摘要
胃癌是最常见的消化道恶性肿瘤之一,在环境、饮食、基因突变、宿主及幽门螺杆菌(Helicobacter pylori, Hp)等众多因素共同参与下,根据Correa描述的肠型胃癌发生的步骤,由正常胃黏膜→浅表性胃炎→萎缩性胃炎→肠上皮化生(Intestinal Metaplasia, IM)→异型增生而逐渐向胃癌演变,这是高度异质性疾病, 具有不同的分子和基因改变。胃癌前病变(Precancerous Lesions of Gastric Cancer, PLGC)是指较易发展为癌组织的病理学变化,包括胃黏膜不完全肠上皮化生和中重度不典型增生(又称上皮内瘤变)。众所周知,Hp感染和伴随的慢性萎缩性胃炎是胃癌发生的两个主要危险因素。大量研究表明Hp感染增加了胃黏膜萎缩、IM及非典型增生的总体发生率,因此,根除Hp可阻断PLGC的进展,从而降低胃黏膜癌变,这个理念被国内外众多研究人员所认可。本文就目前根除Hp后对逆转PLGC作用的最新研究进展做一综述。
Gastric cancer is one of the most common malignant tumors of the digestive tract. With the par-ticipation of many factors, such as environment, diet, gene mutation, host and Helicobacter pylori, etc., according to Correa, the steps of intestinal type gastric cancer gradually develop from normal gastric mucosa to superficial gastritis, atrophic gastritis, intestinal metaplasia to dysplasia, which is a highly heterogeneous disease with different molecular and genetic alterations. Precancerous lesions of gastric cancer (PLGC) are pathological change which are easy to develop into cancerous tissues, including incomplete intestinal metaplasia and moderate severe atypical hyperplasia of gastric mucosa (also known as intraepithelial neoplasia). As we all know, Hp infection and associ-ated chronic atrophic gastritis are the two major risk factors for gastric cancer. A large number of studies have shown that Hp infection increases the overall incidence of gastric mucosal atrophy, IM and atypical hyperplasia. Therefore, eradication of Hp can block the progress of PLGC and reduce the carcinogenesis of gastric mucosa. This idea has been recognized by many researchers at home and abroad. This article reviews the latest research progress in reversing PLGC after Hp eradication.
出处
《临床医学进展》
2018年第8期673-678,共6页
Advances in Clinical Medicine