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    Subjects/Medicine/Viral Hepatitis — Clinical
    Viral Hepatitis — Clinical
    medium
    stethoscope Medicine

    A 32-year-old man from rural India presents with jaundice, dark urine, and hepatomegaly. Serology shows anti-HAV IgM positive and elevated transaminases (ALT 2800 U/L). What is the drug of choice for treatment?

    A. Lamivudine
    B. Sofosbuvir
    C. Ribavirin
    D. Supportive care and monitoring

    Explanation

    ## Acute Hepatitis A: Management Strategy **Key Point:** Hepatitis A is a self-limiting viral infection. There is NO specific antiviral drug of choice — management is entirely supportive. ### Why Supportive Care is the Standard Hepatitis A virus (HAV) causes acute hepatitis that resolves spontaneously in >95% of immunocompetent adults within 3–6 months. The immune response (IgM anti-HAV) clears the virus naturally. **High-Yield:** Unlike HBV and HCV, HAV does not cause chronic infection. No antiviral has been shown to shorten the course or improve outcomes in acute HAV infection. ### Management Principles 1. **Bed rest** during acute phase (if symptomatic) 2. **Nutritional support** — avoid hepatotoxic drugs (acetaminophen, alcohol) 3. **Monitor INR and bilirubin** — assess for fulminant hepatic failure (rare) 4. **Fluid and electrolyte balance** 5. **Avoid hepatotoxic medications** **Clinical Pearl:** Fulminant hepatic failure occurs in <0.5% of cases; if it develops, transfer to a transplant centre for possible liver transplantation. ### Why Other Options Are Wrong | Drug | Role in HAV | Reason Not Used | |------|-------------|------------------| | Ribavirin | Broad-spectrum antiviral | No proven benefit in acute HAV; reserved for HCV and some hemorrhagic fevers | | Lamivudine | Nucleoside reverse transcriptase inhibitor | Used for chronic HBV, not HAV | | Sofosbuvir | NS5B polymerase inhibitor | First-line for HCV, not indicated in HAV | **Warning:** Do not mistake the presence of elevated transaminases or positive serology as an indication for antiviral therapy. The high ALT reflects hepatocellular inflammation, which is self-limited. [cite:Harrison 21e Ch 297]

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