The diagnosis of viral hepatitis is confirmed by serologic testing (see Table 113-1 and Fig. 113-1). The presence of IgM-specific antibody to HAV with low or absent IgG antibody to HAV is presumptive evidence of HAV. There is no chronic carrier state of HAV. The presence of HBsAg signifies acute or chronic infection with HBV. Antigenemia appears early in the illness and is usually transient but is characteristic of chronic infection. Maternal HBsAg status should always be determined when HBV infection is diagnosed in children younger than 1 year of age because of the likelihood of vertical transmission. Hepatitis B early antigen (HBeAg) appears in the serum with acute HBV. The continued presence of HBsAg and HBeAg in the absence of antibody to e antigen (anti-HBe) indicates high risk of transmissibility that is associated with ongoing viral replication. Clearance of HBsAg from the serum precedes a variable window period followed by the emergence of the antibody to surface antigen (anti-HBs), which indicates development of lifelong immunity and is also a marker of immunization. Antibody to core antigen (anti-HBc) is a useful marker for recognizing HBV infection during the window phase (when HBsAg has disappeared but before the appearance of anti-HBs). Anti-HBe is useful in predicting a low degree of infectivity during the carrier state. Seroconversion after HCV infection may occur 6 months after infection. A positive result of HCV enzyme-linked immunosorbent assay should be confirmed with the more specific recombinant immunoblot assay, which detects antibodies to multiple HCV antigens. Detection of HCV RNA by polymerase chain reaction (PCR) is a sensitive marker for active infection, and results of this test may be positive 3 days after inoculation.
Many other viruses may cause hepatitis as part of systemic infection, including Epstein-Barr virus, cytomegalovirus, varicella zoster virus (chickenpox), herpes simplex virus, and adenoviruses. Bacterial infections that may cause hepatitis include Escherichia coli sepsis and leptospirosis. Patients with cholecystitis, cholangitis, and choledocholithiasis may present with acute symptoms and jaundice. Other causes of acute liver disease in childhood include drugs (isoniazid, phenytoin, valproic acid, carbamazepine, oral contraceptives, acetaminophen), toxins (ethanol, poisonous mushroom), Wilson disease, metabolic disease (galactosemia, tyrosinemia), α1-antitrypsin deficiency, tumor, shock, anoxia, and graft-versus-host disease (see Chapter 130).
The treatment of acute hepatitis is largely supportive andinvolves rest, hydration, and adequate nutrition. Hospitalizationis indicated for persons with severe vomiting and dehydration,a prolonged prothrombin time, or signs of hepatic encephalopathy. When the diagnosis of viral hepatitis is established, attention should be directed toward preventing its spread to closecontacts. For HAV, hygienic measures include hand washingand careful disposal of excreta, contaminated diapers or clothing, needles, and other blood-contaminated items.
Chronic HBV infection may be treated with interferon alfa-2b or lamivudine, and HCV may be treated with interferon alfa alone or usually in combination with ribavirin. Mostly adults experience these treatment regimens. The decision to treat is based on the patient’s current age, age at HBV acquisition, development of viral mutations during therapy, and stage of viral infection. Transmission of HBV by vertical transmission or infection early in life often results in chronic HBV infection in an immune tolerant phase, in which interferon usually is not effective.