Conflict of interests: None to declare.
Metabolic syndrome association with fibrosis development in chronic hepatitis B virus inactive carriers
Article first published online: 19 DEC 2013
© 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 29, Issue 1, pages 173–178, January 2014
How to Cite
Mena, Á., Pedreira, J. D., Castro, Á., López, S., Vázquez, P. and Poveda, E. (2014), Metabolic syndrome association with fibrosis development in chronic hepatitis B virus inactive carriers. Journal of Gastroenterology and Hepatology, 29: 173–178. doi: 10.1111/jgh.12432
- Issue published online: 19 DEC 2013
- Article first published online: 19 DEC 2013
- Accepted manuscript online: 13 NOV 2013 05:42AM EST
- Manuscript Accepted: 16 SEP 2013
- Fondo de Investigación Sanitaria. Grant Numbers: CP08/00214, PI10/02166
- Fundación Profesor Novoa Santos, A Coruña
- inactive carriers;
- metabolic syndrome
Background and Aim
There are few data of fibrosis development in chronic hepatitis B (CHB) patients classified as inactive carriers. The aim of this study is to determinate the prevalence of significant fibrosis and probable cirrhosis measured by FibroScan in real inactive CHB carriers and investigate the relationship with virological, epidemiological, and metabolic factors.
Cross-sectional cohort study including CHB inactive carriers. Liver stiffness measurement was performed with transient elastography (FibroScan). Significant fibrosis (≥ F2) was defined as stiffness > 7.5 kPa, and probable cirrhosis as > 11.8 kPa. Factors associated with significant fibrosis were explored with univariate and multivariate adjusted logistic regression analyses.
Ninety-six CHB inactive carriers were analyzed. Of them, 24 (25%) had significant fibrosis and 7 (7%) probable cirrhosis; mean stiffness was 6.2 ± 2.3 kPa.
Of them, 24% had metabolic syndrome, with higher FibroScan value than those without (8.4 kPa vs 5.5 kPa, P < 0.001).
Factors associated with significant fibrosis were (odds ratio, 95% confidence interval, P value): central obesity (7.1, 1.8–27.9, 0.005), elevated fasting glucose (4.3, 1.3–27.9, 0.036), reduced high-density lipoprotein cholesterol (5.2, 1.2–23.6, 0.032) and elevated triglycerides (6.2, 1.4–28.3, 0.019). Factors as age, sex, transaminases, hepatitis B virus DNA or genotype were not related with liver fibrosis.
The presence of metabolic syndrome has a 69% of positive predictive value and 89% of negative predictive value for significant fibrosis.
Different components of metabolic syndrome are associated with fibrosis development in CHB inactive carriers. In the absence of metabolic syndrome, significant fibrosis is uncommon in this population.