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胃炎:临床-病理谱。

Gastritis: The clinico-pathological spectrum.

机构信息

Department of Medicine (DIMED), Surgical Pathology & Cytopathology Unit, Padova University, Padova, Italy; Veneto Tumor Registry (RTV), Azienda Zero, Padova, Italy.

Department of Surgical Oncological & Gastroenterological Sciences (DiSCOG), Gastroenterology Unit, Padova University, Padova, Italy.

出版信息

Dig Liver Dis. 2021 Oct;53(10):1237-1246. doi: 10.1016/j.dld.2021.03.007. Epub 2021 Mar 28.

DOI:10.1016/j.dld.2021.03.007
PMID:33785282
Abstract

The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune-mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies.

摘要

胃疾病的炎症谱包括不同的临床病理实体,其病因最近在国际京都分类中得到确定。胃炎的诊断结合了大体检查(内镜)和组织学(显微镜)的信息。在获得有代表性的黏膜活检样本时,重要的是要考虑胃黏膜的解剖/功能异质性。胃炎包括自限性和非自限性(长期)炎症性疾病,后者在流行病学、生物学和临床上与胃癌的发生有关(即“炎症相关癌症”)。已经提出了不同的炎症相关胃癌发生的生物学模型。幽门螺杆菌(H. pylori)胃炎在全球范围内最为普遍,H. pylori被归类为一级致癌物。基于这些原因,根除 H. pylori 是预防胃癌的主要措施。非自限性胃炎也可能由胃壁细胞的免疫介导破坏引起,导致自身免疫性胃炎。在 H. pylori 相关和自身免疫性胃炎中,非自限性炎症导致胃黏膜萎缩,这是促进胃癌的主要因素。长期随访研究一致表明,胃炎的组织学分期在胃癌二级预防策略中的预后影响。

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