Profiles of liver fibrosis evolution during long-term tenofovir treatment in HIV-positive patients coinfected with hepatitis B.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
12 2021
Historique:
revised: 11 07 2021
received: 05 05 2021
accepted: 19 07 2021
pubmed: 24 7 2021
medline: 4 3 2022
entrez: 23 7 2021
Statut: ppublish

Résumé

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). 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. 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 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.

Sections du résumé

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
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.

Identifiants

pubmed: 34297463
doi: 10.1111/liv.15019
doi:

Substances chimiques

DNA, Viral 0
Tenofovir 99YXE507IL

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2874-2884

Informations de copyright

© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Lorenza N C Dezanet (LNC)

INSERM, Institut Pierre Louis d'Épidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France.

Patrick Miailhes (P)

Hôpital de la Croix-Rousse, Hospices Civils de Lyon, Service de Maladies Infectieuses et Tropicales, Lyon, France.

Caroline Lascoux-Combe (C)

APHP, Hôpital Saint-Louis, Service de Maladies Infectieuses, Paris, France.

Julie Chas (J)

APHP, Hôpital Tenon, Service de Maladies Infectieuses, Paris, France.

Sarah Maylin (S)

APHP, Hôpital Saint-Louis, Laboratoire de Virologie, Paris, France.

Audrey Gabassi (A)

APHP, Hôpital Saint-Louis, Laboratoire de Virologie, Paris, France.
INSERM U944, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.

Hayette Rougier (H)

Institut de Médecine et d'Épidémiologie Appliquée, Paris, France.

Constance Delaugerre (C)

APHP, Hôpital Saint-Louis, Laboratoire de Virologie, Paris, France.
INSERM U944, Institut de Recherche Saint-Louis, Université de Paris, Paris, France.

Karine Lacombe (K)

INSERM, Institut Pierre Louis d'Épidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France.
APHP, Hôpital Saint-Antoine, Service de Maladies Infectieuses et Tropicales, Paris, France.

Anders Boyd (A)

INSERM, Institut Pierre Louis d'Épidémiologie et de Santé Publique, IPLESP, Sorbonne Université, Paris, France.
APHP, Hôpital Saint-Antoine, Service de Maladies Infectieuses et Tropicales, Paris, France.

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