could be attributed to hepatitis C infection. 5 Rarely, acute Patients presenting with clinical and laboratory feahepatitis E has been identified among U.S. or European patures consistent with a diagnosis of acute non-A, non-B tients with a history of recent travel to underdeveloped counhepatitis were evaluated for evidence of hepatitis C or tries. 6 Indeed, because first generation anti-HCV tests were hepatitis E infection and for evidence of severe or profrequently negative early in the course of hepatitis C infection longed disease. Antibody to hepatitis C virus (anti-HCV)
and anti-HEV testing was not widely available, it seemed was detected in 75 of 108 (69%) patients, antibody to heppossible that nearly all cases of acute hepatitis in the U.S. atitis E virus (anti-HEV) in three patients (3%), and neicould be attributed to one of the known hepatitis viruses. 7 ther antibody in 31 (29%) patients. One patient had both However, analysis of fulminant or subfulminant acute nonanti-HCV and anti-HEV. HCV RNA was not detected in A, non-B hepatitis at numerous institutions in the U.S. and sera from any of 20 patients with seronegative (non-Europe has suggested that the majority of such cases cannot ABCDE) hepatitis, but in all 10 patients with anti-HCV be attributed to hepatitis A, B, C, D, or E virus infections who were tested by polymerase chain reaction (PCR).
(non-ABCDE). [8][9][10][11][12][13] In addition, acute non-A, non-B hepatitis Compared with patients with acute hepatitis C, those complicated by development of aplastic anemia is not associwith non-ABCDE hepatitis had a lower incidence of parated with evidence of hepatitis C infection. 14 More recently, enteral risk factors (6% vs. 70%; P Γ΅ .001), higher peak an additional flavivirus associated with human hepatitis has serum bilirubin levels (45% vs. 5% with peak levels ΓΊ15 been identified, [15][16][17] but this agent has been detected in only mg/dL; P Γ΅ .001), more prolonged jaundice (25% vs. 0% a small fraction of cases of acute non-A, non-B hepatitis. 17 with peak bilirubin ΓΊ5 weeks after onset; P Γ΅ .01), more
Previous reports of non-ABCDE hepatitis in the U.S. have severe prothrombin time abnormalities (26% vs. 0% with focused on populations of patients with unique or severe com-ΓΊ3 second prolongation; P Γ΅ .001), more severe hypoalplications of acute non-A, non-B hepatitis seen in tertiary buminemia (39% vs. 9% with albumin Γ΅3 g/dL; P Γ΅ .01), care referral centers. 4,8,11,13,14 Because adult liver transand more frequent major clinical complications (13% vs.
plantation is not performed in any of the hospitals within 0% with encephalopathy; P Γ΅ .01; 10% vs. 0% with death our university medical center, the vast majority of patients or transplant; P Γ
.024). Patients with acute non-ABCDE with acute hepatitis that are seen are either self-referred or hepatitis were less likely to develop chronic hepatitis referred from primary care physicians within our own instituthan those with acute hepatitis C (23% vs. 68%; P Γ΅ .05).
tion and few have developed acute liver failure or other com-Thus, patients with acute non-ABCDE hepatitis are epiplications before initial referral. The present study was dedemiologically distinct from those with acute hepatitis signed to determine the cause and characterize the clinical C and have a significantly more severe acute illness.
course of acute non-A, non-B hepatitis among this population (HEPATOLOGY 1997;25:478-483.) of patients.
For more than a decade before the identification of the
PATIENTS AND METHODS
hepatitis C virus (HCV) and hepatitis E virus (HEV), a signif-