S2954 COVID-19 Infection as a Trigger for Seronegative Autoimmune Hepatitis: A Case Report

Abstract

Introduction: Autoimmune hepatitis (AIH) is an immune-mediated liver disease that commonly develops in a genetically predisposed patient after exposure to an environmental trigger. These triggers include viruses, immunization and drugs. Both COVID-19 infection and vaccination have been linked to the development of AIH. Case Description/Methods: A 58-year-old male patient, known to have vitiligo and mild rheumatic mitral stenosis presented to our hospital complaining of flu-like symptoms. The patient denied any history of alcohol intake, substance abuse, over-the-counter or herbal medications, or family history of liver or autoimmune disease. His chronic medications included aspirin and bisoprolol. He tested positive for COVID-19 PCR, so he was admitted for observation. Chest X-ray showed no abnormality, and he was not started on any medication. His laboratory investigations (Table 1) were remarkable for ALT of 271 and AST of 175 U/L. During hospitalization, liver enzymes were trending down but remained elevated. The hepatitis workup (Table 1) was notable for an elevated IgG level of 16.9 g/l (normal range 7-16). His radiological investigations included US abdomen that revealed mildly increased echotexture, MRI liver that was only remarkable for tiny cyst 2 mm, and liver elastography that showed a stiffness average of 5.77 kPa indicating mild stiffness. The patient was offered a liver biopsy, but he was reluctant. During follow-up, his LFTs remained elevated but were fluctuating (Figure 1a). On week 31, he finally agreed for liver biopsy that showed moderate interface and portal tract inflammatory cell infiltrate composed mainly of lymphocytes with occasional eosinophils (Figure 1b,c). The histopathological findings were suggestive of AIH. On week 34, he was started on prednisone 40 mg. LFTs on week 36 were completely normal. The prednisone was tapered over the following two months. Six months later, repeat LFTs were also normal. Discussion: Our patient had an elevation of LFTs after COVID-19 infection that persisted for weeks and promptly responded to steroids therapy. Drug-induced liver injury was less likely as he didn’t receive any hepatotoxic medications prior to or during his hospitalization. In our patient, the Revised Original Score for Autoimmune Hepatitis (AIH) was 17, indicating definite AIH. The proposed mechanism of AIH development after COVID-19 infection is the molecular mimicry between spike protein S1 and multiple human tissue proteins. More studies are needed to examine this association.Figure 1.: a: Trend of LFTs over time. b,c: histopathological images showing interface and portal tract inflammation. Abbreviations alphabetically: Bx: biopsy - d/c: discharge - Dx: diagnosis - f/u: followup - Rx: treatment Table 1. - shows extensive hepatitis workup Laboratory test result Reference ALT 271 0-40 U/L AST 175 0-37 U/L ALP 38.9 40-129 U/L Antinuclear ab Negative Negative Anti Mitochondrial ab Negative Negative Anti Mitochondrial M2 ab Negative Negative Anti Smooth Muscle ab Negative Negative Anti Liver Kidney Microsomes Negative Negative Hepatitis B Core ab Reactive non-reactive Hepatitis B Core Ab IgM non-reactive non-reactive Hepatitis B Surface Antigen Non-reactive Non-reactive Hepatitis B e Ab Non-reactive Non-reactive Hepatitis B e Antigen Non-reactive Non-reactive Hepatitis A Ab IgM Non-reactive Non-reactive Hepatitis C Ab Non-reactive Non-reactive Hepatitis E IgG Reactive Non-reactive Hepatitis E IgM Non-reactive Non-reactive Herpes Simplex virus Ab IgM Non-reactive Non-reactive Parvovirus Ab IgM Non-reactive Non-reactive Alpha-1 anti-trypsin 37 20-53 µmol/L Ceruloplasmin 33 14 to 40 mg/dL CMV PCR Negative Negative EBV PCR Negative Negative HBV PCR Negative Negative