Hepatitis A-Induced Fulminant Hepatic Failure Linked to Autoimmune Hepatitis in a Child Amidst Diagnostic Challenges of Dengue and Malaria.

Hepatitis A virus (HAV) typically causes a self-limiting illness in children. Rarely, it can progress to fulminant hepatic failure (FHF), and even less commonly, may be followed by features suggestive of autoimmune hepatitis (AIH). The diagnostic overlap can be particularly challenging in tropical regions, where endemic infections such as dengue and malaria may present with similar clinical features. We report a previously healthy five-year-old girl who presented with a four-day history of high-grade fever, abdominal pain, vomiting and lethargy. Examination revealed pallor, icterus, hepatosplenomegaly, and right-sided pleural effusion. Initial investigations showed thrombocytopenia, leukopenia, and ascites, prompting a provisional diagnosis of dengue hemorrhagic fever. However, dengue serology was negative. Further workup revealed HAV IgM positivity and Plasmodium vivax parasitemia. Her condition worsened with bilateral pleural effusions and altered mental status, consistent with mild hepatic encephalopathy. She was managed conservatively without liver transplantation using intravenous antibiotics, oral antimalarials, lactulose, rifaximin, and transfusional support. Clinical stabilisation was achieved, and she was discharged. Persistent transaminitis on follow-up prompted further evaluation, revealing antinuclear antibody (ANA) positivity (1:320, speckled), suggestive of evolving type 1 AIH. Oral corticosteroid therapy was initiated, leading to a favourable response. She continues on outpatient follow-up with improving liver function. While definitive confirmation of AIH was limited by the absence of serum IgG, smooth muscle antibody (SMA), and liver biopsy, the findings were suggestive of an evolving autoimmune process. This case highlights the diagnostic pitfalls in co-endemic regions and underscores the importance of re-evaluating children with persistently elevated liver enzymes following acute viral hepatitis.