Immune-mediated hepatitis with the Moderna vaccine
Immune-mediated hepatitis secondary to #COVIDVaccination (Moderna):
https://www.journal-of-hepatology.eu/article/S0168-8278(21)02093-6/fulltext
"Long-term follow up of identified individuals will be essential in determining the prognosis of this immune-mediated liver injury."Immune-mediated hepatitis with the Moderna vaccine, no longer a coincidence but confirmed.
Published:October 04, 2021DOI:https://doi.org/10.1016/j.jhep.2021.09.031
Case description
47-year-old Caucasian man, previously completely well, received 1st Moderna vaccine dose on the 26 April 2021. He noted malaise and jaundice three days after. Investigations on the 30th April showed serum bilirubin 190 μmol/L (normal 0-20), ALT 1048 U/L (normal 10-49), ALP 229 U/L (normal 30-130), albumin 41 g/L (normal 35-50). Blood count, renal function and INR were normal. Liver function tests (LFTs) last checked 4 years previously were normal. He denied paracetamol use and reported minimal alcohol intake. Ultrasound scan, CT thorax, abdomen and pelvis and MRI pancreas performed to exclude malignancy, showed no significant findings. Serum IgG was raised at 25.1 g/L (normal 6-16), IgM 2.2 g/L(0.5-2) and serum was positive for Anti-Nuclear Antibody. Serological tests for HAV, HBV, HCV, HEV, EBV and CMV were negative.
His jaundice faded and LFTs improved: bilirubin falling on 25th June to 69 μmol/L and ALT to 332 U/L. The patient received his 2nd Moderna vaccine dose on the 6 July 2021 (despite reporting the jaundice to the vaccination centre) and the jaundice returned a few days after. Blood tests on 20th July found bilirubin 355 μmol/L, ALT 1084 U/L and a raised PT 18.4 seconds. After liver biopsy on the 21st July 2021 he was commenced onto Prednisolone 40 mg/day and was transferred to our service.
On examination, he was alert, deeply jaundiced, with hepatomegaly but no ascites. Repeat abdominal ultrasound showed a mildly fatty liver, patent portal and hepatic vein flow, with no ascites. Review of the liver biopsy showed acute active hepatitis: widespread areas of bridging necrosis, marked interface hepatitis, lymphoplasmatic inflammation including eosinophils, ballooned hepatocytes, multi-nucleated giant cells, and emperipolesis (Figure 1). There was minimal fibrosis, Ishak stage 1. The pattern of injury on histology was consistent with acute hepatitis, with features of autoimmune hepatitis or possible drug-induced liver injury (DILI), triggering an autoimmune-like hepatitis.
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