High viral load is a risk factor for hepatocellular carcinoma in patients with chronic hepatitis B virus infection

被引:90
作者
Ohata, K
Hamasaki, K
Toriyama, K
Ishikawa, H
Nakao, K
Eguchi, K
机构
[1] Nagasaki Univ, Sch Med, Dept Internal Med 1, Nagasaki 8528501, Japan
[2] Nagasaki Univ, Dept Pathol, Inst Trop Med, Nagasaki 852, Japan
[3] Nagasaki Univ, Hlth Res Ctr, Nagasaki 852, Japan
关键词
hepatitis B virus; hepatitis B virus DNA; hepatocellular carcinoma; risk factor;
D O I
10.1111/j.1440-1746.2004.03360.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background and Aims: Hepatitis B virus (HBV) is considered a major risk factor for the progression to liver cirrhosis and hepatocellular carcinoma (HCC). The serum level of HBV-DNA is correlated with progression of the disease. The aim of the present study was to determine the relationship between the level of HBV-DNA and hepatocarcinogenesis in patients with chronic HBV infection. Methods: The authors studied 73 patients who were diagnosed with chronic HBV infection at Nagasaki University Hospital (Nagasaki, Japan) between January 1980 and December 1999. The significance of age, sex, habitual drinking, serum alanine aminotransferase level, HBV viral load, interferon treatment, hepatic fibrosis and hepatic inflammation on the development of HCC were examined using univariate and multivariate analyses. Results: The cumulative incidence rates of HCC were 14%, 29% and 48% at 5, 10 and 15 years after liver biopsy, respectively. Multivariate analysis identified high viral load, together with age and severe fibrosis, as independent and significant risk factors (P = 0.045, 0.047 and 0.013, respectively) for HCC. Conclusions: The present findings indicate that high viral load is a risk factor for HCC in patients with chronic HBV infection. Patients with a high HBV viral load should be carefully monitored for HCC. (C) 2004 Blackwell Publishing Asia Pty Ltd.
引用
收藏
页码:670 / 675
页数:6
相关论文
共 39 条
[1]  
BENVEGNU L, 1994, CANCER, V74, P2442, DOI 10.1002/1097-0142(19941101)74:9<2442::AID-CNCR2820740909>3.0.CO
[2]  
2-#
[3]   Evidence for an association between the aetiology of cirrhosis and pattern of hepatocellular carcinoma development [J].
Benvegnù, L ;
Noventa, F ;
Bernardinello, E ;
Pontisso, P ;
Gatta, A ;
Alberti, A .
GUT, 2001, 48 (01) :110-115
[4]  
BRUNETTO MR, 1995, J HEPATOL, V22, P42
[5]   NATURAL-HISTORY OF CHRONIC HEPATITIS-B VIRUS-INFECTION IN TAIWAN - STUDIES OF HEPATITIS-B VIRUS-DNA IN SERUM [J].
CHU, CM ;
KARAYIANNIS, P ;
FOWLER, MJF ;
MONJARDINO, J ;
LIAW, YF ;
THOMAS, HC .
HEPATOLOGY, 1985, 5 (03) :431-434
[6]   HEPATOCELLULAR-CARCINOMA [J].
COLOMBO, M .
JOURNAL OF HEPATOLOGY, 1992, 15 (1-2) :225-236
[7]  
DESMET VJ, 1994, HEPATOLOGY, V19, P1513, DOI 10.1002/hep.1840190629
[8]   The long-term course of chronic hepatitis B [J].
Di Marco, V ;
Lo Iacono, O ;
Cammà, C ;
Vaccaro, A ;
Giunta, M ;
Martorana, G ;
Fuschi, P ;
Almasio, PL ;
Craxì, A .
HEPATOLOGY, 1999, 30 (01) :257-264
[9]   CLINICAL, VIROLOGICAL AND HISTOLOGIC OUTCOME FOLLOWING SEROCONVERSION FROM HEBEAG TO ANTI-HBE IN CHRONIC HEPATITIS TYPE-B [J].
FATTOVICH, G ;
RUGGE, M ;
BROLLO, L ;
PONTISSO, P ;
NOVENTA, F ;
GUIDO, M ;
ALBERTI, A ;
REALDI, G .
HEPATOLOGY, 1986, 6 (02) :167-172
[10]  
Feitelson MA, 1999, J CELL PHYSIOL, V181, P188