Role of hepatitis B virus genotypes and quantitative HBV DNA in metastasis and recurrence of hepatocellular carcinoma

✍ Scribed by Yuehua Huang; Zhanhui Wang; Shengli An; Bin Zhou; Yuanping Zhou; Henry Lik-Yuen Chan; Jinlin Hou

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 126 KB
• Volume: 80
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.21117

✦ Synopsis

Abstract

Identification of risk factors for recurrence and metastasis of HCC is important for the prognosis of HCC surveillance in chronic HBV infection. In this article, 125 HCC patients recruited were followed up prospectively for tumor metastasis and recurrence for a median of 104 (10–130) weeks. HBV DNA level was detected by LightCycler‐based real‐time fluorescence quantitative polymerase chain reaction‐restriction system. HBV genotypes were determined by using PCR restriction‐fragment length polymorphism. BCP and PC mutations were performed by PCR and direct sequencing of amplified products. Among 125 HCC patients, 19 patients were excluded because of the lack of follow‐up data and the remaining 106 patients were followed up of 2 years and entered into analysis. Sixty‐nine patients had tumor metastasis or recurrence during the follow‐up and the cumulative probability of HCC metastasis or recurrence was 65.1%. On multivariate analysis, genotype C and HBV DNA level were the risk factors for HCC recurrence or metastasis. The incidence of recurrence or metastasis increased with baseline HBV DNA level in a dose‐response relationship ranging from 22% for HBV DNA level of less than 3 log~10~ copies/ml to 80% for HBV DNA level of 5 log~10~ copies/ml or greater (P = 0.012). Fifty‐seven (74.0%) and 12 (41.4%) patients had metastasis or recurrence in patients with genotype C and B, respectively. The adjusted OR of recurrence or metastasis for genotype C compared with genotype B was 9.755 (P = 0.009). In conclusion, elevated HBV DNA level and genotype C are strong risk predictors of HCC metastasis or recurrence. J. Med. Virol. 80:591–597, 2008. © 2008 Wiley‐Liss, Inc.