Effect of hepatitis B virus on steatosis in hepatitis C virus co-infected subjects: A multi-centre study and systematic review

Publication

Effect of hepatitis B virus on steatosis in hepatitis C virus co-infected subjects: A multi-centre study and systematic review

Journal Paper/Review - Apr 17, 2018

Goossens N, Semmo N, Mullhaupt B, Semela David, Malinverni R, Moradpour D, Heim M, Trincucci G, Rubbia-Brandt L, Negro F, Wedemeyer H, Adinolfi L E, de Vito C, Mangia A, Clément S, Cenderello G, Barrera F, D'Ambrosio R, Coppola N, Zampino R, Stanzione M, BOSTIC Study Group

Citation

Goossens N, Semmo N, Mullhaupt B, Semela D, Malinverni R, Moradpour D, Heim M, Trincucci G, Rubbia-Brandt L, Negro F, Wedemeyer H, Adinolfi L, de Vito C, Mangia A, Clément S, Cenderello G, Barrera F, D'Ambrosio R, Coppola N, Zampino R, Stanzione M, BOSTIC Study Group. Effect of hepatitis B virus on steatosis in hepatitis C virus co-infected subjects: A multi-centre study and systematic review. J Viral Hepat 2018; 25:920-929.

Type

Journal Paper/Review (English)

Journal

J Viral Hepat 2018; 25

Publication Date

Apr 17, 2018

Issn Electronic

1365-2893

Pages

920-929

Brief description/objective

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 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.