Tseng Chin-Hsiao, Tseng Farn-Hsuan
Chin-Hsiao Tseng, Department of Internal Medicine, National Taiwan University College of Medicine, Taipei 100, Taiwan.
World J Gastroenterol. 2014 Feb 21;20(7):1701-11. doi: 10.3748/wjg.v20.i7.1701.
This article reviews the epidemiological evidence linking diabetes and gastric cancer and discusses some of the potential mechanisms, confounders and biases in the evaluation of such an association. Findings from four meta-analyses published from 2011 to 2013 suggest a positive link, which may be more remarkable in females and in the Asian populations. Putative mechanisms may involve shared risk factors, hyperglycemia, Helicobacter pylori (H. pylori) infection, high salt intake, medications and comorbidities. Diabetes may increase the risk of gastric cancer through shared risk factors including obesity, insulin resistance, hyperinsulinemia and smoking. Hyperglycemia, even before the clinical diagnosis of diabetes, may predict gastric cancer in some epidemiological studies, which is supported by in vitro, and in vivo studies. Patients with diabetes may also have a higher risk of gastric cancer through the higher infection rate, lower eradication rate and higher reinfection rate of H. pylori. High salt intake can act synergistically with H. pylori infection in the induction of gastric cancer. Whether a higher risk of gastric cancer in patients with diabetes may be ascribed to a higher intake of salt due to the loss of taste sensation awaits further investigation. The use of medications such as insulin, metformin, sulfonylureas, aspirin, statins and antibiotics may also influence the risk of gastric cancer, but most of them have not been extensively studied. Comorbidities may affect the development of gastric cancer through the use of medications and changes in lifestyle, dietary intake, and the metabolism of drugs. Finally, a potential detection bias related to gastrointestinal symptoms more commonly seen in patients with diabetes and with multiple comorbidities should be pointed out. Taking into account the inconsistent findings and the potential confounders and detection bias in previous epidemiological studies, it is expected that there are still more to be explored for the clarification of the association between diabetes and gastric cancer.
本文回顾了将糖尿病与胃癌联系起来的流行病学证据，并讨论了评估这种关联时的一些潜在机制、混杂因素和偏差。2011年至2013年发表的四项荟萃分析结果表明存在正相关，这在女性和亚洲人群中可能更为显著。推测的机制可能涉及共同的风险因素、高血糖、幽门螺杆菌（H. pylori）感染、高盐摄入、药物和合并症。糖尿病可能通过包括肥胖、胰岛素抵抗、高胰岛素血症和吸烟在内的共同风险因素增加患胃癌的风险。在一些流行病学研究中，即使在糖尿病临床诊断之前，高血糖也可能预测胃癌，这得到了体外和体内研究的支持。糖尿病患者也可能因幽门螺杆菌的感染率较高、根除率较低和再感染率较高而患胃癌的风险更高。高盐摄入可与幽门螺杆菌感染协同作用诱发胃癌。糖尿病患者患胃癌风险较高是否归因于味觉丧失导致盐摄入量增加有待进一步研究。使用胰岛素、二甲双胍、磺脲类药物、阿司匹林、他汀类药物和抗生素等药物也可能影响患胃癌的风险，但其中大多数尚未得到广泛研究。合并症可能通过药物使用以及生活方式、饮食摄入和药物代谢的改变影响胃癌的发生。最后，应指出与糖尿病患者和多种合并症患者中更常见的胃肠道症状相关的潜在检测偏差。考虑到先前流行病学研究结果不一致以及潜在的混杂因素和检测偏差，预计在阐明糖尿病与胃癌之间的关联方面仍有更多有待探索之处。
