title: Fulminant hepatitis due to HBV/HDV coinfection.
abstract: The diagnosis of acute viral hepatitis is based on a thorough history (with a detailed review of possible modes of transmission), consistent physical findings (in which stigmata of chronic liver disease are absent), and laboratory tests confirming the presence of acute hepatocyte damage. Specific etiologic entities can be identified by serologic testing. In some cases, infection by more than one hepatitis virus may be revealed. The occurrence of HBV/HDV coinfection may lead to typical, uncomplicated acute hepatitis. In some patients, however, the development of a prolonged prothrombin time and encephalopathy indicates the presence of fulminant disease. The management of patients with such disease usually requires admission to an intensive care unit in order to increase the likelihood that complications will be recognized at an early stage, when intervention might make a difference. Standard interventions include vigorous treatment of hypoglycemia, attention to electrolyte and acid-base disturbances, and antibiotic therapy for bacterial sepsis. Despite aggressive management by experienced teams, fatality rates remain exceedingly high: As many as 75% to 100% of patients with severe encephalopathy die. Liver transplantation has been attempted in a number of cases. Its role remains ambiguous. Survival rates of 50% to 60% have been reported, but selection bias may turn out to have contributed to this apparently favorable outcome. In the patient under discussion, results of a follow-up physical two months after discharge were entirely normal. Liver chemistries were within normal limits, but a test for HBsAg was still positive. During the course of the examination, the patient admitted to having accidentally pricked his skin nearly two months before the onset of his illness while holding a needle that a friend had used for the intravenous injection of heroin. One year later, HBsAg was no longer detectable, but tests for anti-HBc and anti-HBs were both positive. The anti-HBc positivity was attributable to IgG rather than IgG anti-HBc. A test for anti-HDV was negative.
mesh_terms: D000208:Acute Disease; D000328:Adult; D006508:Hepatitis Antibodies / Q000032:analysis; D006509:Hepatitis B / Q000150:complications* / Q000175:diagnosis / Q000276:immunology / Q000628:therapy; D006510:Hepatitis B Antibodies / Q000032:analysis; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D003699:Hepatitis D / Q000150:complications* / Q000175:diagnosis / Q000276:immunology / Q000628:therapy; D003698:Hepatitis Delta Virus / Q000276:immunology; D006801:Humans; D008297:Male
chemical_list: D006508:Hepatitis Antibodies; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens