Gillen D, el-Omar E M, Wirz A A, Ardill J E, McColl K E
University Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland.
Gastroenterology. 1998 Jan;114(1):50-7. doi: 10.1016/s0016-5085(98)70632-8.
BACKGROUND & AIMS: Helicobacter pylori-induced hypergastrinemia is accompanied by increased acid secretion in patients with duodenal ulcer (DU) but not in infected healthy volunteers. The aim of this study was to investigate the mechanism underlying this difference.
Thirty-four H. pylori-negative and 20 H. pylori-positive healthy volunteers and 15 H. pylori-positive patients with DU were studied. Maximal acid output and sensitivity to gastrin (gastrin concentration required to achieve 50% maximal acid output) were assessed by examining the dose response to gastrin 17. Inhibitory control was tested by comparing the maximal acid response to cholecystokinin octapeptide with that for gastrin 17.
Sensitivity to gastrin was similar in patients with DU (median, 69.5 ng.L-1; range, 26.2-142) and H. pylori-negative healthy volunteers (median, 82.2 ng.L-1; range, 17.7-410); H. pylori-positive healthy volunteers were less sensitive than either (164.5 ng.L-1; range, 44.8 to > 3360 ng.L-1). Patients with DU had higher maximal acid output (51.2 mmol.h-1; range, 30.8-73.7 mmol.h-1) than either infected healthy volunteers (37.8 mmol.h-1; range, 0.0-65.0 mmol.h-1; P < 0.04) or uninfected healthy volunteers (35.3 mmol.h-1; range, 21.3-67.3 mmol.h-1; P < 0.002). The maximal acid output in both groups of healthy subjects was similar. The proportion of maximal acid output to gastrin 17 achieved by cholecystokinin was similar in patients with DU (36.6%; range, 21.5%-58.2%) and H. pylori-negative healthy volunteers (28.7%; range, 5.9%-85.8%).
A combination of decreased sensitivity to gastrin in infected healthy volunteers and increased maximal acid secretory capacity in patients with DU underlies their different acid response to H. pylori-induced hypergastrinemia.
十二指肠溃疡（DU）患者中，幽门螺杆菌诱导的高胃泌素血症伴有胃酸分泌增加，但在受感染的健康志愿者中并非如此。本研究旨在探讨这种差异背后的机制。
对34名幽门螺杆菌阴性和20名幽门螺杆菌阳性的健康志愿者以及15名幽门螺杆菌阳性的DU患者进行了研究。通过检测对胃泌素17的剂量反应来评估最大胃酸分泌量和对胃泌素的敏感性（达到最大胃酸分泌量50%所需的胃泌素浓度）。通过比较对八肽胆囊收缩素与胃泌素17的最大胃酸反应来测试抑制性控制。
DU患者（中位数为69.5 ng.L-1；范围为26.2 - 142）和幽门螺杆菌阴性的健康志愿者（中位数为82.2 ng.L-1；范围为17.7 - 410）对胃泌素的敏感性相似；幽门螺杆菌阳性的健康志愿者比两者的敏感性都低（164.5 ng.L-1；范围为44.8至> 3360 ng.L-1）。DU患者的最大胃酸分泌量（51.2 mmol.h-1；范围为30.8 - 73.7 mmol.h-1）高于受感染的健康志愿者（37.8 mmol.h-1；范围为0.0 - 65.0 mmol.h-1；P < 0.04）或未受感染的健康志愿者（35.3 mmol.h-1；范围为21.3 - 67.3 mmol.h-1；P < 0.002）。两组健康受试者的最大胃酸分泌量相似。八肽胆囊收缩素达到的胃泌素17最大胃酸分泌量比例在DU患者（36.6%；范围为21.5% - 58.2%）和幽门螺杆菌阴性的健康志愿者（28.7%；范围为5.9% - 85.8%）中相似。
受感染的健康志愿者对胃泌素的敏感性降低以及DU患者最大胃酸分泌能力增加，共同构成了他们对幽门螺杆菌诱导的高胃泌素血症不同胃酸反应的基础。
