Love Jack W
Med Hypotheses. 2008;70(6):1103-7. doi: 10.1016/j.mehy.2007.12.011. Epub 2008 Feb 15.
Evidence is reviewed that Helicobacter pylori infection may cause a deficiency of the hormone secretin that allows peptic ulcer disease to develop by impairing the body's defenses to gastric acid. Secretin is released into the circulation from the S-cells of the duodenal crypts in response to gastric acid entering the duodenum. Once in the circulation, secretin has five well-documented effects that protect the upper intestine from gastric acid: it stimulates secretion of bicarbonate rich exocrine pancreatic juice; it stimulates secretion of alkaline bile; it stimulates secretion of alkaline mucus from the duodenal submucosal glands of Brunner; it inhibits the humoral phase of gastric secretion; and it inhibits gastric motility, thereby delaying gastric emptying. Impaired secretin release and reduced duodenal S-cells have been documented in peptic ulcer patients compared with control patients. Clinical evidence that patients with H. pylori infection and peptic ulceration have increased gastric secretion and motility and decreased duodenal bicarbonate response to gastric acid, all of which normalize after eradication of the infection, could be explained by reversible impairment of the secretin mechanism. Gastric metaplasia in the duodenum with H. pylori infection is known to reduce the S-cell population. The fact that not all patients with H. pylori infection develop peptic ulceration suggests that degree of secretin deficiency determined by extent of the infection must reach a critical level for peptic ulceration to occur. Peptic ulceration may be a hormonal deficiency disease, a result of secretin deficiency caused by H. pylori infection. It may be the first example of a specific hormonal deficiency disease caused by a specific bacterial infection.
有证据表明，幽门螺杆菌感染可能导致促胰液素缺乏，从而通过削弱人体对胃酸的防御能力引发消化性溃疡疾病。促胰液素是十二指肠隐窝的S细胞在胃酸进入十二指肠时释放到循环系统中的。一旦进入循环系统，促胰液素具有五种已被充分证实的保护上消化道免受胃酸侵害的作用：它刺激富含碳酸氢盐的外分泌胰液分泌；刺激碱性胆汁分泌；刺激十二指肠Brunner黏膜下腺分泌碱性黏液；抑制胃分泌的体液期；抑制胃蠕动，从而延迟胃排空。与对照患者相比，消化性溃疡患者中促胰液素释放受损和十二指肠S细胞减少的情况已有记录。临床证据显示，幽门螺杆菌感染和消化性溃疡患者的胃酸分泌和胃蠕动增加，十二指肠对胃酸的碳酸氢盐反应降低，而在根除感染后所有这些情况都恢复正常，这可以用促胰液素机制的可逆性损伤来解释。已知幽门螺杆菌感染导致的十二指肠胃化生会减少S细胞数量。并非所有幽门螺杆菌感染患者都会发生消化性溃疡这一事实表明，由感染程度决定的促胰液素缺乏程度必须达到临界水平才会发生消化性溃疡。消化性溃疡可能是一种激素缺乏性疾病，是幽门螺杆菌感染导致促胰液素缺乏的结果。它可能是由特定细菌感染引起的特定激素缺乏性疾病的首个例子。
