Sipponen P
Department of Pathology, Jorvi Hospital, Espoo, Finland.
Ital J Gastroenterol Hepatol. 1998 Oct;30 Suppl 3:S270-2.
Helicobacter pylori acquisition induces chronic gastritis that affects antrum, corpus or both. In approximately half of the cases, Helicobacter pylori gastritis slowly (years, decades) develops to atrophic gastritis, thereby resulting in severe abnormalities in the function of the stomach. In humans, the appearance of intestinal metaplasia associates with atrophic gastritis (loss of normal antral and/or oxyntic glands), and intestinal metaplasia linearly increases in grade and extent with increasing age and progression of atrophy. Several mechanisms may play in role in the development of atrophic gastritis and intestinal metaplasia; i.e., including genetic liability of the host to destruction of cells and glands, specific cytotoxic strains of Helicobacter pylori, environmental factors other than the bacterial ones, and some functional properties of the stomach, such as output of acid and intragastric acidity. Atrophic and metaplastic alterations may also result from genotoxic and mutagenic injuries which are triggered by the inflammation, or are exogenous.
幽门螺杆菌感染会引发慢性胃炎，影响胃窦、胃体或两者。在大约一半的病例中，幽门螺杆菌胃炎会缓慢（数年、数十年）发展为萎缩性胃炎，从而导致胃部功能严重异常。在人类中，肠化生的出现与萎缩性胃炎（正常胃窦和/或胃底腺的丧失）相关，并且随着年龄增长和萎缩进展，肠化生的程度和范围呈线性增加。萎缩性胃炎和肠化生的发展可能涉及多种机制；即包括宿主对细胞和腺体破坏的遗传易感性、幽门螺杆菌的特定细胞毒性菌株、除细菌因素以外的环境因素，以及胃的一些功能特性，如胃酸分泌和胃内酸度。萎缩和化生改变也可能由炎症引发的基因毒性和致突变性损伤或外源性损伤导致。
