure suggests that continued monitoring of liver fibrosis and interventions to mitigate progression in people with HIV after HCV cure remains essential.