Gastroenterology · Viral Hepatitis
The facts most likely to be tested
Hepatitis A virus is a non-enveloped, single-stranded RNA picornavirus transmitted primarily via the fecal-oral route.
Clinical presentation typically involves abrupt onset of fever, jaundice, hepatomegaly, and elevated aminotransferases following a period of travel to endemic areas or consumption of contaminated shellfish.
The diagnosis of acute infection is confirmed by the presence of anti-HAV IgM antibodies in the serum.
Hepatitis A infection is self-limiting and does not progress to chronic hepatitis, cirrhosis, or hepatocellular carcinoma.
Post-exposure prophylaxis for close contacts consists of the Hepatitis A vaccine or immune globulin administered within two weeks of exposure.
The Hepatitis A vaccine is recommended for all children at age 1 year, as well as adults with chronic liver disease, men who have sex with men, or those traveling to endemic regions.
Patients with acute Hepatitis A should be advised to avoid acetaminophen and alcohol to prevent further drug-induced liver injury.
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A 28-year-old male presents to the urgent care clinic with a 5-day history of fatigue, nausea, and dark-colored urine. He recently returned from a two-week backpacking trip in rural Southeast Asia where he consumed local street food. Physical examination reveals scleral icterus and right upper quadrant tenderness. Laboratory studies demonstrate an ALT of 1,200 U/L, an AST of 950 U/L, and a total bilirubin of 4.5 mg/dL.
Which of the following serologic markers is most likely to be positive in this patient?
Anti-HAV IgM
The patient's clinical presentation of acute hepatitis following travel to an endemic area is classic for Hepatitis A, which is confirmed by the presence of IgM antibodies against the virus.
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Etiology / Epidemiology
Fecal-oral transmission via contaminated food/water or close contact. High risk in international travelers and daycare settings.
Clinical Manifestations
Abrupt onset of prodromal fever, malaise, and jaundice. Look for hepatomegaly and dark urine.
Diagnosis
Diagnosis confirmed by IgM anti-HAV antibodies. Elevated ALT/AST > 1000 IU/L is classic.
Treatment
Management is supportive care. Avoid hepatotoxins like alcohol and acetaminophen.
Prognosis
Self-limiting disease with 0% chronicity. Rare risk of fulminant hepatic failure.
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Epidemiology & Etiology
Caused by the HAV virus, a non-enveloped RNA virus. Primarily transmitted via the fecal-oral route in areas with poor sanitation. Outbreaks are frequently linked to contaminated shellfish or infected food handlers.
Pertinent Anatomy
The virus targets hepatocytes in the liver. Inflammation leads to portal triad infiltration and subsequent cholestasis.
Pathophysiology
Following ingestion, the virus replicates in the liver and is excreted in bile. The host immune response, specifically CD8+ T-cell activation, causes hepatocellular injury. This results in the classic icteric phase of clinical illness.
Clinical Manifestations
Patients present with an abrupt onset of fever, nausea, and right upper quadrant pain. Physical exam reveals jaundice, hepatomegaly, and clay-colored stools. Fulminant hepatic failure is a rare but life-threatening complication characterized by encephalopathy and coagulopathy.
Diagnosis
The gold standard for acute infection is IgM anti-HAV. Total anti-HAV (IgG) indicates prior exposure or vaccination. Liver enzymes typically show ALT/AST > 1000 IU/L with a predominance of ALT.
Treatment
Treatment is strictly supportive care with hydration and rest. Avoid hepatotoxins including alcohol and acetaminophen. Post-exposure prophylaxis with HAV vaccine or immune globulin is indicated for close contacts within 2 weeks.
Prognosis
The disease is self-limiting and does not progress to a chronic state. 100% recovery is expected in the vast majority of patients. Monitor for signs of acute liver failure such as rising INR or altered mental status.
Differential Diagnosis
Hepatitis B: presence of HBsAg and anti-HBc
Hepatitis C: usually asymptomatic, anti-HCV positive
Choledocholithiasis: elevated alkaline phosphatase and dilated bile ducts
Drug-induced liver injury: history of recent medication change
Autoimmune hepatitis: elevated ANA or anti-smooth muscle antibodies