Relationship between the production of autoantibodies to oxidized low-density lipoprotein and hepatic steatosis in patients with chronic hepatitis C

Abstract

Persistent hepatitis C virus (HCV) infection induces oxidative stress and eventually leads to hepatic steatosis. Oxidatively modified autoantigens, including oxidized low-density lipoprotein (ox-LDL), were identified in patients with systemic lupus erythematosus. Chronic HCV infection often evokes autoimmune phenomena, such as autoantibody production and/or concurrent autoimmune diseases. We examined the relationship between the production of antibodies to ox-LDL (anti-ox-LDL) and hepatic steatosis in patients with chronic hepatitis C (CH-C). Anti-ox-LDL levels were determined by the enzyme-linked immunosorbent assay method. The severity of hepatic steatosis was evaluated using the classification proposed by Brunt and colleagues. The effect of antiviral treatment was also investigated. Twenty-two (52%) of the 42 patients with CH-C had no hepatic steatosis (grade 0), while 12 (29%) and 8 (19%) had grade 1 and 2 hepatic steatosis, respectively. The overall serum immunoglobulin G (IgG) level in patients with grade 2 steatosis was significantly higher than that in patients with grade 0 steatosis (1,999±340 vs. 1,465±196 mg/dl, p<0.0001). The mean anti-ox-LDL level in grade 2 steatosis patients was also higher than that in grade 0 steatosis patients (754±479 vs. 361±274 mU/ml, p=0.0165). A close correlation was apparent between anti-ox-LDL and serum IgG levels (r=0.390, p=0.0107). There was no significant difference in the level of anti-ox-LDL between CH-C patients who acquired sustained virological response (SVR) and those who exhibited non-SVR. These findings suggest that anti-ox-LDL in patients with CH-C is induced in the process of hepatic steatosis and that the emergence of anti-ox-LDL does not affect antiviral treatment.