Malik Tayyab Hamid, Sayahan Mujtaba Yousef Al, Al Ahmed Hussain Ali, Hong Xu
Department of Gastroenterology and Endoscopy Center, First Hospital of Jilin University, Xinmin Street, Changchun-130021, China.
Norman Bethune Health Science Center, Jilin University, Changchun, China.
J Coll Physicians Surg Pak. 2017 Mar;27(3):166-172.
Gastric intestinal metaplasia, an intermediate lesion in the development of intestinal-type gastric cancer, is observed in the milieu of long standing non-atrophic gastritis and atrophic gastritis. Most patients with intestinal metaplasia remain asymptomatic unless cobalamin deficiency occurs secondary to loss of glands (that produce intrinsic factor and acid). Genetic events that predispose to development of gastric intestinal metaplasia remains an enigma. Mechanisms leading to the progression of atrophy to metaplasia still needs to be comprehensively explored. Many studies in the literature describe a positive effect of typing intestinal metaplasia and concluded that intestinal metaplasia type III carries the highest risk for developing gastric cancer while others refute it. It is well established that Helicobacter pylori infection is the most important factor for the development of chronic gastritis, gastric intestinal metaplasia as well as gastric cancer. Countries with a higher prevalence of Helicobacter pylori infection and gastric cancer also have a high tendency of being prevalent for intestinal metaplasia. However, it remains elusive whether eradication of Helicobacter pylori infection tends to regress gastric intestinal metaplasia or reduce the subsequent risk of cancer development. Putting together, more prospective cohort studies should be designed to identify factors (antioxidants; anti-inflammatory drugs; food therapy) that may contribute in the regression of intestinal metaplasia, when used simultaneously with eradication therapy. Furthermore, molecular markers for evaluation of intestinal metaplasia, and the potential point-of-no-return should be further investigated. Consensus is also required to advocate a timeframe for surveillance of patients with gastric intestinal metaplasia.
胃黏膜肠化生是肠型胃癌发生发展过程中的一种中间病变，可见于长期非萎缩性胃炎和萎缩性胃炎环境中。大多数肠化生患者无症状，除非因腺体（产生内因子和胃酸）丧失继发钴胺素缺乏。导致胃黏膜肠化生发生的遗传事件仍是一个谜。萎缩进展为化生的机制仍需全面探索。文献中的许多研究描述了肠化生分型的积极作用，并得出结论，III型肠化生发生胃癌的风险最高，而其他研究则予以反驳。幽门螺杆菌感染是慢性胃炎、胃黏膜肠化生以及胃癌发生的最重要因素，这一点已得到充分证实。幽门螺杆菌感染和胃癌患病率较高的国家，肠化生的流行趋势也较高。然而，根除幽门螺杆菌感染是否会使胃黏膜肠化生消退或降低随后发生癌症的风险仍不明确。综上所述，应设计更多前瞻性队列研究，以确定在根除治疗同时使用时可能有助于肠化生消退的因素（抗氧化剂、抗炎药物、食物疗法）。此外，还应进一步研究评估肠化生的分子标志物以及潜在的不可逆转点。对于倡导胃黏膜肠化生患者的监测时间框架也需要达成共识。
