2479 Autoimmune Hepatitis Triggered by Hepatitis A: An Interesting Case and Review of Pathophysiology

Abstract

INTRODUCTION: Autoimmune hepatitis (AIH) is an immune-mediated disorder of the liver, whose pathophysiology involves triggering of T-cell mediated events by environmental agents in the liver in a host genetically predisposed to this disease. One trigger described in literature has been the hepatitis A virus (HAV). Hence, occasionally cases which clinically appear to be that of relapsing HAV are in fact concealing underlying autoimmune hepatitis that has been provoked from the initial episode of HAV. We describe one such case. CASE DESCRIPTION/METHODS: A 45 year old Caucasian male with past medical history of chronic hepatitis C and acute hepatitis two months prior to admission was admitted for multifocal pneumonia. During his initial evaluation, the patient was found to have generalized jaundice, and laboratory evaluation revealed elevated transaminases with a hepatocellular pattern. He was initially thought to have reactivation of the hepatitis A, however non-improvement with conservative measures led to further serological testing, which revealed positive anti-smooth muscle antibody. Autoimmune hepatitis was confirmed by biopsy, and patient was started or oral steroids. The patient's clinical status and liver function improved significantly, and he was discharged with outpatient follow-up. DISCUSSION: It is hypothesized that environmental agents trigger T-cell–mediated events directed at liver antigens in a host genetically predisposed to AIH, leading to a progressive necro-inflammatory and fibrotic process in the liver. Studies have shown hepatotropic viruses including HAV to be associated with AIH. Defects in suppressor-inducer T lymphocytes specifically controlling immune responses to the asialoglycoprotein receptor may be the cause of susceptibility. It has also been shown that humoral immune responses to liver cell surface antigens are frequently provoked by hepatitis A and B viruses. Newer research is also exploring molecular mimicry between the infectious particle and the liver constituent as the mechanism, although specific data has not been discovered on HAV. In the setting of the recent outbreaks of HAV, such pathology may become more commonplace. It is important for a clinician to distinguish between relapses of HAV (documented to be between 3-20% of patients in the first 6 months) and onset of AIH, as treatment modalities and prognosis are vastly different. A high level of awareness of this pathology allows for its prompt recognition and the potential for successful treatment.