Hepatitis

Inflammation of the liver due to various causes – most often hepatitis viruses (A, B, C, D, E), but also alcohol, drugs/toxins, or autoimmune disease. It can be acute (resolves <6 months) or chronic (persistent inflammation ≥6 months).

• Hundreds of millions worldwide have chronic hepatitis B or C, leading to cirrhosis and hepatocellular carcinoma (HCC) and over 1 million deaths annually. Differentiating hepatitis types (A–E) is a common clinical and exam challenge. Vaccination (for A and B) and antiviral therapies (for B and C) help prevent these serious outcomes.

• General symptoms of acute hepatitis include fatigue, fever, nausea, jaundice (yellow skin/eyes), dark urine, and right upper quadrant pain. Many cases (especially in children or chronic infections) can be asymptomatic.
• Acute viral hepatitis (e.g. Hepatitis A) typically causes very high AST/ALT elevations (often >1000 U/L) with jaundice, but is usually self-limited. Chronic hepatitis (especially Hep B, C) often has mild or no initial symptoms and may only present later with signs of cirrhosis (e.g. hepatomegaly, spider angiomata).
• Multiple etiologies exist: most commonly viral hepatitis (A, B, C, D, E). Other causes include alcoholic hepatitis (due to chronic alcohol use), drug-induced or toxic hepatitis (e.g. acetaminophen overdose, certain drugs/supplements), and autoimmune hepatitis (immune-mediated liver injury).

1. Use serologies to identify the cause: e.g. IgM anti-HAV confirms acute Hepatitis A; HBsAg (hepatitis B surface antigen) indicates active Hep B infection, and IgM anti-HBc indicates acute HBV (vs IgG anti-HBc in chronic/past); anti-HCV antibody (with HCV RNA) confirms Hep C infection.
2. Assess acute vs chronic: acute hepatitis is defined by <6 months duration (often with IgM antibodies in viral hepatitis), whereas persistence of HBsAg or HCV RNA >6 months indicates chronic infection. Markers of liver function (bilirubin, PT/INR) help gauge severity (acute liver failure if coagulopathy/encephalopathy).
3. Consider other causes if viral tests are negative: review medications and toxins (for drug-induced hepatitis), check autoimmune markers (ANA, anti–smooth muscle antibody, IgG) for autoimmune hepatitis, and evaluate for rare causes (Wilson disease, hemochromatosis, NAFLD, etc.). Imaging (ultrasound) can assess liver anatomy and rule out biliary obstruction.

1. Supportive care is the mainstay for acute hepatitis: rest, adequate hydration, and avoiding hepatotoxins (e.g. alcohol, acetaminophen). Hospitalize if severe symptoms or coagulopathy, and consider transplant evaluation if acute liver failure develops.
2. Chronic viral hepatitis may require antiviral therapy. Chronic HBV is treated with long-term antivirals (e.g. tenofovir or entecavir) to suppress viral replication and slow disease progression. Chronic HCV is treated with direct-acting antivirals, which can cure >95% of cases, eliminating the virus.
3. For autoimmune hepatitis, immunosuppressive therapy (corticosteroids ± azathioprine) induces remission. Alcoholic hepatitis is managed by alcohol cessation (and corticosteroids if severe). Acetaminophen overdose is treated with N-acetylcysteine antidote to prevent fulminant liver failure.
4. Prevention: Vaccines are available for Hepatitis A and B (and Hep E in some regions). Post-exposure prophylaxis can prevent disease (HAV immunoglobulin; HBV vaccine ± HBIG for neonates or needlestick exposures). Safe practices (e.g. clean water, safe sex, not sharing needles) reduce transmission.

• Mnemonic: "Vowels hit your bowels" – Hepatitis A and E are fecal-oral infections (contaminated food or water).
• Hepatitis D is Dependent on Hep B (it's a "defective" virus requiring HBV coinfection).
• Hepatitis C virus has no 3′→5′ proofreading, leading to high mutation rates and no vaccine available.

• Acute hepatitis with signs of acute liver failure (e.g. confusion, encephalopathy, INR >1.5, severe jaundice) indicates fulminant hepatitis – a life-threatening emergency requiring critical care and possible transplant.
• In chronic HBV/HCV patients, onset of decompensated cirrhosis (ascites, variceal bleeding, coagulopathy) is a dire sign – high risk of mortality from liver failure or HCC; such patients need urgent specialized management (e.g. transplant evaluation).

1. Elevated aminotransferases ± jaundice → suspect hepatitis.
2. Order acute viral hepatitis panel: IgM anti-HAV, HBsAg and IgM anti-HBc, and anti-HCV (with reflex HCV RNA).
3. If all viral tests negative, evaluate for non-viral causes: review medications and alcohol use, check autoimmune markers (ANA, SMA, IgG), and consider Wilson disease, etc. as appropriate.
4. Determine if acute vs chronic (duration <6 months vs ≥6 months). Acute infection often shows IgM antibodies and symptomatic presentation; chronic infection if HBsAg or HCV RNA persists >6 months (often with milder symptoms).
5. Initiate management: supportive care for acute cases; if chronic HBV or HCV, refer for antiviral therapy. Admit patients with severe acute hepatitis or any features of liver failure.

• Young adult with recent travel developing acute jaundice, fever, and markedly elevated ALT; positive IgM anti-HAV → Acute Hepatitis A (fecal–oral transmission, self-limited).
• Unvaccinated 30‑year‑old immigrant from an HBV-endemic region, asymptomatic with elevated ALT; tests show HBsAg positive for >6 months and signs of cirrhosis → Chronic Hepatitis B (likely perinatally acquired; high risk of cirrhosis/HCC).
• 55‑year‑old with history of IV drug use and new-onset ascites; AST and ALT mildly elevated, HCV antibody and RNA positive → Chronic Hepatitis C with cirrhosis (blood-borne infection leading to chronic liver disease).