Anticarcinogenic impact of interferon on patients with chronic hepatitis C: a Large-scale long-term study in a single center

被引:8
作者
Ikeda, K
Arase, Y
Saitoh, S
Kobayashi, M
Someya, T
Hosaka, T
Sezaki, H
Akuta, N
Suzuki, F
Suzuki, Y
Kumada, H
机构
[1] Toranomon Gen Hosp, Dept Gastroenterol, Minato Ku, Tokyo 1058470, Japan
[2] Okinaka Mem Inst Med Res, Tokyo, Japan
关键词
cirrhosis; fibrosis; hepatitis C virus; hepatocellular carcinoma; interferon;
D O I
10.1159/000087268
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Background: The anticarcinogenic capacity of interferon (IFN) was assessed in a cohort of Japanese patients with chronic hepatitis C en masse. Patients and Methods: The rate of hepatocarcinogenesis was analyzed in 2,166 patients with chronic hepatitis C, of whom 1,654 had received IFN therapy while 512 had not. Results: Crude rates of hepatocarcinogenesis in treated and untreated patients were 2.6 and 4.6% at the end of the 5th year, 5.8 and 12.7% at the 10th year and 13.9 and 23.9% at the 15th year (after completion of IFN therapy for those treated) (p<0.001). IFN decreased the hazard ratio of carcinogenesis to 0.42 (p<0.001) in multivariate analysis with adjustments for significant covariates including fibrotic stage, gamma-glutamyl transpeptidase level, gender, platelet count and age. Among the 1,654 patients treated with IFN, 606 (36.6%) achieved persistent loss of hepatitis C virus (HCV) RNA and an additional 266 (16.1%) gained normal levels of alanine aminotransferase without loss of HCV RNA for 6 months or longer after the completion of IFN therpay. Cumulative rates of hepatocarcinogenesis in sustained virological responders and biochemical responders were 1.4 and 2.0% at the end of the 5th year, 1.9 and 3.6% at the 10th year and 1.9 and 7.5% at the 15th year, respectively. The hazard ratio of sustained virological response was 0.10 (p<0.001), and that of biochemical response was 0.12 (p<0.001). Normalization of aminotransferase levels after IFN therapy without loss of serum HCV RNA decreased hepatocarcinogenesis. Conclusion: IFN significantly decreased the rate of hepatocarcinogenesis in patients with chronic hepatitis C as a whole in Japan, even in those who fail to clear HCV RNA from serum. Copyright (C) 2006 S. Karger AG, Basel.
引用
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页码:82 / 90
页数:9
相关论文
共 36 条
[1]  
Benvegnù L, 1998, CANCER-AM CANCER SOC, V83, P901, DOI 10.1002/(SICI)1097-0142(19980901)83:5<901::AID-CNCR15>3.0.CO
[2]  
2-Z
[3]  
Brunetto MR, 1998, LANCET, V351, P1535
[4]   Interferon and prevention of hepatocellular carcinoma in viral cirrhosis:: an evidence-based approach [J].
Cammà, C ;
Giunta, M ;
Andreone, P ;
Craxì, A .
JOURNAL OF HEPATOLOGY, 2001, 34 (04) :593-602
[5]   COMPARISON OF 1 OR 3 MU OF INTERFERON ALFA-2B AND PLACEBO IN PATIENTS WITH CHRONIC NON-A, NON-B HEPATITIS [J].
CAUSSE, X ;
GODINOT, H ;
CHEVALLIER, M ;
CHOSSEGROS, P ;
ZOULIM, F ;
OUZAN, D ;
HEYRAUD, JP ;
FONTANGES, T ;
ALBRECHT, J ;
MESCHIEVITZ, C ;
TREPO, C .
GASTROENTEROLOGY, 1991, 101 (02) :497-502
[6]  
CHAYAMA K, 1991, HEPATOLOGY, V13, P1040
[7]  
COX DR, 1972, J R STAT SOC, V34, P248
[8]   TREATMENT OF CHRONIC HEPATITIS-C WITH RECOMBINANT INTERFERON-ALFA - A MULTICENTER RANDOMIZED, CONTROLLED TRIAL [J].
DAVIS, GL ;
BALART, LA ;
SCHIFF, ER ;
LINDSAY, K ;
BODENHEIMER, HC ;
PERRILLO, RP ;
CAREY, W ;
JACOBSON, IM ;
PAYNE, J ;
DIENSTAG, JL ;
VANTHIEL, DH ;
TAMBURRO, C ;
LEFKOWITCH, J ;
ALBRECHT, J ;
MESCHIEVITZ, C ;
ORTEGO, TJ ;
GIBAS, A .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (22) :1501-1506
[9]  
Di Bisceglie Adrian M., 1998, Hepatology, V28, P1161, DOI 10.1002/hep.510280436
[10]   RECOMBINANT INTERFERON-ALFA THERAPY FOR CHRONIC HEPATITIS-C - A RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED TRIAL [J].
DIBISCEGLIE, AM ;
MARTIN, P ;
KASSIANIDES, C ;
LISKERMELMAN, M ;
MURRAY, L ;
WAGGONER, J ;
GOODMAN, Z ;
BANKS, SM ;
HOOFNAGLE, JH .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (22) :1506-1510