Predictive factors for hepatocellular carcinoma in chronic hepatitis B using structural equation modeling: a prospective cohort study.

Aged Carcinoma, Hepatocellular / epidemiology Hepatitis B, Chronic / epidemiology Humans Liver Neoplasms / epidemiology Male Prospective Studies Risk Factors

Epidemiology Hepatitis B virus Hepatocarcinogenesis Hepatocellular carcinoma Liver cancer

Journal

Clinics and research in hepatology and gastroenterology

ISSN: 2210-741X

Titre abrégé: Clin Res Hepatol Gastroenterol

Pays: France

ID NLM: 101553659

Informations de publication

Date de publication:
09 2021

Historique:

received: 09 02 2021

accepted: 11 04 2021

pubmed: 1 5 2021

medline: 26 2 2022

entrez: 30 4 2021

Statut: ppublish

Résumé

The factors predicting hepatocellular carcinoma (HCC) occurrence in chronic hepatitis B need to be precisely known to improve its detection. We identified pathways and individual predictive factors associated with HCC in the ANRS CO22 HEPATHER cohort. The study analyzed HBV-infected patients recruited at 32 French expert hepatology centers from August 6, 2012, to December 31, 2015. We excluded patients with chronic HCV, HDV and a history of HCC, decompensated cirrhosis or liver transplantation. Structural equation models were developed to characterize the causal pathways leading to HCC occurrence. The association between clinical characteristics (age, gender, body-mass index, liver fibrosis, alcohol consumption, smoking status, diabetes, hypertension, dyslipidemia, alpha-fetoprotein, HBV DNA levels, antiviral therapy) and incident HCC was quantified. Among the 4489 patients included, 33 patients reported incident HCC. The median follow-up was 45.5 months. Age (β = 0.18 by decade, 95% CI 0.14-0.23), male gender (β = 0.23, 95% CI 0.18-0.29), metabolic syndrome (β = 0.28, 95% CI 0.22-0.33), alcohol consumption (β = 0.09, 95% CI 0.05-0.14) and HBV DNA (β = 0.25, 95% CI 0.170.34) had a significant and direct effect on the occurrence of advanced liver fibrosis. Liver fibrosis (β = 0.71, 95% CI 0.55-0.87) predicted, in turn, the occurrence of HCC. Liver fibrosis mediates the effects of age, gender, alcohol, metabolic syndrome and HBV DNA on the occurrence of HCC. Elderly men with chronic hepatitis B, risky alcohol use, advanced liver fibrosis, metabolic syndrome and high HBV DNA levels should be monitored closely to detect the development of HCC.

Sections du résumé

BACKGROUND & AIMS

METHODS

The study analyzed HBV-infected patients recruited at 32 French expert hepatology centers from August 6, 2012, to December 31, 2015. We excluded patients with chronic HCV, HDV and a history of HCC, decompensated cirrhosis or liver transplantation. Structural equation models were developed to characterize the causal pathways leading to HCC occurrence. The association between clinical characteristics (age, gender, body-mass index, liver fibrosis, alcohol consumption, smoking status, diabetes, hypertension, dyslipidemia, alpha-fetoprotein, HBV DNA levels, antiviral therapy) and incident HCC was quantified.

RESULTS

Among the 4489 patients included, 33 patients reported incident HCC. The median follow-up was 45.5 months. Age (β = 0.18 by decade, 95% CI 0.14-0.23), male gender (β = 0.23, 95% CI 0.18-0.29), metabolic syndrome (β = 0.28, 95% CI 0.22-0.33), alcohol consumption (β = 0.09, 95% CI 0.05-0.14) and HBV DNA (β = 0.25, 95% CI 0.170.34) had a significant and direct effect on the occurrence of advanced liver fibrosis. Liver fibrosis (β = 0.71, 95% CI 0.55-0.87) predicted, in turn, the occurrence of HCC.

CONCLUSIONS

Liver fibrosis mediates the effects of age, gender, alcohol, metabolic syndrome and HBV DNA on the occurrence of HCC. Elderly men with chronic hepatitis B, risky alcohol use, advanced liver fibrosis, metabolic syndrome and high HBV DNA levels should be monitored closely to detect the development of HCC.

Identifiants

DOI: 10.1016/j.clinre.2021.101713 PMID: 33930591

pubmed: 33930591

pii: S2210-7401(21)00092-9

doi: 10.1016/j.clinre.2021.101713

pii:

doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

Pagination

101713