Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Masonic Cancer Center, Minneapolis, Minnesota 55455, USA.
Cancer Epidemiol Biomarkers Prev. 2010 Sep;19(9):2287-97. doi: 10.1158/1055-9965.EPI-10-0362. Epub 2010 Aug 10.
Epidemiologic findings of tobacco and alcohol use in relation to gastric cancer are inconsistent. Well-designed prospective studies examining their relationship are sparse.
The association between cigarette smoking/alcohol intake and gastric cancer risk was examined in a population-based prospective cohort of 18,244 middle-aged and older men in Shanghai, China, who were enrolled in the study during 1986-1989. After up to 20 years of follow-up, 391 incident gastric cancer cases were identified. Cox proportional hazards regression models were used to estimate hazard ratios (HR) and corresponding 95% confidence intervals (95% CI).
Ever smokers experienced a statistically significant increased risk of gastric cancer (HR, 1.59; 95% CI, 1.27-1.99) compared with nonsmokers after adjustment for alcohol intake and other confounders. Among nondrinkers, smokers experienced 80% increased risk of gastric cancer (HR, 1.81; 95% CI,1.36, 2.41). Conversely, heavy drinkers experienced a statistically significant increase in risk of gastric cancer (HR, 1.46; 95% CI, 1.05-2.04) among all subjects and a statistically nonsignificant 80% increased risk among never smokers. Further adjustment for Helicobacter pylori serology, serum levels of beta-carotene and vitamin C, and urinary level of total isothiocyanates in combination with glutathione S-transferase (GST) M1 and GSTT1 genotypes did not materially change the associations between smoking/alcohol consumption and gastric cancer risk.
These results suggest that cigarette smoking and alcohol consumption may exert independent effects on the development of gastric cancer in this high-risk population.
Modification of these lifestyle choices may reduce the incidence of gastric cancer.
有关烟草和酒精使用与胃癌之间关系的流行病学研究结果不一致。目前，很少有精心设计的前瞻性研究来检验它们之间的关系。
在中国上海，对 18244 名中年及以上男性进行了一项基于人群的前瞻性队列研究，在 1986-1989 年期间对他们进行了研究。在最多 20 年的随访期间，共发现 391 例胃癌新发病例。采用 Cox 比例风险回归模型来估计风险比（HR）及其相应的 95%置信区间（95%CI）。
调整酒精摄入量和其他混杂因素后，与从不吸烟者相比，曾经吸烟者患胃癌的风险显著增加（HR，1.59；95%CI，1.27-1.99）。在不饮酒者中，吸烟者患胃癌的风险增加了 80%（HR，1.81；95%CI，1.36-2.41）。相反，在所有受试者中，重度饮酒者患胃癌的风险显著增加（HR，1.46；95%CI，1.05-2.04），而在从不吸烟者中，这种风险增加则无统计学意义（HR，1.12；95%CI，0.76-1.65）。进一步调整幽门螺杆菌血清学、β-胡萝卜素和维生素 C 血清水平以及谷胱甘肽 S-转移酶（GST）M1 和 GSTT1 基因型与总异硫氰酸酯结合物后，吸烟/饮酒与胃癌风险之间的关联并未发生实质性变化。
这些结果表明，在这种高危人群中，吸烟和饮酒可能对胃癌的发生有独立的影响。
改变这些生活方式的选择可能会降低胃癌的发病率。
