World J Gastroenterol. 2012 Mar 28;18(12):1279-85. doi: 10.3748/wjg.v18.i12.1279.
Chronic atrophic gastritis (CAG) is an inflammatory condition characterized by the loss of gastric glandular structures which are replaced by connective tissue (non-metaplastic atrophy) or by glandular structures inappropriate for location (metaplastic atrophy). Epidemiological data suggest that CAG is associated with two different types of tumors: Intestinal-type gastric cancer (GC) and type I gastric carcinoid (TIGC). The pathophysiological mechanisms which lead to the development of these gastric tumors are different. It is accepted that a multistep process initiating from Helicobacter pylori-related chronic inflammation of the gastric mucosa progresses to CAG, intestinal metaplasia, dysplasia and, finally, leads to the development of GC. The TIGC is a gastrin-dependent tumor and the chronic elevation of gastrin, which is associated with CAG, stimulates the growth of enterochromaffin-like cells with their hyperplasia leading to the development of TIGC. Thus, several events occur in the gastric mucosa before the development of intestinal-type GC and/or TIGC and these take several years. Knowledge of CAG incidence from superficial gastritis, its prevalence in different clinical settings and possible risk factors associated with the progression of this condition to gastric neoplasias are important issues. This editorial intends to provide a brief review of the main studies regarding incidence and prevalence of CAG and risk factors for the development of gastric neoplasias.
慢性萎缩性胃炎（CAG）是一种炎症性疾病，其特征是胃腺结构丧失，被结缔组织（非化生性萎缩）或不适当位置的腺结构（化生性萎缩）所取代。流行病学数据表明，CAG 与两种不同类型的肿瘤有关：肠型胃癌（GC）和 I 型胃类癌（TIGC）。导致这些胃肿瘤发展的病理生理机制是不同的。人们普遍认为，从与幽门螺杆菌相关的胃黏膜慢性炎症开始的多步骤过程进展为 CAG、肠化生、异型增生，最终导致 GC 的发生。TIGC 是一种胃泌素依赖性肿瘤，与 CAG 相关的慢性胃泌素升高刺激肠嗜铬样细胞生长，导致 TIGC 的发生。因此，在发生肠型 GC 和/或 TIGC 之前，胃黏膜中会发生多个事件，这些事件需要数年时间。了解从浅表性胃炎到 CAG 的发病率、不同临床环境中的患病率以及与该疾病进展为胃肿瘤相关的可能危险因素是重要的问题。本社论旨在简要回顾关于 CAG 的发病率和患病率以及发展为胃肿瘤的危险因素的主要研究。
