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Acute viral hepatitis is a systemic infection predominantly affecting the liver. Clinically characterized by malaise, nausea, vomiting, diarrhea, and low-grade fever followed by dark urine, jaundice, and tender hepatomegaly; may be subclinical and detected on basis of elevated aspartate and alanine aminotransferase (AST and ALT) levels. Hepatitis B may be associated with immune-complex phenomena, including arthritis, serum sickness-like illness, glomerulonephritis, and a polyarteritis nodosa–like vasculitis. Hepatitis-like illnesses may be caused not only by hepatotropic viruses (A, B, C, D, E) but also by other viruses (Epstein-Barr, CMV, coxsackievirus, etc.), alcohol, drugs, hypotension and ischemia, and biliary tract disease (Table 163-1).



27-nm picornavirus (hepatovirus) with single-stranded RNA genome.

Clinical Course

FIGURE 163-1

Scheme of typical clinical and laboratory features of HAV.


Recovery within 6–12 months, usually with no clinical sequelae; a small proportion will have one or two apparent clinical and serologic relapses; in some cases, pronounced cholestasis suggesting biliary obstruction may occur; rare fatalities (fulminant hepatitis), no chronic carrier state.


IgM anti-HAV in acute or early convalescent serum sample.


Fecal-oral transmission; endemic in underdeveloped countries; food-borne and waterborne epidemics; outbreaks in day-care centers, residential institutions.


After exposure: immune globulin 0.02 mL/kg IM within 2 weeks to household and institutional contacts (not casual contacts at work). Before exposure: inactivated HAV vaccine 1 mL IM (unit dose depends on formulation); half dose to children; repeat at 6–12 months; target travelers, military ...

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