Thanks to Kevin and Brayden for presenting a 36yo F with no medical history presenting with acute abdominal pain, nausea, and anorexia. Her AST/ALTs were in the thousands and she was ultimately diagnosed with acute hepatitis A! Incidentally her HB Core Ab came back “borderline…”

AST ALT Elevation

• If AST/ALTs are in the thousands, there are only a few entities that can cause this:
  • Ischemia (shock liver)
  • Toxins (Tylenol is most common), Amanita aka magic mushrooms, herbal supplements (we don’t know what they put in these!)
  • Acute viral hepatitis (HAV, HBV, HCV, HEV, HSV, CMV, VZV, parvovirus)
• Less common:
  • Autoimmune hepatitis
  • Acute Budd Chiari
  • Reactivation HBV, HDV
  • HLH (we seem to see this a lot in this hospital for some reason?)
  • Malignant infiltration
  • HELLP
  • Wilsonian Crisis (severe hemolysis and impending acute liver failure in setting of Wilson’s)
• For acute viral hepatitis, ALT is typically higher than AST.

Hepatitis A

Epidemiology

• Global, 1.4 mil cases per year, can be sporadic or epidemic form
• Fecal oral route, either person-to-person contact or ingestion of contaminated food or water.
• Other risk factors: Sexual transmission (anal/oral sex), day care, consumption of raw or undercooked shellfish, veggies, or eating food prepared by an infected food handler.

Presentation

• Incubation period: 15-50 days, average of 28 days.
• Acute onset N/V, fever, anorexia, abd pain are typical.
• Bilirubinuria, pale stools can also be seen within a few days.
• Jaundice + pruritus. Jaundice peaks within 2 weeks.
• Exam: Jaundice, hepatomegaly, RUQ pain.
• Serum aminotransferases often > 1000 IU/dL, bili typically < 10, alk phos can be nrl to mildly elevated. ALT is commonly higher than AST.
• Kids: Can be asymptomatic.

Diagnosis

• Serum Anti-HAV IgM is diagnostic, detectable at time of symptom onset, remain detectable for 3-6 months after infection.
• Anti-HAV IgG: remain detectable for decades, protective vs future infections. Detection of anti-HAV IgM and IgG reflects past infection or vaccination.

Management

• Primarily supportive, but transfer to a transplant center might be indicated if pt goes into fulminant liver failure (severe acute liver injury with encephalopathy and impaired synthetic function i.e. INR >5 in patients without pre-existing liver disease)
• Report to public health! Fax a confidential morbidity report over to Santa Clara County Department of Public Health
  • https://www.sccgov.org/sites/phd-p/report/Documents/morb-110a.pdf

Vaccination

• Single Antigen inactivated virus: 2 IM doses 6-18 months apart
• Combo HAV and HBV inactivated virus vaccine: Adults only, 0, 1, 6 mo (3 doses total)

Prognosis

• Generally pretty good, less than 1% go into fulminant hepatic failure.
• Risk factors for severe complications: > 50, underlying liver dz
• Other Complications
  • Relapsing hepatitis: Up to to 10% of pts experience a relapse of sx 6 months after the acute episode for ~ < 3 weeks. Multiple relapses can occur. These patients usually make a complete recovery
  • Autoimmune hepatitis: HAV can trigger development of autoimmune hepatitis.
  • Cholestatic hepatitis: Prolonged period of jaundice > 3 months, typically self-resolving

Hepatitis B serologies made ridiculously simple