MULTIPLE VIRAL INFECTION AS THE MOST COMMON CAUSE OF FULMINANT AND SUBFULMINANT VIRAL HEPATITIS IN AN AREA ENDEMIC FOR HEPATITIS B: APPLICATION AND LIMITATIONS OF THE POLYMERASE CHAIN REACTION.

Wu JC; Chen CL; Hou MC; Chen TZ; Lee SD; Lo KJ; Department of Medicine, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China. Hepatology, 1994 Apr, 19:4, 836-40

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.


DIAGNOSTIC SIGNIFICANCE OF IGM ANTIBODY TO HEPATITIS DELTA VIRUS IN FULMINANT HEPATITIS B.

Tassopoulos NC; Koutelou MG; Macagno S; Zorbas P; Rizzetto M; Department of Medicine, Western Attica General Hospital, Athens, Greece. J Med Virol, 1990 Mar, 30:3, 174-7

The prevalence of hepatitis delta virus (HDV) infection was studied in 25 adult patients with fulminant hepatitis who were admitted consecutively to our unit from February, 1986, to September, 1988. Enzyme and radioimmunoassays were used for the detection of serological markers of HAV, HBV, and HDV (HDAg, IgM anti-HD, total [IgG] anti-HD) infections. Two hundred twenty-nine serum samples (three to 19 samples/patient) were tested for serological markers of HDV infection. Of the 25 patients, 17 (68%) were HBsAg-positive, and the remaining eight (32%) were HBsAg-negative on admission to the hospital. All patients were seropositive for IgM anti-HBc. Serological markers of HDV infection were detected in 13 (52%) of the 25 patients. In particular, HDV infection was observed in nine (53%) of the 17 HBsAg-positive and in four (50%) of the eight HBsAg-negative patients with type B fulminant hepatitis. Survival was 16.7% for patients with hepatitis B and 57.8% for patients with B and D coinfection. Coinfections were responsible for fulminant hepatitis in 100% of drug addicts and 40% in patients who were not drug addicts. All patients with HBV/HDV coinfections became seropositive for IgM anti-HD. The results show that HDV infection has a significant role (52%) in type B fulminant hepatitis in an area with a moderate prevalence of HBV infections, that it should be tested in cases with early clearance of HBsAg, and that it does not seem to be accompanied by a high fatality rate.


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