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?

Question

Accepted Answer

B. Acute hepatitis A with preserved synthetic function. ## 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]

Answer

A. Autoimmune hepatitis with acute presentation

Answer

C. Acute hepatitis A with fulminant hepatic failure

Answer

D. Chronic hepatitis B with acute exacerbation

Explanation

Clinical Diagnosis: Acute Hepatitis A

Key Clinical Features

Diagnostic Reasoning

Pathophysiology

Why Fulminant Failure Is Not Present Here

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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