Published online Sep 27, 2014. doi: 10.4254/wjh.v6.i9.677
Revised: July 8, 2014
Accepted: August 27, 2014
Published online: September 27, 2014
Processing time: 160 Days and 22.7 Hours
AIM: To evaluate steatosis, insulin resistance (IR) and patatin-like phospholipase domain-containing 3 (PNPLA3) and their relation to disease progression in hepatitis B and C viruses (HCV-HBV) co-infected patients.
METHODS: Three hundred and thirty patients with biopsy proven chronic hepatitis were enrolled: 66 had HBV-HCV, 66 HBV and 198 HCV infection. Prevalence of steatosis, IR and PNPLA3 polymorphisms and their relation to anthropometric, biochemical, virological and histological parameters were evaluated.
RESULTS: Prevalence of steatosis in group HBV-HCV was similar to that in HCV (47.0% vs 49.5%, respectively); group HBV showed the lowest steatosis (33.3%). Group HBV-HCV had a lesser degree of steatosis than HCV (P = 0.016), lower HCV RNA levels (P = 0.025) and lower prevalence and degree of IR (P = 0.01). PNPLA3 polymorphisms were associated with steatosis. Group HBV-HCV showed higher levels of liver fibrosis than group HCV (P = 0.001), but similar to that observed in HBV group. In HBV-HCV group, liver fibrosis was not associated with steatosis, IR or PNPLA3. HBV infection was the independent predictor of advanced liver fibrosis.
CONCLUSION: HBV-HCV co-infected patients have lower degree of hepatic steatosis, IR and HCV RNA than HCV mono-infected; co-infected patients showed a more rapid liver fibrosis progression that seems to be due to the double infection and/or HBV dominance.
Core tip: We evaluated the prevalence and role of steatosis, insulin resistance and patatin-like phospholipase domain-containing 3 (PNPLA3) polymorphisms on disease progression in hepatitis B and C viruses (HCV-HBV) co-infected patients. The data showed that HBV-HCV patients have lower levels of liver steatosis and insulin resistance than HCV mono-infected patients. HBV seems to interact with HCV reducing HCV replication and HCV-related metabolic features. Thus, the influence of HCV-related steatosis and insulin resistance as well as PNPLA3 polymorphism do not significantly impact liver fibrosis progression in HBV-HCV patients. The more rapid progression of liver fibrosis observed in HBV-HCV co-infected patients seems to be mostly associated with HBV infection.