A 32-year-old man from rural India presents with jaundice, dark urine, and abdominal pain for 10 days. He reports consuming contaminated water 6 weeks ago. On examination, he is afebrile with hepatomegaly and right upper quadrant tenderness. Laboratory findings show: total bilirubin 8.2 mg/dL, ALT 2840 IU/L, AST 2100 IU/L, alkaline phosphatase 180 IU/L, albumin 3.8 g/dL, PT normal. Serology shows anti-HAV IgM positive, anti-HAV IgG negative. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Acute Hepatitis A ### Key Clinical Features **Key Point:** The combination of acute jaundice, markedly elevated transaminases (ALT > AST), normal PT, and anti-HAV IgM positivity is pathognomonic for acute hepatitis A. ### Serological Interpretation | Marker | Acute HAV | Chronic HAV | Interpretation | |--------|-----------|-------------|----------------| | Anti-HAV IgM | **Positive** | Negative | Active/recent infection | | Anti-HAV IgG | Negative | **Positive** | Past immunity | | HAV RNA | Detectable early | Not detectable | Acute phase | **High-Yield:** Anti-HAV IgM is the diagnostic marker of acute hepatitis A; it appears at symptom onset and persists for 3–6 months. ### Epidemiological Context - **Fecal-oral transmission** via contaminated water (6-week incubation period fits HAV) - Rural India: endemic area for HAV due to poor sanitation - Afebrile presentation is typical (unlike bacterial infections) ### Laboratory Pattern 1. **Transaminitis:** ALT > AST (hepatocellular injury) 2. **Preserved synthetic function:** Normal PT and albumin (acute hepatitis, no cirrhosis) 3. **Cholestasis:** Elevated bilirubin and mild alkaline phosphatase rise 4. **No hemolysis:** Direct hyperbilirubinemia (conjugated) ### Clinical Pearl **Clinical Pearl:** Hepatitis A is self-limited; fulminant hepatic failure occurs in <1% of immunocompetent adults. Prognosis is excellent with supportive care. No chronic sequelae. ### Pathophysiology Acute hepatitis A causes **acute hepatocellular inflammation** with portal tract infiltration by lymphocytes and Kupffer cell hyperplasia. Viral replication in hepatocytes leads to cytolysis and transaminase release. The intact PT indicates preserved hepatic synthetic function, ruling out fulminant failure. [cite:Robbins 10e Ch 18]