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Increased Incidence of Fulminant Hepatic Failure in Previously Unrecognized HBsAg Carriers with Acute Hepatitis Independent of Etiology

  • Clinical and Epidemiological Study
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Abstract

Background:

Previous studies have shown a high risk of fulminant hepatitis in HBsAg carriers with acute hepatitis. The etiology of acute hepatitis in HBsAg carriers was heterogeneous. This study aimed to correlate the incidence of fulminant hepatitis with the etiology in HBsAg carriers with acute hepatitis.

Patients and Methods:

The incidence of fulminant hepatitis was studied in 334 adults hospitalized for overt acute viral hepatitis. There were 12 patients with acute hepatitis A, 17 with acute hepatitis B, 70 with acute hepatitis C, five with acute hepatitis E, 53 with acute hepatitis non-A-E, and 177 previously unrecognized HBsAg carriers with acute hepatitis (patients who were positive for HBsAg but negative for IgM antibody against hepatitis B core antigen). Of the latter, 64 (36%) had serological evidence of non-B hepatotropic virus superinfection.

Results:

The incidence of fulminant hepatitis was 3.2% (5/157) in patients with acute hepatitis A, B, C, E or non-A-E, and 20.3% (36/177) in HBsAg carriers with acute hepatitis (p < 0.001). HBsAg carriers were at a 9-fold increased risk of fulminant hepatitis than noncarriers. Among HBsAg carriers with acute hepatitis, the incidence of fulminant hepatitis showed no significant difference between patients with viral superinfection (23% or 15/64) and those without (19% or 21/113). The incidence of fulminant hepatitis in HBsAg carriers with viral superinfection also showed no significant difference between different etiologies of virus superinfection.

Conclusion:

There is a 9-fold increased risk of fulminant hepatitis in HBsAg carriers with acute hepatitis, independent of the underlying etiology.

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Correspondence to C. M. Chu.

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Chu, C.M., Liaw, Y.F. Increased Incidence of Fulminant Hepatic Failure in Previously Unrecognized HBsAg Carriers with Acute Hepatitis Independent of Etiology. Infection 33, 136–139 (2005). https://doi.org/10.1007/s15010-005-4094-4

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  • DOI: https://doi.org/10.1007/s15010-005-4094-4

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