A 32-year-old man from rural Maharashtra presents with jaundice, dark urine, and abdominal discomfort for 10 days. He reports consuming contaminated water from a local well 4 weeks ago. On examination, he is afebrile with mild hepatomegaly. Laboratory investigations show: ALT 1200 IU/L, AST 980 IU/L, total bilirubin 8.2 mg/dL, alkaline phosphatase 180 IU/L, albumin 3.8 g/dL, PT-INR 1.1. Anti-HAV IgM is positive; anti-HBc and anti-HCV are negative. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Acute Hepatitis A ### Key Clinical Features **Key Point:** This patient has acute hepatitis A with preserved hepatic synthetic function, as evidenced by normal PT-INR (1.1) and adequate albumin (3.8 g/dL). ### Diagnostic Reasoning | Feature | Finding | Significance | |---------|---------|---------------| | **Epidemiology** | Rural water exposure, 4-week incubation | Classic HAV transmission | | **Serology** | Anti-HAV IgM positive | Acute HAV infection | | **Transaminases** | ALT 1200, AST 980 (markedly elevated) | Hepatocellular necrosis | | **Bilirubin** | 8.2 mg/dL (conjugated predominant) | Cholestasis from inflammation | | **Synthetic function** | PT-INR 1.1, albumin 3.8 | **Preserved** — no fulminant failure | | **Negative serology** | Anti-HBc, anti-HCV negative | Rules out B and C | **High-Yield:** Fulminant hepatic failure in acute HAV is rare (~0.1–0.4% in immunocompetent adults) and presents with coagulopathy (PT-INR >1.5) and encephalopathy. This patient has neither. ### Pathophysiology Hepatitis A causes acute hepatocellular inflammation and necrosis via direct viral cytotoxicity and immune-mediated injury. Unlike HBV and HCV, HAV does not cause chronic infection; recovery is complete in >95% of immunocompetent hosts. **Clinical Pearl:** The waterborne epidemiology, acute presentation with preserved synthetic function, and positive anti-HAV IgM in the setting of negative HBc and HCV serology make acute hepatitis A the diagnosis. The normal PT-INR excludes fulminant failure. ### Why Fulminant Failure Is Not Present Here 1. PT-INR is normal (1.1) — coagulopathy absent 2. No mention of encephalopathy or altered mental status 3. Albumin is maintained at 3.8 g/dL [cite:Robbins 10e Ch 18]