Webb P M, Forman D
Department of Social and Preventive Medicine, Medical School, University of Queensland, Herston, Australia.
Baillieres Clin Gastroenterol. 1995 Sep;9(3):563-82. doi: 10.1016/0950-3528(95)90049-7.
In 1985, gastric cancer was the second most common cause of cancer death in the world. The rapid decline in gastric cancer rates over the last few decades has been attributed to a decline in the prevalence of environmental risk factors for gastric cancer and/or an increase in the prevalence of protective factors. One such risk factor could be the bacterium Helicobacter pylori. Epidemiological studies have shown that areas with high gastric cancer rates often have a correspondingly high prevalence of H. pylori and prospective studies have shown that subjects with serological evidence of H. pylori infection were significantly more likely to go on to develop gastric cancer than those who did not. Helicobacter pylori itself does not appear to be either genotoxic or mutagenic. Infection is, however, associated with increased cell turnover, a chronic immune response accompanied by increased levels of reactive oxygen metabolites and a reduction in gastric levels of ascorbic acid, all conditions that could favour the development of cancer. Nonetheless, the majority of those who are infected with H. pylori do not go on to develop gastric cancer and other factors, such as the strain of the infecting organism or consumption of dietary antioxidants including vitamin C, could also affect the risk of cancer. Finally, it has been estimated that more than one third, and possibly as many as 90% of gastric cancers might be attributable to infection with H. pylori. Prevention and treatment of infection are, therefore, possible approaches to reducing gastric cancer rates. It is, however, unclear what, if any, effect eradication of the infection would have on an individual's risk of gastric cancer and, to date, anti-Helicobacter therapy has only been shown to be of potential benefit in the treatment of low grade gastric MALT lymphomas.
1985年，胃癌是全球第二大常见癌症死因。过去几十年间胃癌发病率的迅速下降归因于胃癌环境风险因素患病率的降低和/或保护因素患病率的增加。其中一个风险因素可能是幽门螺杆菌。流行病学研究表明，胃癌发病率高的地区幽门螺杆菌的患病率通常也相应较高，前瞻性研究表明，有血清学证据证明感染幽门螺杆菌的受试者比未感染者患胃癌的可能性显著更高。幽门螺杆菌本身似乎既没有基因毒性也没有致突变性。然而，感染与细胞更新增加、伴有活性氧代谢产物水平升高的慢性免疫反应以及胃内抗坏血酸水平降低有关，所有这些情况都可能有利于癌症的发展。尽管如此，大多数感染幽门螺杆菌的人并不会患胃癌，其他因素，如感染菌株或包括维生素C在内的膳食抗氧化剂的摄入，也可能影响患癌风险。最后，据估计，超过三分之一甚至可能多达90%的胃癌可能归因于幽门螺杆菌感染。因此，预防和治疗感染可能是降低胃癌发病率的方法。然而，目前尚不清楚根除感染对个体患胃癌的风险会有何种影响（如果有影响的话），而且迄今为止，抗幽门螺杆菌治疗仅在治疗低度胃黏膜相关淋巴组织淋巴瘤方面显示出潜在益处。
