Covid-19-vaccine-pfizer-biontech

Author Information

An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 61-year-old woman developed autoimmune hepatitis (AIH) following administration of COVID-19-Vaccine-Pfizer-BioNTech for COVID-19 immunisation.

The woman presented with fatigue, malaise, nausea, anorexia and yellow eyes for 2 weeks. She had been receiving valsartan for hypertension and levothyroxine for Hashimoto's thyroiditis. Eight months previously, she had COVID-19 with mild symptoms. About a month prior to presentation, she had received COVID-19-Vaccine-Pfizer-BioNTech [Pfizer/BioNTech BNT162b2 mRNA vaccine; route and dose not stated]. Physical examination showed jaundice throughout the body, predominantly in the sclera. The abdominal examination revealed no defense or tenderness, with non-palpable liver and spleen. Laboratory tests showed increased ALT, AST, gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), total bilirubin and direct bilirubin. She tested negative for hepatitis A, B, C, Epstein-Barr virus and cytomegalovirus serology. Serum copper and ceruloplasmin levels were within the normal range. She tested positive for antinuclear antibody (ANA) and anti-smooth muscle antibody (ASMA). The immunoglobulin G level was increased. Ultrasound revealed a normal liver size, with a homogeneous parenchymal echo pattern. The gallbladder was filled with several millimetric stones. The common bile duct and intrahepatic biliary tract were normal. No thrombus was detected in the splenic vein and portal vein. The magnetic resonance cholangiopancreatography (MRCPI) revealed that the bile ducts were of normal diameter, without stone or sludge. The abdominal CT scan revealed no space-occupying formation. A percutaneous liver biopsy showed narrow sinusoids and lymphocyte infiltration, severe portal and periportal lymphocyte infiltration, periseptal interface hepatitis, 4–5 spotty necrosis in each high magnification field of view, and limiting plate disorder, without confluent necrosis. Masson's trichrome staining showed mild fibrosis. Her Ishak histological activity index was 10/18 and fibrosis score was stage 2/6. The simplified autoimmune hepatitis score was 7. She was diagnosed with AIH.

The woman's treatment was started with oral prednisolone. After 14 days, azathioprine was started as steroid-sparing therapy. On the 35th day of the treatment, she did not have any complaints, with resolution of icterus. Her laboratory results were normal except for mildly elevated transaminase and bilirubin levels. She continued prednisolone and azathioprine. Based on the absence of a history of hepatotoxic drug use for liver disease, a history of Hashimoto's disease, negative viral serology, biochemical/histopathological findings compatible with AIH, simplified AIH score and good response to immunosuppressive treatment, the AIH was attributed to COVID-19-Vaccine-Pfizer-BioNTech. However, the possibility of the presence of an underlying silent autoimmune hepatitis could not be ruled out.