• Terapevt Arkh · Mar 2023

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

    • E S Sbikina, E V Vinnitskaya, S N Batskikh, Y G Sandler, K G Saliev, T Y Khaimenova, and D S Bordin.
    • Loginov Moscow Clinical Scientific Center.
    • Terapevt Arkh. 2023 Mar 30; 95 (2): 173178173-178.

    BackgroundDespite the well-studied pathogenesis, the etiology of autoimmune liver disease (AILD) remains unknown.AimTo determine the significance of hepatitis A, B, C and E viruses in the development and progression of AILD.Materials And MethodsA 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 48-65 years. 125 patients - without liver disease - control group (median age 55 years, IQR 46-65 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).ResultsAb(IgG) to HAV and HBV were detected in patients with AILD significantly more often than in the control group (74.8% vs 54.4%; p<0.001). 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% [1.481-4.190]). The highest risk of developing PBC was found in patients with antibodies to HAV and HBV (OR 3.008, 95% CI [1.633-5.542] and OR 2.515, 95% CI [1.242-5.093]). In patients with severe liver fibrosis (F3-F4 according to METAVIR), antibodies to HAV and HBV were detected significantly more often than in patients with F0-F2 [85% vs 65%; p=0.008].ConclusionIn 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.

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