THE SOMATOSTATIN-GASTRIN LINK OF HELICOBACTER-PYLORI INFECTION
THE SOMATOSTATIN-GASTRIN LINK OF HELICOBACTER-PYLORI INFECTION
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DOI：
10.3109/07853899509002471
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发表时间：
1995-10-01
影响因子：
4.4
通讯作者：
CALAM, J
中科院分区：
文献类型：
--
作者：
CALAM, J
幽门螺杆菌是新发现的十二指肠溃疡(DU)的病因，但胃酸分泌仍然是必需的，并且在DU患者中升高。Wry团队和其他人提出了幽门螺杆菌本身是否会改变胃生理的问题。这种感染被发现减少了局部抑制肽生长抑素的表达，并增加了促酸激素胃泌素的释放。幽门螺杆菌感染可双向改变胃酸分泌。胃酸在第一次感染时会暂时消失，如果幽门螺杆菌导致胃萎缩，酸可能会在以后减少。DU患者的壁细胞质量大约是正常水平的两倍，这增加了他们的最大分泌能力，但尚不清楚这是否与幽门螺杆菌有关。然而，正如内分泌变化所预期的那样，感染确实改变了对酸分泌的生理控制。在禁食、酸性食物刺激和输注胃泌素释放肽的过程中，胃酸分泌增加。幽门螺杆菌对酸的这些相反作用之间的平衡可能是决定幽门螺杆菌感染的临床结局的关键，高酸分泌会导致DU，而胃溃疡和胃癌患者则发现低酸分泌。幽门螺杆菌胃炎释放的炎性细胞因子可能引起胃生理的某些改变。
Helicobacter pylori is the new-found cause of duodenal ulcers (DU), but acid secretion remains necessary and is elevated in DU patients. Wry group and others have asked whether H. pylori itself alters gastric physiology. This infection has been found to decrease local expression of the inhibitory peptide somatostatin, and to increase release of the acid-stimulating hormone gastrin. H. pylori infection can alter acid secretion in both directions. Acid disappears temporarily on first infection, and may dwindle later if H. pylori causes gastric atrophy. DU patients have approximately twice the normal parietal cell mass, which increases their maximal secretory capacity, but it is not clear whether or not this is due to H. pylori. However, the infection certainly does change physiological control of acid secretion, as expected from the endocrine changes. Acid secretion is elevated during fasting, during stimulation with an acidic meal and during infusions of gastrin-releasing peptide. The balance between these opposing effects of H. pylori on acid may be crucial in determining the clinical outcome of H. pylori infection, High-acid secretion leads to DUs whilst low acid secretion is found in patients with gastric ulcers and gastric cancer. Inflammatory cytokines released in H. pylori gastritis may cause some of these changes in gastric physiology.