Jencks David S, Adam Jason D, Borum Marie L, Koh Joyce M, Stephen Sindu, Doman David B
Dr Jencks and Dr Adam are gastroenterology fellows in the Division of Gastroenterology and Liver Diseases at George Washington University Medical Center and are affiliated with Medical Faculty Associates, both in Washington, DC.
Dr Borum is a professor of medicine at George Washington University School of Medicine in Washington, DC; director of the Division of Gastroenterology and Liver Diseases at George Washington University Medical Center; and is affiliated with Medical Faculty Associates.
Gastroenterol Hepatol (N Y). 2018 Feb;14(2):92-101.
Gastric intestinal metaplasia is a precancerous change of the mucosa of the stomach with intestinal epithelium, and is associated with an increased risk of dysplasia and cancer. The pathogenesis to gastric cancer is proposed by the Correa hypothesis as the transition from normal gastric epithelium to invasive cancer via inflammation followed by intramucosal cancer and invasion. Multiple risk factors have been associated with the development of gastric intestinal metaplasia interplay, including infection and associated genomics, host genetic factors, environmental milieu, rheumatologic disorders, diet, and intestinal microbiota. Globally, screening guidelines have been established in countries with high incidence. In the United States, no such guidelines have been developed due to lower, albeit increasing, incidence. The American Society for Gastrointestinal Endoscopy recommends a case-by-case patient assessment based upon epidemiology, genetics, and environmental risk factors. Studies have examined the use of a serologic biopsy to stratify risk based upon factors such as status and virulence factors, along with serologic markers of chronic inflammation including pepsinogen I, pepsinogen II, and gastrin. High-risk patients may then be advised to undergo endoscopic evaluation with mapping biopsies from the antrum (greater curvature, lesser curvature), incisura angularis, and corpus (greater curvature, lesser curvature). Surveillance guidelines have not been firmly established for patients with known gastric intestinal metaplasia, but include repeat endoscopy at intervals according to the histologic risk for malignant transformation.
胃黏膜肠化生是胃黏膜向肠上皮化生的一种癌前病变,与发育异常和癌症风险增加相关。科雷亚假说提出了胃癌的发病机制,即从正常胃上皮通过炎症,继而发展为黏膜内癌和浸润癌,最终发展为浸润性癌。多种风险因素与胃黏膜肠化生的发生相互作用有关,包括感染及相关基因组学、宿主遗传因素、环境、风湿性疾病、饮食和肠道微生物群。在全球范围内,高发病率国家已制定了筛查指南。在美国,由于发病率较低(尽管在上升),尚未制定此类指南。美国胃肠内镜学会建议根据流行病学、遗传学和环境风险因素对患者进行个案评估。研究已经探讨了使用血清活检根据诸如状态和毒力因子等因素以及包括胃蛋白酶原I、胃蛋白酶原II和胃泌素在内的慢性炎症血清学标志物来分层风险。然后,高危患者可能会被建议接受内镜评估,并对胃窦(大弯侧、小弯侧)、角切迹和胃体(大弯侧、小弯侧)进行定位活检。对于已知胃黏膜肠化生的患者,监测指南尚未完全确立,但包括根据恶性转化的组织学风险定期进行重复内镜检查。