Assessment of the possible impact of hepatitis viruses on the development and course of autoimmune liver diseases

Abstract

Background. Despite the well-studied pathogenesis, the etiology of autoimmune liver disease (AILD) remains unknown. Aim. To determine the significance of hepatitis A, B, C and E viruses in the development and progression of AILD. Materials and methods. A single-center case-control study included 139 patients with AILD: autoimmune hepatitis AIH (n=46), primary biliary cholangitis PBS (n=74), primary sclerosing cholangitis PSC (n=19). Median age 56 years, IQR 4865 years. 125 patients without liver disease control group (median age 55 years, IQR 4665 years). Testing of blood serum samples for anti-HAV IgG, anti-HEV IgG, HBsAg, anti-HBc IgG, anti-HCV was carried out by solid-phase ELISA. All patients underwent fibroelastography. Needle liver biopsy 70 patients: AIH (n=37), PBC (n=28) and PSC (n=5). Results. Ab(IgG) to HAV and HBV were detected in patients with AILD significantly more often than in the control group (74.8% vs 54.4%; p0.001). An increased risk of developing AILD was established in patients with the presence of antibodies to HAV, HBV and HEV (OR 2.491, CI 95% [1.4814.190]). The highest risk of developing PBC was found in patients with antibodies to HAV and HBV (OR 3.008, 95% CI [1.6335.542] and OR 2.515, 95% CI [1.2425.093]). In patients with severe liver fibrosis (F3F4 according to METAVIR), antibodies to HAV and HBV were detected significantly more often than in patients with F0F2 [85% vs 65%; p=0.008]. Conclusion. In our work, we have demonstrated the relationship of past hepatitis A, B, E and AILD, as well as the high risk of developing severe fibrosis in patients with AILD and markers of hepatitis A and B viruses indicates the possible involvement of these viruses in the pathogenesis of AILD.