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Contribution of hepatitis C virus to non‐A, non‐B fulminant hepatitis in Japan
Author(s) -
Yoshiba Makoto,
Dehara Kazuhiko,
Inoue Kazuaki,
Okamoto Hiroaki,
Mayumi Makoto
Publication year - 1994
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840190405
Subject(s) - fulminant hepatitis , group b , medicine , gastroenterology , group a , coma (optics) , jaundice , hepatitis b virus , fulminant , hepatitis b , hepatitis , hepatitis c virus , virus , immunology , physics , optics
To assess the contribution of hepatitis C virus to non‐A, non‐B fulminant hepatitis in Japan, we compared 10 major clinical features among 7 patients with type B fulminant hepatitis (type B group), 13 patients with non‐A, non‐B fulminant hepatitis with evidence of hepatitis C virus infection (type C group) and 10 patients without evidence of hepatitis C virus infection (NANB group). Duration from first symptom to coma and that from onset of jaundice to coma was significantly longer in the type C group (median = 39 and 25 days, respectively) and in the non‐A, non‐B group (median = 29 and 12 days, respectively) than in the type B group (median = 9 and 2 days, respectively) (p < 0.01). The maximum median AST level was significantly lower in the type C (1,689 U/L) and non‐A, non‐B groups (1,353 U/L) than in the type B group (5,780 U/L) (p < 0.05). Serum transaminase levels showed a single peak in six of seven of the type B patients, whereas they formed two or more peaks in all of the type C patients and in most of the non‐A, non‐B group (p < 0.05). Six of seven in the type B group, 6 of 13 in the type C group and 4 of 10 in the non‐A, non‐B group survived (p < 0.05). We found no significant difference in any of the 10 clinical features between the type C and non‐A, non‐B groups. Compared with type B fulminant hepatitis, type C and most cases of non‐A, non‐B fulminant hepatitis in Japan are, thus, characterized by slower and less severe but more persistent hepatocyte destruction. (H EPATOLOGY 1994;19:829–835.)

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