Cigarette smoking and the colorectal adenoma-carcinoma sequence: a hypothesis to explain the paradox.
Cigarette smoking and the colorectal adenoma-carcinoma sequence: a hypothesis to explain the paradox.
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吸烟和结直肠腺瘤-癌序列：解释悖论的假设。
DOI：
10.1093/oxfordjournals.aje.a009379
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发表时间：
1998
影响因子：
5
通讯作者：
Neugut,AI
中科院分区：
文献类型：
--
作者：
Terry,MB;Neugut,AI
作为公认的结直肠癌的前驱病变，结直肠腺瘤性息肉已经被研究以提高对结直肠癌病因学的认识。虽然大多数已知的结直肠癌危险因素也与结直肠腺瘤的发生有关，但吸烟与结直肠腺瘤有很强的一致性关系，但通常与结直肠癌无关。这个悖论的解释是未知的。根据1986-1988年在纽约市进行的一项基于结肠镜检查结果的大型病例对照研究中收集的数据，作者调查了由于结肠直肠腺瘤受试者被纳入癌症病例对照研究的对照组而可能出现悖论的可能性。作者发现，重度吸烟（吸烟40包-年）和腺瘤风险之间的风险增加具有统计学意义（比值比（OR）= 1.61，95%置信区间（CI）1.06-2.44）。他们使用“人造”对照组来模拟典型的未筛查的、基于人群的对照组，没有发现大量吸烟（OR = 1.02，95%CI 0.52-1.99）增加结直肠癌的风险。当作者在多个病例组（新诊断的腺瘤、原位癌、粘膜内癌和结直肠癌）的多分割模型中将这些结直肠癌病例与通过结肠镜检查的无腺瘤对照组进行比较时，他们发现吸烟20-39包-年的风险升高，尽管没有统计学意义，并且在所有四个病例组中相似。最高吸烟类别的风险（s40包-年）在所有四个病例组中都有更强烈的升高，尽管只有新诊断的腺瘤和原位癌病例有统计学意义（腺瘤OR = 1.59，95% CI 1.05-2.42，原位癌OR = 2.05，95% CI 1.01-4.15，粘膜内癌OR = 1.30，95% CI 0.61-2.77;结直肠癌OR = 1.30，95% CI 0.64-2.65）。虽然作者的研究由于缺乏关于结直肠癌风险的统计学显著性而被削弱，但这些数据为以下假设提供了一些支持：吸烟与结直肠癌风险之间的关联可能被纳入腺瘤受试者的对照组所掩盖。他们还表明，吸烟对结肠直肠腺瘤-癌序列的主要影响发生在腺瘤形成和原位癌发展的早期阶段.Am J Epidemiol 1998; 147：903-10.
As recognized precursor lesions to colorectal cancer, colorectal adenomatous polyps have been studied to enhance knowledge of colorectal cancer etiology. Although most of the known risk factors for colorectal cancer are also associated with the occurrence of colorectal adenomas, cigarette smoking has had a strong, consistent relationship with colorectal adenomas but is generally not associated with colorectal cancer. The explanation for this paradox is unknown. With data collected in 1986–1988 during a large case-control study based on colonoscopy results in New York City, New York, the authors investigated the possibility that the paradox may arise because subjects with colorectal adenomas were included in the control group of cancer case-control studies. The authors found a statistically significant increased risk between heavy cigarette smoking (smokers with 40 pack-years of smoking) and risk of adenoma (odds ratio (OR) = 1.61, 95% confidence interval (Cl) 1.06–2.44). They saw no increased colorectal cancer risk from heavy cigarette smoking (OR = 1.02, 95% Cl 0.52–1.99) using a “manufactured” control group to simulate a typical unscreened, population-based control group. When the authors compared these colorectal cancer cases with an adenoma-free control group examined by colonoscopy in a polytomous model with several case groups (newly diagnosed adenomas, carcinoma in situ, intramucosal carcinoma, and colorectal cancer), they found that the risk for 20–39 pack-years of smoking was elevated, although not statistically significant, and was similar for all four case groups. The risk for the highest smoking category (s40 pack-years) was more strongly elevated in all four case groups, although it was statistically significant for only the newly diagnosed adenoma and the carcinoma in situ cases (adenomas, OR = 1.59, 95% Cl 1.05–2.42; carcinoma in situ, OR = 2.05, 95% Cl 1.01–4.15; intramucosal carcinoma, OR = 1.30, 95% Cl 0.61–2.77; and colorectal cancer, OR = 1.30, 95% Cl 0.64–2.65). While the authors’ study is weakened by the lack of statistical significance concerning risk for colorectal cancer, these data offer some support for the hypothesis that the association between cigarette smoking and risk of colorectal cancer may have been masked by inclusion in the control group of subjects with adenomas. They also suggest that the major effect of smoking on the colorectal adenoma-carcinoma sequence occurs in the earlier stages of the formation of adenoma and the development of carcinoma in situ.Am J Epidemiol1998; 147: 903–10.