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慢性乙型肝炎病毒感染患者罹患胰腺癌的风险:REVEAL-HBV 队列研究的数据。

Risk of pancreatic cancer in chronic hepatitis B virus infection: data from the REVEAL-HBV cohort study.

机构信息

Research and Development, Bristol-Myers Squibb Company, Wallingford, CT, USA.

出版信息

Liver Int. 2010 Mar;30(3):423-9. doi: 10.1111/j.1478-3231.2009.02147.x. Epub 2009 Oct 16.

DOI:10.1111/j.1478-3231.2009.02147.x
PMID:19840258
Abstract

BACKGROUND AND AIMS

The relationship between the hepatitis B virus (HBV) and pancreatic cancer remains unclear. Because HBV has been isolated from pancreatic tissue, we hypothesized that HBV may play a role in the development of pancreatic carcinoma.

METHODS

This cohort was recruited between 1991 and 1992. Serum samples obtained at enrolment were tested for HBsAg and HBeAg by radioimmunoassay. Pancreatic cancer diagnosis was ascertained through data linkage with profiles of the National Cancer Registry and Death Certification System in Taiwan from 1 January 1991 to 31 December 2007. Multivariate-adjusted hazards ratios (HR(adj)) with 95% confidence intervals (CI) were derived using Cox proportional hazards models.

RESULTS

In total 22 471 subjects were followed up for 342 186 person-years and 48 had pancreatic cancer. Chronic carriers of HBsAg had a significantly increased risk of pancreatic cancer showing an HR(adj) (95% CI) of 1.95 (1.01-3.78). This association was most striking in females, individuals < or =50 years, non-smokers and non-drinkers. The HR(adj) (95% CI) of developing pancreatic cancer was 5.73 (1.73-19.05) for HBeAg-seropositive carriers and 1.64 (0.79-3.42) for HBeAg-seronegative carriers compared with HBsAg-seronegative non-carriers. An increased risk of pancreatic cancer was observed for HBsAg-seropositives with HBV DNA > or =300 copies/ml (HR(adj), 2.44; 95% CI, 1.20-4.95), but not for HBsAg-seropositives with HBV DNA <300 copies/ml (HR(adj), 0.64; 95% CI, 0.09-4.67).

CONCLUSIONS

In addition to the well-established risk of hepatocellular carcinoma, chronic HBV infection may be associated with an increased risk of pancreatic cancer.

摘要

背景与目的

乙型肝炎病毒(HBV)与胰腺癌之间的关系仍不清楚。由于 HBV 已从胰腺组织中分离出来,我们假设 HBV 可能在胰腺癌的发展中起作用。

方法

本队列于 1991 年至 1992 年期间招募。通过放射免疫测定法检测入组时获得的血清样本中的 HBsAg 和 HBeAg。通过与台湾国家癌症登记处和死亡认证系统的资料进行链接,从 1991 年 1 月 1 日至 2007 年 12 月 31 日确定胰腺癌的诊断。使用 Cox 比例风险模型得出多变量调整后的风险比(HR(adj))和 95%置信区间(CI)。

结果

共有 22471 名受试者接受了 342186 人年的随访,有 48 人患有胰腺癌。慢性 HBsAg 携带者患胰腺癌的风险显著增加,HR(adj)(95%CI)为 1.95(1.01-3.78)。这种关联在女性、<或=50 岁、不吸烟者和不饮酒者中最为明显。与 HBsAg 阴性非携带者相比,HBeAg 阳性携带者发生胰腺癌的 HR(adj)(95%CI)为 5.73(1.73-19.05),HBeAg 阴性携带者为 1.64(0.79-3.42)。对于 HBV DNA >或=300 拷贝/ml 的 HBsAg 阳性者,观察到胰腺癌的风险增加(HR(adj),2.44;95%CI,1.20-4.95),但 HBV DNA <300 拷贝/ml 的 HBsAg 阳性者则无此风险(HR(adj),0.64;95%CI,0.09-4.67)。

结论

除了已确立的肝癌风险外,慢性 HBV 感染可能与胰腺癌风险增加有关。

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