Naylor Gregory, Axon Anthony
Centre for Digestive Diseases, Department of Gastroenterology, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, United Kingdom.
Can J Gastroenterol. 2003 Jun;17 Suppl B:13B-17B. doi: 10.1155/2003/350347.
Gastric bacteria can either be ingested or ascend from the distal bowel; however, their survival is usually limited by gastric acidity and motility. A reduction in gastric acid can result in bacterial overgrowth in the stomach and proximal small bowel, and the number of organisms rises as the intragastric pH rises. The increased risk of noncardia gastric cancer seen in patients with hypochlorhydria may be explained by an excess of nitrites and N-nitroso compounds (NOCs). These compounds are found in the diet of populations with a high gastric cancer risk, but can also be produced by the organisms that exist in the hypochlorhydria stomach. It has long been hypothesized that nitrites and NOCs act as one of the triggers in the atrophy-metaplasia-dysplasia-carcinoma path. However, although indirect data have linked the premalignant changes of metaplasia and dysplasia to NOCs, direct measurement of gastric nitrites and NOCs has not confirmed such a link. The role of Helicobacter pylori in bacterial overgrowth is mainly as a cause of hypochlorhydria resulting from atrophic gastritis, leading to a reduction in the parietal cell mass. Acid-suppressing drugs can result in bacterial overgrowth and increased nitrites and NOCs, although there is no current evidence for an increased risk of gastric cancer in patients taking them. One explanation is that the stomach appears to be colonized by different organisms than those in patients with hypochlorhydria for other reasons. There is some evidence that bacterial overgrowth per se can cause gastric inflammation in mice; however, although in humans the degree of gastric inflammation is greater when overgrowth is more prominent this may simply reflect the greater degree of hypochlorhydria in patients with a more severe H pylori-induced inflammation.
胃内细菌可通过摄入或从远端肠道上行进入；然而，它们的存活通常受胃酸和胃动力的限制。胃酸减少会导致胃和近端小肠细菌过度生长，随着胃内pH值升高，细菌数量增加。胃酸缺乏患者患非贲门胃癌风险增加，可能是由于亚硝酸盐和N-亚硝基化合物（NOCs）过量所致。这些化合物存在于胃癌高发人群的饮食中，但也可由胃酸缺乏的胃内存在的微生物产生。长期以来，人们一直假设亚硝酸盐和NOCs是萎缩-化生-发育异常-癌途径的触发因素之一。然而，尽管间接数据将化生和发育异常的癌前变化与NOCs联系起来，但胃内亚硝酸盐和NOCs的直接测量并未证实这种联系。幽门螺杆菌在细菌过度生长中的作用主要是作为萎缩性胃炎导致胃酸缺乏的原因，导致壁细胞数量减少。抑酸药物可导致细菌过度生长以及亚硝酸盐和NOCs增加，尽管目前没有证据表明服用这些药物的患者患胃癌的风险增加。一种解释是，与因其他原因胃酸缺乏的患者相比，胃内似乎定殖着不同的微生物。有一些证据表明，细菌过度生长本身可在小鼠中引起胃炎症；然而，尽管在人类中，过度生长越明显，胃炎症程度越高，但这可能仅仅反映了幽门螺杆菌诱导的炎症更严重的患者胃酸缺乏程度更高。
