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

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

Resolved Hepatitis B: Achieved or Imaginary Wellbeing?

Aim. Assessment of the clinical impact of previous hepatitis B infection (PHB).Key points. PHB is characterized by the presence of viral DNA in the organism (including intrahepatic cccDNA and integrated DNA). Possible virus persistence in the PHB patient's hepatocytes potentiates the agent transmission risk via haemotransfusion, organ transplantation and haemodialysis. Occult HBV infection in PHB individuals can reactivate at background immunosuppressive or chemotherapies. PHB with chronic liver diseases of various aetiology significantly rises the risk of cirrhosis and hepatic cancer. The PHB association with autoimmune liver diseases and extrahepatic gastrointestinal cancer needs a careful research to confirm the possible involvement of hepatitis B virus in morbid genesis.Conclusion. No clinical signs of acute or chronic disease, HBsAg clearance and negative viral DNA load in blood of PHB individuals do not necessarily imply a complete disease eradication.PHB elicitation improves accuracy of the overall prognosis, reduces the virus transmission risk and prevents the reactivation of HBV infection

Risk of Cirrhosis in Patients with Non-alcoholic Fatty Liver Disease and Previous Viral Hepatitis B

Previous viral hepatitis B increases the risk of cirrhosis in various chronic liver diseases.Aim. Assessment of association between previous hepatitis B and the severity of liver fibrosis in patients with nonalcoholic fatty liver disease (NAFLD).Materials and methods. A single-centre cross-sectional trial included 110 HBsAg- and anti-HCV-negative patients with confirmed NAFLD (median (IQR) age 60 (53-66) years). Obesity, type 2 diabetes and dyslipidemia were in 78 (70.9%), 64 (58.2%) and 77 (70%) individuals, respectively. To confirm previous and occult hepatitis B virus (HBV) infection, blood of all participants was examined for anti-HBc (IgG) and HBV DNA. Liver biopsy was performed in 35 patients (31.8%), other patients had transient elastography with steatometry and/or a serum FibroMax™ assay (FibroTest+SteatoTest+NashTest).Results. In 85 patients, liver fibrosis was scored F0-F2 with METAVIR, 25 persons had severe fibrosis (F4 in 23, F3 in 2). Patients with severe fibrosis were significantly older than persons with F0-F2 and had more frequent type 2 diabetes. Anti-HBc was detected in 10 of 25 (40%) patients with F3-F4 and in 7 of 85 (8.2%) persons with F0-F2 (p <0.001). None of anti-HBc-positive individuals had HBV DNA in blood. Presence of anti-HBc was the major factor directly associated with severe liver fibrosis (OR 7.339; 95% CI 2.189-24.604; p = 0.001).Conclusion. Anti-HBc-positive patients with NAFLD have a much higher risk of severe liver fibrosis compared to patients without previous viral hepatitis B