Effect of hepatitis B virus on steatosis in hepatitis C virus co‐infected subjects: A multi‐centre study and systematic review. Issue 8 (17th April 2018)

• Record Type: Journal Article
• Authors: Goossens, N.; de Vito, C.; Mangia, A.; Clément, S.; Cenderello, G.; Barrera, F.; D'Ambrosio, R.; Coppola, N.; Zampino, R.; Stanzione, M.; Adinolfi, L. E.; Wedemeyer, H.; Semmo, N.; Müllhaupt, B.; Semela, D.; Malinverni, R.; Moradpour, D.; Heim, M.; Trincucci, G.; Rubbia‐Brandt, L.; Negro, F.
• Other Names: Piazzolla Valeria investigator.; Santoro Rosanna investigator.; Dufour Jean‐Francois investigator.; Brunner Barbara investigator.; Weber Achim investigator.; Herranz Maribelle investigator.; Mathieu Adeline investigator.; Clerc Olivier investigator.; Elisabetta Degasperi investigator.; Floriana Facchetti investigator.; Macera Margherita investigator.; Pisaturo Mariantonietta investigator.; Stornaiuolo Gianfranca investigator.; Rinaldi Luca investigator.; George Jacob investigator.; Mix Carola investigator.; Cornberg Markus investigator.
• Is Part Of: Journal of viral hepatitis. Volume 25:Issue 8(2018)
• Page Start: 920
• Page End: 929
• Publication Date: 2018-04-17
• Subjects: hepatitis C virus -- hepatitis C‐hepatitis B coinfection -- metabolic syndrome -- steatosis; Hepatitis, Viral -- Periodicals; Hepatitis, Viral, Animal; Hepatitis, Viral, Human; 616.3623
• DOI: 10.1111/jvh.12891
• Languages: English
• ISSNs: 1352-0504

Abstract

Summary: It remains unclear whether hepatitis B virus (HBV) infection may modify the severity of viral steatosis in patients coinfected with chronic hepatitis C virus (HCV). We examined the influence of coinfection with HBV on prevalence of steatosis in chronic hepatitis C in a multi‐centre cohort of HBV‐HCV subjects, and by performing a systematic review and meta‐analysis of the literature. We centrally and blindly assessed steatosis prevalence and severity in a cohort of HBV‐HCV coinfected subjects compared to HCV and HBV monoinfected controls and we performed a systematic review of studies addressing the prevalence of steatosis in HBV‐HCV subjects compared to HCV controls. In the clinical cohort, we included 85 HBV‐HCV, 69 HBV and 112 HCV subjects from 16 international centres. There was no significant difference in steatosis prevalence between the HBV‐HCV and the HCV groups (33% vs 45%, P = .11). In subgroup analysis, lean HBV‐HCV subjects with detectable HBV DNA had less steatosis than lean HCV subjects matched for HCV viremia (15% vs 45%, P = .02). Our literature search identified 5 additional studies included in a systematic review. Overall, prevalence of steatosis > 5% was similar in HBV‐HCV infection compared to HCV (pooled odds ratio [OR] 0.91, 95% CI 0.53‐1.6) although there was significant heterogeneity (I 2 69%, P = .007). In conclusion, although the prevalence of steatosis is similar in HBV‐HCV compared to HCV subjects, our analysis suggests that there may be an inhibitory effect of HCV‐induced steatogenesis by HBV in certain subgroups of patients.