Authors' Affiliations: Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt-Ingram Cancer Center, and Division of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; International Epidemiology Institute, Rockville, Maryland; and Division of Genome Modifications and Carcinogenesis, Infection and Cancer Program, German Cancer Research Center (DFKZ), Heidelberg, Germany.
Cancer Epidemiol Biomarkers Prev. 2013 Nov;22(11):1964-74. doi: 10.1158/1055-9965.EPI-13-0702. Epub 2013 Sep 17.
There is biologic plausibility as to why infection with Helicobacter pylori, the leading cause of gastric cancer, may also increase the risk of colorectal cancer, but the epidemiologic findings have been inconsistent. We assessed the association of H. pylori protein-specific infection and colorectal cancer risk in the prospective cohort, the Southern Community Cohort Study.
Multiplex serology was used to measure antibodies to 15 H. pylori proteins in prediagnostic blood among 188 incident colorectal cancer cases and 370 controls matched by age, race, sex, and blood collection timing. Conditional logistic regression was used to calculate ORs and 95% confidence intervals (CI).
Overall H. pylori prevalence was not associated with colorectal cancer risk (OR, 1.03; 95% CI, 0.59-1.77). However, seropositivity to any of five specific H. pylori proteins (VacA, HP231, HP305, NapA, and HcpC) was associated with a significant 60% to 80% increase in odds of risk. These associations became even stronger when limited to colon cancer risk, particularly for the known H. pylori toxin VacA (OR, 2.24; 95% CI, 1.22-4.11), including a significant, positive dose-response association by VacA antibody levels in quartiles (P < 0.05). Associations with VacA seropositivity were especially strong for early-onset and late-stage cancers.
The findings raise the hypothesis that individuals with high levels of antibodies to specific H. pylori proteins may be at higher risk of colon cancer.
Further investigation of the H. pylori-colorectal cancer association is warranted to determine the possibility of protein-specific antibody levels as a risk biomarker.
感染幽门螺杆菌（导致胃癌的主要原因）也可能增加结直肠癌风险，这其中存在生物学上的可能性，但流行病学研究结果并不一致。我们在前瞻性队列研究——南方社区队列研究中评估了幽门螺杆菌蛋白特异性感染与结直肠癌风险之间的关联。
在 188 例结直肠癌病例和 370 例按年龄、种族、性别和采血时间匹配的对照者的前瞻性血样中，采用多重血清学方法检测 15 种幽门螺杆菌蛋白的抗体。采用条件 logistic 回归计算比值比（OR）和 95%置信区间（CI）。
总体上，幽门螺杆菌感染与结直肠癌风险无关（OR，1.03；95%CI，0.59-1.77）。然而，对五种特定幽门螺杆菌蛋白（VacA、HP231、HP305、NapA 和 HcpC）中的任何一种的血清阳性均与风险的比值比显著增加 60%至 80%相关。当将研究对象限定为结肠癌风险时，这些关联变得更强，特别是对已知的幽门螺杆菌毒素 VacA 而言（OR，2.24；95%CI，1.22-4.11），包括按 VacA 抗体水平四分位数的显著正剂量-反应关联（P<0.05）。与 VacA 血清阳性相关的关联在发病早和晚期癌症中尤为强烈。
这些发现提出了一种假设，即高水平的针对特定幽门螺杆菌蛋白的抗体的个体可能具有更高的结肠癌风险。
进一步研究幽门螺杆菌与结直肠癌的关联，以确定特定蛋白抗体水平作为风险生物标志物的可能性是有必要的。
