CONTRIBUTION OF HEPATITIS-C VIRUS TO NON-A, NON-B FULMINANT-HEPATITIS IN JAPAN

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作者
YOSHIBA, M [1 ]
DEHARA, K [1 ]
INOUE, K [1 ]
OKAMOTO, H [1 ]
MAYUMI, M [1 ]
机构
[1] JICHI MED SCH,DIV IMMUNOL,MINAMI KAWACHI,TOCHIGI 32904,JAPAN
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R57 [消化系及腹部疾病];
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摘要
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.
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页码:829 / 835
页数:7
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共 29 条
[1]  
AKBAR SMF, 1991, GASTROENTEROL JPN, V27, P514
[2]   FULMINANT AND SUBFULMINANT LIVER-FAILURE - DEFINITIONS AND CAUSES [J].
BERNUAU, J ;
RUEFF, B ;
BENHAMOU, JP .
SEMINARS IN LIVER DISEASE, 1986, 6 (02) :97-106
[3]   PERSISTENT NON-A, NON-B HEPATITIS IN EXPERIMENTALLY INFECTED CHIMPANZEES [J].
BRADLEY, DW ;
MAYNARD, JE ;
POPPER, H ;
EBERT, JW ;
COOK, EH ;
FIELDS, HA ;
KEMLER, BJ .
JOURNAL OF INFECTIOUS DISEASES, 1981, 143 (02) :210-218
[4]   MULTIPLICATION OF HEPATITIS-B VIRUS IN FULMINANT HEPATITIS-B [J].
BRECHOT, C ;
BERNUAU, J ;
THIERS, V ;
DUBOIS, F ;
GOUDEAU, A ;
RUEFF, B ;
TIOLLAIS, P ;
BENHAMOU, JP .
BMJ-BRITISH MEDICAL JOURNAL, 1984, 288 (6413) :270-271
[5]   ISOLATION OF A CDNA CLONE DERIVED FROM A BLOOD-BORNE NON-A, NON-B VIRAL-HEPATITIS GENOME [J].
CHOO, QL ;
KUO, G ;
WEINER, AJ ;
OVERBY, LR ;
BRADLEY, DW ;
HOUGHTON, M .
SCIENCE, 1989, 244 (4902) :359-362
[6]  
COCK KM, 1986, ANN INTERN MED, V105, P546
[7]   NON-A, NON-B HEPATITIS - EVOLVING EPIDEMIOLOGIC AND CLINICAL PERSPECTIVE [J].
DIENSTAG, JL ;
ALTER, HJ .
SEMINARS IN LIVER DISEASE, 1986, 6 (01) :67-81
[8]  
DIENSTAG JL, 1983, GASTROENTEROLOGY, V85, P439
[9]   HEPATITIS-C VIRUS-RNA AND HEPATITIS-B VIRUS-DNA IN SERUM AND LIVER OF PATIENTS WITH FULMINANT-HEPATITIS [J].
FERAY, C ;
GIGOU, M ;
SAMUEL, D ;
REYES, G ;
BERNUAU, J ;
REYNES, M ;
BISMUTH, H ;
BRECHOT, C .
GASTROENTEROLOGY, 1993, 104 (02) :549-555
[10]   LATE ONSET HEPATIC-FAILURE - CLINICAL, SEROLOGICAL AND HISTOLOGICAL FEATURES [J].
GIMSON, AES ;
OGRADY, J ;
EDE, RJ ;
PORTMANN, B ;
WILLIAMS, R .
HEPATOLOGY, 1986, 6 (02) :288-294