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Hepatitis B Virus DNA in Fulminant Hepatitis B

KEVIN M. DE COCK, M.D., M.R.C.P., D.T.M.&H.; SUGANTHA GOVINDARAJAN, M.D.; BOONTAR VALINLUCK, B.S.; and ALLAN G. REDEKER, M.D.
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▸Correspondence should be addressed to Kevin M. De Cock, MD.; Special Pathogens Branch, Division of Viral Diseases, Centers for Disease Control, 1600 Clifton Road, N.E.; Atlanta, GA 30333. Reprints are not available.


University of Southern California Liver Unit, Rancho Los Amigos Medical Center; Downey, California.


Ann Intern Med. 1986;105(4):546-547. doi:10.7326/0003-4819-105-4-546
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This excerpt has been provided in the absence of an abstract.

Patients with fulminant hepatitis B have hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) detected for shorter periods than do patients with nonfulminant infections, and they show early and enhanced production of antibodies to HBsAg, HBeAg, and hepatitis B core antigen (HBcAg) (1-3). These observations have been interpreted as evidence that fulminant hepatitis results from the host's immunologic response to the infection rather than from hepatitis B virus replication.

Modern techniques for detecting hepatitis B virus DNA in serum provide the most sensitive method available for showing active viral replication (4-6). We examined hepatitis B virus DNA

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