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Abstract

We tested serum samples from 25 fulminant hepatitis and 7 subfulminant hepatitis patients for hepatitis A, B, C, D and E viral markers and nucleic acids by means of polymerase chain reaction to determine the role of each virus on such catastrophic events in an area endemic for hepatitis B. Of these 32 patients, 14 (44%) were hepatitis B virus carriers with hepatitis D virus superinfection (1 with hepatitis C virus infection), 3 others had coexisting hepatitis B virus and hepatitis C virus infections, 6 had reactivation of underlying chronic hepatitis B, 4 had acute hepatitis B, 2 had acute hepatitis C and 1 had acute hepatitis E. Pathogenesis in the remaining two cases was unclear. Serum hepatitis B virus DNA was detectable in most carriers without superinfection and in one third of those with superinfection detected on polymerase chain reaction (6 of 7 vs. 6 of 16, p < 0.05). Of the polymerase chain reaction–positive samples, only 17% yielded positive results on spot hybridization. Hepatitis B virus DNA was the only marker to indicate coexisting hepatitis B virus infection in one patient positive for hepatitis C virus antibody. Only three of the six hepatitis C virus–infected cases were positive for hepatitis C virus antibody; diagnoses in the remaining three were established by means of detection of hepatitis C virus RNA. Of the hepatitis D virus–infected patients, infection in only half was diagnosed by means of total hepatitis D virus antibody assay. Twelve (86%) were positive for anti-hepatitis D virus IgM and nine (64%) had detectable hepatitis D virus RNA on reverse transcription–polymerase chain reaction. Only one third of reverse transcription–polymerase chain reaction positive cases had positive results on Northern-blot hybridization. Hepatitis D virus RNA was the only marker indicating hepatitis D virus infection in two (14%) of the hepatitis D virus–infected patients. In conclusion, most fulminant and subfulminant viral hepatitis in Taiwan is caused by multiple viral infection (hepatitis B virus with hepatitis D virus or hepatitis C virus), which might be underestimated if only one kind of marker were used. (HEPATOLOGY 1994;19:836–840.)