Vincenzo Malagnino1, Julie Bottero2, Patrick Miailhes3, Caroline Lascoux-Combe4, Pierre-Marie Girard5,6, Fabien Zoulim7, Karine Lacombe5,6, Anders Boyd5,6. 1. Department of System Medicine, Clinical of Infectious Diseases, Tor Vergata University of Rome, Rome, Italy. 2. Unite de Maladies Infectieuses et Tropicales, CHU Jean Verdier, GH HUPSS, Bondy, France. 3. Service des Maladies Infectieuses et Tropicales, Hopital de la Croix-Rousse, Hospices Civils de Lyon, Lyon, France. 4. Service des Maladies Infectieuses et Tropicales, Hopital Saint-Louis, AP-HP, Paris, France. 5. Service des Maladies Infectieuses et Tropicales, Hôpital Saint-Antoine, AP-HP, Paris, France. 6. Inserm UMR-S1136, Sorbonne Université, Institut PierreLouis d'Épidémiologie et de Santé Publique, Paris, France. 7. Centre de Recherche sur le Cancer de Lyon, INSERM, Unité 1052, CNRS, UMR 5286, Lyon, France.
Abstract
INTRODUCTION: Infection with hepatitis B virus (HBV) genotype G has been associated with increased liver fibrosis levels compared with other genotypes in cross-sectional studies, yet its role in fibrosis evolution remains to be established. METHODS: In this prospective cohort study, 158 human immunodeficiency virus (HIV)-HBV coinfected patients had available HBV genotyping at baseline. Liver fibrosis was assessed at baseline and every 6 to 12 months by the FibroTest (BioPredictive, Paris, France). Risk factors for fibrosis regression (F3-F4 to F0-F1-F2) and progression (F0-F1-F2 to F3-F4) between baseline and end of follow-up were evaluated. RESULTS: Most patients were male (88.6%) with a median age of 39 years. HBV genotype A was more prevalent compared with other HBV genotypes (62.7% vs D = 10.8%, E = 10.8%, and G = 15.8%). Patients were followed up for a median of 83 months (IQR = 37-97). In the 43 (27.2%) patients with F3-F4 baseline liver fibrosis, 7 (16.2%) regressed to F0-F1-F2 fibrosis at the last follow-up visit. In the 115 (72.8%) with F0-F1-F2 fibrosis at baseline, 19 (16.5%) progressed to F3-F4 fibrosis at last visit. In multivariable analysis, fibrosis progression was independently associated with older age (P <0.005), baseline CD4+ cell count less than 350/mm 3 ( P <0.01), longer antiretroviral therapy duration ( P <0.03), and HBV genotype G infection (vs non-G, P <0.01). When examining averages over time, the rate of FibroTest increase was faster in genotype G vs non-G-infected patients with baseline F0-F1-F2 fibrosis ( P for interaction = 0.002). CONCLUSION: In HIV-HBV coinfected patients, HBV genotype G is an independent risk factor for liver fibrosis progression as determined by noninvasive markers. HBV genotype G-infected patients with low initial liver fibrosis levels may require more careful monitoring.
INTRODUCTION:Infection with hepatitis B virus (HBV) genotype G has been associated with increased liver fibrosis levels compared with other genotypes in cross-sectional studies, yet its role in fibrosis evolution remains to be established. METHODS: In this prospective cohort study, 158 human immunodeficiency virus (HIV)-HBV coinfectedpatients had available HBV genotyping at baseline. Liver fibrosis was assessed at baseline and every 6 to 12 months by the FibroTest (BioPredictive, Paris, France). Risk factors for fibrosis regression (F3-F4 to F0-F1-F2) and progression (F0-F1-F2 to F3-F4) between baseline and end of follow-up were evaluated. RESULTS: Most patients were male (88.6%) with a median age of 39 years. HBV genotype A was more prevalent compared with other HBV genotypes (62.7% vs D = 10.8%, E = 10.8%, and G = 15.8%). Patients were followed up for a median of 83 months (IQR = 37-97). In the 43 (27.2%) patients with F3-F4 baseline liver fibrosis, 7 (16.2%) regressed to F0-F1-F2 fibrosis at the last follow-up visit. In the 115 (72.8%) with F0-F1-F2 fibrosis at baseline, 19 (16.5%) progressed to F3-F4 fibrosis at last visit. In multivariable analysis, fibrosis progression was independently associated with older age (P <0.005), baseline CD4+ cell count less than 350/mm 3 ( P <0.01), longer antiretroviral therapy duration ( P <0.03), and HBV genotype Ginfection (vs non-G, P <0.01). When examining averages over time, the rate of FibroTest increase was faster in genotype G vs non-G-infectedpatients with baseline F0-F1-F2 fibrosis ( P for interaction = 0.002). CONCLUSION: In HIV-HBV coinfectedpatients, HBV genotype G is an independent risk factor for liver fibrosis progression as determined by noninvasive markers. HBV genotype G-infectedpatients with low initial liver fibrosis levels may require more careful monitoring.