el-Omar E, Penman I, Dorrian C A, Ardill J E, McColl K E
University Department of Medicine and Therapeutics, Western Infirmary, Glasgow.
Gut. 1993 Aug;34(8):1060-5. doi: 10.1136/gut.34.8.1060.
Helicobacter pylori (H pylori) raises serum gastrin but it is unclear whether this stimulates increased acid secretion. Gastrin mediated acid secretion and plasma gastrin after the intravenous infusion of gastrin releasing peptide was studied in nine H pylori negative and nine H pylori positive healthy volunteers, and in 11 duodenal ulcer patients. Nine of the last group were re-examined one month after eradication of H pylori. The median acid output (mmol/h) to gastrin releasing peptide (40 pmol/kg/h) in the H pylori positive healthy volunteers was 15.1 (range 3.3-38.3), which was three times that of the H pylori negative healthy volunteers (median = 5.5, range 1.0-9.0) (p < 0.02). The median acid output in the duodenal ulcer patients with H pylori was 37 (range 8.5-57), which was > six times that of the H pylori negative healthy volunteers. Eradication of H pylori in the duodenal ulcer patients lowered their acid secretion by a median of 66% (range 30%-80%) (p < 0.01) and to values equivalent to the H pylori positive healthy volunteers. The pepsin output in response to gastrin releasing peptide followed the same pattern as the acid output. The median plasma gastrin concentrations during gastrin releasing peptide were similar in the H pylori positive duodenal ulcer patients (150 ng/l, range 95-400) and H pylori positive healthy volunteers (129 ng/l, range 23-420) and both were appreciably higher than H pylori negative healthy volunteers (60 ng/l, range 28-135) (p < 0.005 for each). Eradication of H pylori lowered the plasma gastrin in the duodenal ulcer patients to values equivalent to the H pylori negative healthy volunteers. These findings show a threefold increase in acid secretion in H pylori positive healthy volunteers that is explained by H pylori induced hypergastrinaemia and a sixfold increase in acid secretion in the duodenal ulcer patients that is explained by the combination of H pylori induced hypergastrinaemia and an exaggerated acid response to stimulation by gastrin. Eradicating H pylori lowers gastrin mediated acid secretion by 66% in duodenal ulcer patients as a result of the resolution of the hypergastrinaemia. Increased gastrin mediated acid secretion seems to be the key factor in the pathophysiology of duodenal ulceration and explains the role of H pylori infection in the disorder.
幽门螺杆菌（H pylori）可使血清胃泌素升高，但尚不清楚这是否会刺激胃酸分泌增加。在9名幽门螺杆菌阴性和9名幽门螺杆菌阳性的健康志愿者以及11名十二指肠溃疡患者中，研究了静脉输注胃泌素释放肽后胃泌素介导的胃酸分泌和血浆胃泌素情况。最后一组中的9名患者在根除幽门螺杆菌1个月后再次接受检查。幽门螺杆菌阳性健康志愿者对胃泌素释放肽（40 pmol/kg/h）的胃酸分泌中位数（mmol/h）为15.1（范围3.3 - 38.3），是幽门螺杆菌阴性健康志愿者的3倍（中位数 = 5.5，范围1.0 - 9.0）（p < 0.02）。幽门螺杆菌阳性的十二指肠溃疡患者的胃酸分泌中位数为37（范围8.5 - 57），是幽门螺杆菌阴性健康志愿者的6倍多。十二指肠溃疡患者根除幽门螺杆菌后，胃酸分泌中位数降低了66%（范围30% - 80%）（p < 0.01），降至与幽门螺杆菌阳性健康志愿者相当的值。胃蛋白酶对胃泌素释放肽的分泌模式与胃酸分泌相同。幽门螺杆菌阳性的十二指肠溃疡患者（150 ng/l，范围95 - 400）和幽门螺杆菌阳性健康志愿者（129 ng/l，范围23 - 420）在胃泌素释放肽刺激期间的血浆胃泌素浓度中位数相似，且均明显高于幽门螺杆菌阴性健康志愿者（60 ng/l，范围28 - 135）（每组p < 0.005）。十二指肠溃疡患者根除幽门螺杆菌后，血浆胃泌素降至与幽门螺杆菌阴性健康志愿者相当的值。这些发现表明，幽门螺杆菌阳性健康志愿者的胃酸分泌增加了3倍，这可由幽门螺杆菌诱导的高胃泌素血症来解释；十二指肠溃疡患者的胃酸分泌增加了6倍，这可由幽门螺杆菌诱导的高胃泌素血症以及对胃泌素刺激的过度胃酸反应共同解释。根除幽门螺杆菌可使十二指肠溃疡患者胃泌素介导的胃酸分泌降低66%，这是高胃泌素血症得到缓解的结果。胃泌素介导的胃酸分泌增加似乎是十二指肠溃疡病理生理学的关键因素，并解释了幽门螺杆菌感染在该疾病中的作用。
