False positive anti-hepatitis A virus immunoglobulin M in autoimmune hepatitis/primary biliary cholangitis overlap syndrome: A case report

Abstract

BACKGROUND

Autoimmune hepatitis (AIH) is an immune-mediated liver disease affecting all age groups. Associations between hepatitis A virus (HAV) and AIH have been described for many years. Herein, we report a case of an AIH/primary biliary cholangitis (PBC) overlap syndrome with anti-HAV immunoglobulin M (IgM) false positivity.

CASE SUMMARY

A 55-year-old man was admitted with manifestations of anorexia and jaundice along with weakness. He had marked transaminitis and hyperbilirubinemia. Viral serology was positive for HAV IgM and negative for others. Autoantibody screening was positive for anti-mitochondria antibody but negative for others. Abdominal ultrasound imaging was normal. He was diagnosed with acute hepatitis A. After symptomatic treatment, liver function tests gradually recovered. Several months later, his anti-HAV IgM positivity persisted and transaminase and bilirubin levels were also more than 10 times above of the upper limit of normal. Liver histology was prominent, and HAV RNA was negative. Therefore, AIH/primary biliary cholangitis (PBC) overlap syndrome diagnosis was made based on the “Paris Criteria”. The patient was successfully treated by immunosuppression.

CONCLUSION

This case highlights that autoimmune diseases or chronic or acute infections, may cause a false-positive anti-HAV IgM result because of cross-reacting antibodies. Therefore, the detection of IgM should not be the only method for the diagnosis of acute HAV infection. HAV nucleic acid amplification tests should be employed to confirm the diagnosis.

Keywords: Autoimmune hepatitis, Primary biliary cholangitis, Hepatitis A virus, Case report

Core Tip: Autoimmune hepatitis (AIH)/primary biliary cholangitis (PBC) overlap syndrome is the specific clinical manifestation of AIH, which is an immune-mediated liver disease. Environmental factors including viral infections have been documented to externally trigger AIH. The association between hepatitis A virus (HAV) and AIH has been described for many years. But relying solely on anti- HAV immunoglobulin M (IgM) to diagnose acute HAV infection is not adequate. This case highlights that false-positive anti-HAV IgM might be caused by the cross-reaction of antibodies in individuals with autoimmune diseases or chronic or acute infections. HAV nucleic acid amplification can be used more broadly during the diagnosis workup to confirm HAV infection, especially in patients testing positive for anti-HAV IgM with a low cutoff value.