Autoimmune hepatitis developed after acute liver failure due to hepatitis A. A case-report

Introduction and Objectives

In this report, the relationship between Hepatitis A Virus (HAV) and Autoimmune Hepatitis (HAI) will be analyzed, demonstrating the presence of HAI after an acute HAV infection, highlighting the time between diagnoses and seroconversion with antibodies, as well as clinical characteristics and evolution.

Materials and Patients

30-year-old male patient, with no personal pathological history who presents with general malaise, fever and jaundice. The clinical examination was within normal limits except for slight jaundice. The admission biochemical analyzes were as follows: Hb 14.2 g/dL, Leukocytes 8,550 /mm3, Total bilirubin 9.5 mg/dL Direct bilirubin 2.2 mg/, ALT 6155 UI/L, AST 3940 UI/L, Alkaline Phosphatase 1 15U /L. and Prothrombin time 51.0 seconds; INR 4.95. a viral hepatitis profile with positive anti-HAV IgM antibodies and an imaging examination of the liver and bile ducts with inflammatory changes. The diagnosis of hepatitis A and acute liver failure was made.

The patient suffers rapid clinical and biochemical deterioration, with multiple organ failure requiring admission to an intensive care unit and advanced life management area due to acute respiratory failure syndrome, general support stockings and three sessions of single-step albumin dialysis were indicated. He showed stabilization and improvement in his general condition.

Results

27 days after initial evaluation, fatigue and fever of unknown origin were present. Liver function test with BT 25.58 mg/dl, BD 17.55.0 mg/dl, ALT 38 U/l, AST 100 U/l and ALP 105 U/l and INR 1.5. He presented positive antinuclear antibodies with a cytoplasmic pattern with a titer of 1:80, SMOOTH MUSCLE 3+ intermediate filament pattern. DILUTION 1:80 immunoglobulin G 3260 mg/dl. A liver biopsy was performed, which showed changes compatible with autoimmune hepatitis (fig. 1). In the previous context, the diagnosis of autoimmune hepatitis triggered by HAV was made and treatment was started with prednisone 50 mg every 24 hours PO in a reduced dose of azathioprine 50 mg every 24 hours. At one month of follow-up, PFH was found to have decreased and the established treatment continued.

Conclusions

Atypical courses of hepatitis A virus infection have a global prevalence of 7(1). Some case reports of HAI indicate that viruses that cause acute hepatitis, such as hepatitis A virus (HAV), hepatitis of hepatitis B (HBV) and Epstein-Barr virus, can trigger HAY (2) studies suggest a deficiency of suppressor T cells specific for the asialoglycoprotein receptor that would be involved in immunological abnormalities, including antigen presentations, were involved in the appearance of HAI after acute HA.(3)

Failure to normalize liver tests after OAB should raise concern for HAI, particularly in those with seroconversion to SMA positivity. (4) always having cholestasis that could arise after an acute episode of HAV infection.