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

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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 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).

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%; 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].

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.

About the authors

Evgeniya S. Sbikina

Loginov Moscow Clinical Scientific Center

Author for correspondence.
Email: e.sbikina@mknc.ru
ORCID iD: 0000-0003-2195-9643

мл. науч. сотр. отд. гепатологии

Russian Federation, Moscow

Elena V. Vinnitskaya

Loginov Moscow Clinical Scientific Center

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0002-0344-8375

д-р мед. наук, зав. отд. гепатологии

Russian Federation, Moscow

Sergey N. Batskikh

Loginov Moscow Clinical Scientific Center

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0002-5917-203X

канд. мед. наук, ст. науч. сотр. отд. гепатологии

Russian Federation, Moscow

Yuliay G. Sandler

Loginov Moscow Clinical Scientific Center

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0003-4291-812X

канд. мед. наук, ст. науч. сотр. отд. гепатологии

Russian Federation, Moscow

Kirill G. Saliev

Loginov Moscow Clinical Scientific Center

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0002-4581-7052

мл. науч. сотр. отд. гепатологии

Russian Federation, Moscow

Tatyana Yu. Khaimenova

Loginov Moscow Clinical Scientific Center

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0002-4599-4040

канд. мед. наук, зав. отд-нием хронических заболеваний печени

Russian Federation, Moscow

Dmitry S. Bordin

Loginov Moscow Clinical Scientific Center; Yevdokimov Moscow State University of Medicine and Dentistry; Tver State Medical University

Email: e.sbikina@mknc.ru
ORCID iD: 0000-0003-2815-3992

д-р мед. наук, зав. отд. патологии поджелудочной железы, желчных путей и верхних отделов пищеварительного тракта, проф. каф. пропедевтики внутренних болезней и гастроэнтерологии, проф. каф. общей врачебной практики и семейной медицины

Russian Federation, Moscow; Moscow; Tver

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Copyright (c) 2023 Sbikina E.S., Vinnitskaya E.V., Batskikh S.N., Sandler Y.G., Saliev K.G., Khaimenova T.Y., Bordin D.S.

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This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
 
 


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