TY - JOUR
T1 - Profiles of liver fibrosis evolution during long-term tenofovir treatment in HIV-positive patients coinfected with hepatitis B
AU - Dezanet, Lorenza N.C.
AU - Miailhes, Patrick
AU - Lascoux-Combe, Caroline
AU - Chas, Julie
AU - Maylin, Sarah
AU - Gabassi, Audrey
AU - Rougier, Hayette
AU - Delaugerre, Constance
AU - Lacombe, Karine
AU - Boyd, Anders
N1 - Funding Information: This work was supported by SIDACTION and the ANRS. Gilead Sciences, Inc. provided an unrestricted grant for the French HIV‐HBV cohort and was not involved in any part of the data collection, analysis and manuscript writing. Funding Information: The authors are grateful to the patients and the clinical teams for their commitment to the French HIV‐HBV Cohort. This study was sponsored by the Institut de Médecine et d'Epidémiologie Appliquée (IMEA). LNCD was awarded a post‐doctoral fellowship from the France REcherche Nord&sud Sida‐hiv Hépatites (ANRS). Funding Information: This work was supported by SIDACTION and the ANRS. Gilead Sciences, Inc. provided an unrestricted grant for the French HIV-HBV cohort and was not involved in any part of the data collection, analysis and manuscript writing. The authors are grateful to the patients and the clinical teams for their commitment to the French HIV-HBV Cohort. This study was sponsored by the Institut de M?decine et d'Epid?miologie Appliqu?e (IMEA). LNCD was awarded a post-doctoral fellowship from the France REcherche Nord&sud Sida-hiv H?patites (ANRS). Publisher Copyright: © 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2021/12
Y1 - 2021/12
N2 - Background & Aims: Data on liver fibrosis evolution and its involvement in liver-related morbidity are scarce in individuals with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) co-infection during treatment. We identified profiles of liver fibrosis evolution in coinfected patients undergoing tenofovir (TDF). Methods: We included 169 HIV-HBV-coinfected patients on TDF-based antiretroviral therapy. Virological and clinical data were obtained at TDF-initiation and every 6-12 months. From data on non-invasive liver fibrosis assessments collected yearly (FibroTest®), we established clusters of individuals with similar liver fibrosis evolution using group-based trajectory models. Results: Four profiles of liver fibrosis evolution were established from a median follow-up of 7.6 years (IQR = 3.1-13.1): low fibrosis with no progression (29.6%, profile A), low fibrosis with progression (22.5%, profile B), moderate fibrosis with high fluctuation (39.6%, profile C), and cirrhosis with no regression (8.3%, profile D). When compared to profile A, baseline HBeAg-positive status was associated with profiles B (P =.007) and C (P =.004), older age with profiles C (P <.001) and D (P =.001), exposure to second-generation protease inhibitors with profile C (P =.004), and CD4+ <500/mm3 at the last visit with profiles C (P =.02) and D (P =.002). Incident liver-related events occurred in profiles other than A (B, n = 1/38; C, n = 6/67; D, n = 3/14) and all five cases of hepatocellular carcinoma occurred in profiles C (n = 2) and D (n = 3). Conclusions: TDF-treated HIV-HBV coinfected individuals do not seem to benefit from comparable levels of liver fibrosis regression as in HBV mono-infection. Liver-related morbidity occurs mainly in those with fluctuating or consistently high fibrosis levels.
AB - Background & Aims: Data on liver fibrosis evolution and its involvement in liver-related morbidity are scarce in individuals with human immunodeficiency virus (HIV) and hepatitis B virus (HBV) co-infection during treatment. We identified profiles of liver fibrosis evolution in coinfected patients undergoing tenofovir (TDF). Methods: We included 169 HIV-HBV-coinfected patients on TDF-based antiretroviral therapy. Virological and clinical data were obtained at TDF-initiation and every 6-12 months. From data on non-invasive liver fibrosis assessments collected yearly (FibroTest®), we established clusters of individuals with similar liver fibrosis evolution using group-based trajectory models. Results: Four profiles of liver fibrosis evolution were established from a median follow-up of 7.6 years (IQR = 3.1-13.1): low fibrosis with no progression (29.6%, profile A), low fibrosis with progression (22.5%, profile B), moderate fibrosis with high fluctuation (39.6%, profile C), and cirrhosis with no regression (8.3%, profile D). When compared to profile A, baseline HBeAg-positive status was associated with profiles B (P =.007) and C (P =.004), older age with profiles C (P <.001) and D (P =.001), exposure to second-generation protease inhibitors with profile C (P =.004), and CD4+ <500/mm3 at the last visit with profiles C (P =.02) and D (P =.002). Incident liver-related events occurred in profiles other than A (B, n = 1/38; C, n = 6/67; D, n = 3/14) and all five cases of hepatocellular carcinoma occurred in profiles C (n = 2) and D (n = 3). Conclusions: TDF-treated HIV-HBV coinfected individuals do not seem to benefit from comparable levels of liver fibrosis regression as in HBV mono-infection. Liver-related morbidity occurs mainly in those with fluctuating or consistently high fibrosis levels.
KW - group-based trajectory models
KW - hepatic fibrosis
KW - hepatitis B virus
KW - human immunodeficiency virus
UR - http://www.scopus.com/inward/record.url?scp=85111600135&partnerID=8YFLogxK
U2 - https://doi.org/10.1111/liv.15019
DO - https://doi.org/10.1111/liv.15019
M3 - Article
C2 - 34297463
SN - 1478-3223
VL - 41
SP - 2874
EP - 2884
JO - Liver international
JF - Liver international
IS - 12
ER -