Contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan

✍ Scribed by Makoto Yoshiba; Kazuhiko Dehara; Kazuaki Inoue; Hiroaki Okamoto; Makoto Mayumi

• Publisher: John Wiley and Sons
• Year: 1994
• Tongue: English
• Weight: 669 KB
• Volume: 19
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840190405

✦ Synopsis

To assess the contribution of hepatitis C virus to non-A, non-B fulminant hepatitis in Japan, we compared 10 mqjor 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 (1,363 U/L) than in the type B group (5,780 U/L) (p < 0.06). 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 < 0.06). W e 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. (FIEPATOLOGY 1994;19:829-836.)

Fulminant liver failure (FLF) is characterized by rapid and progressive deterioration of liver function due to extensive hepatocellular destruction. Various factors such as viruses, drugs, toxins and circulatory and metabolic disorders are implicated as causes. All viruses that cause acute hepatitis, such as hepatitis A virus (HAW, HBV, non-A, non-B (NANB) hepatitis virus, cytomegalovirus, Epstein-Barr virus and herpes simplex virus are known to cause fulminant hepatitis (1).

Recently, hepatitis C virus (HCV) has been identified