From Hepatitis E to Autoimmune Hepatitis: Aftermath of a trip to Qatar

• Published in: Annals of hepatology Vol. 29; p. 101448
• Main Authors: Duran-Azamar, Pamela, Martínez-Pérez, Genesis P., Cano-Contreras, Ana D., Grube-Pagola, Peter, Amezcua-Toledo, Luis A., Troche, José M. Remes
• Format: Journal Article
• Language: English
• Published: Elsevier España, S.L.U 01.02.2024; Elsevier
• Subjects: Gastroenterology and Hepatology
• ISSN: 1665-2681; 2659-5982
• DOI: 10.1016/j.aohep.2024.101448

Autoimmune hepatitis (AIH) is a chronic immune-mediated disease with an estimated frequency of 11 to 25 subjects per 100 000 population. It has been reported that viral hepatitis can be a trigger for chronic active hepatitis with AIH criteria. Hepatitis E virus is infrequent in our environment, but it is recognized as the cause of about 20 million new infections per year, being described in case reports as a triggering factor of AIH. We present the case of a 39-year-old woman who debuts with jaundice and general condition attack, this, 20 days after her return from Qatar, referring to have consumed raw meat during her stay, denying chronic degenerative history, alcohol and drug consumption. Liver function tests showed changes with R factor >5 compatible with hepatocellular pattern, liver ultrasound showed no liver or biliary changes. AgsVHB (-), HCV (-), VHA IgG (+), IgM (-), AC VHE IgG (-), IgM (+), immunoglobulins IgA 342, IgG 1777 U, IgM 97 U, negative ANA, AML, AMA, anti-LKM-1 antibodies were reported, which was considered probable acute hepatitis E. Cholangioresonance was performed due to the increase in bilirubin at the expense of direct bilirubin, confirming the absence of biliary tract changes. The patient was stable for 4 weeks with clinical improvement and a gradual decrease in bilirubin and transaminases, without evidence of liver damage or encephalopathy. After this period, the patient presented again with an abrupt rise in transaminases of more than 20 times the LSN. In view of these findings, an ultrasound-guided liver biopsy was performed. The histopathological report was consistent with autoimmune hepatitis, and treatment with prednisone and azathioprine was initiated, to which the patient responded favourably. The patient is currently asymptomatic and stable. It is important to consider that acute hepatitis due to HEV is increasingly recognised, although sometimes misdiagnosed and confused with other liver diseases. It is also important to highlight that autoimmune diseases may be preceded by a viral infection due to an inadequate immune response, which forces us to highlight liver biopsy as a useful tool when serological markers are insufficient.