University of Adelaide, Adelaide, South Australia, Australia.
J Gastroenterol Hepatol. 2018 Jul;33(7):1321-1326. doi: 10.1111/jgh.14090. Epub 2018 Mar 12.
Humans and Helicobacter pylori have evolved and adapted over tens of thousands of years. Yet peptic ulcer disease appeared to be rare prior to the 19th century. The prevalence of peptic ulcer disease increased between 1850 and 1900 and culminated in a cohort at high risk that was born at the end of the 19th century. This coincided with the provision of safe water and improvements in sanitation and personal hygiene. One hypothesis for the emergence of peptic ulcer disease focuses on the rate of development of atrophic gastritis induced by H. pylori. The hypothesis developed in this article focuses on delay in the age of acquisition of H. pylori to a time when immune and inflammatory responses to the infection were more mature. Whereas the acquisition of H. pylori in infancy usually resulted in mild pangastritis, hypochlorhydria, and a low risk for peptic ulcer disease, delayed acquisition could cause either more severe pangastritis (predisposing to gastric ulceration) or gastritis largely restricted to the antrum of the stomach (predisposing to duodenal ulceration). The decline in the prevalence of peptic ulcer disease over the past 100 years parallels the decline in the prevalence of H. pylori. The epidemic of ulcer disease in the first half of the 20th century seems likely to be an adverse effect of important public health measures undertaken in the latter half of the 19th century.
人类和幽门螺杆菌已经进化和适应了数万年。然而，在 19 世纪之前，消化性溃疡病似乎很少见。消化性溃疡病的患病率在 1850 年至 1900 年间增加，并在 19 世纪末出生的高危人群中达到高峰。这与安全用水的提供、卫生和个人卫生条件的改善同时发生。消化性溃疡病出现的一个假设集中在幽门螺杆菌引起的萎缩性胃炎的发展速度上。本文提出的假设集中在幽门螺杆菌感染获得年龄的延迟上，此时对感染的免疫和炎症反应更加成熟。虽然婴儿期感染幽门螺杆菌通常会导致轻度全胃炎、低胃酸分泌和消化性溃疡病的风险较低，但延迟感染可能导致更严重的全胃炎（易患胃溃疡）或主要局限于胃窦的胃炎（易患十二指肠溃疡）。过去 100 年来消化性溃疡病患病率的下降与幽门螺杆菌患病率的下降相吻合。20 世纪上半叶溃疡病的流行似乎是 19 世纪后半叶实施的重要公共卫生措施的不利影响。
