Hurlimann S, Dür S, Schwab P, Varga L, Mazzucchelli L, Brand R, Halter F
Gastrointestinal Unit, Inselspital, Berne, Switzerland.
Am J Gastroenterol. 1998 Aug;93(8):1277-85. doi: 10.1111/j.1572-0241.1998.409_x.x.
There is strong evidence accumulating that chronic infection with Helicobacter pylori (H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis.
H. pylori status was assessed by CLO test and histology (two biopsies each from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender. Gastritis score was assessed by a pathologist, who was unaware of the acid secretory data. Following determination of BAO, the relation of pentagastrin and gastric acid secretion was established with a cumulative pentagastrin dose response curve for the dose range 0.03-6.0 microg/kg(-1) h(-1) and MAO (Vmax) and pentagastrin sensitivity (ED50) were determined. Basal and postprandial gastrin release was measured by radioimmunoassay.
There was a significant higher gastritis score in the H. pylori-positive compared with the H. pylori-negative subjects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. pylori-negative groups. No correlation was seen between the gastritis score, basal acid output (BAO) peak acid output (PAO), maximum acid output (MAO), ED50 values and the plasma gastrin values. There was, however, a considerable larger variation of the PAO and MAO data of the H. pylori-infected subjects and >50% of the respective data was above or below the relatively low range of the respective values of the noninfected subjects.
H. pylori-induced gastritis does not regularly enhance maximum acid output in nonulcer patients, nor does it modify the sensitivity of the parietal cell to gastrin. H. pylori infection is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum acid secretory capacity in certain subgroups of patients.
越来越多的确凿证据表明，幽门螺杆菌（H. pylori）慢性感染会干扰胃酸分泌调节的抑制途径。然而，十二指肠溃疡病（DU）患者中常见的最大胃酸分泌量（MAO）增加以及壁细胞对胃泌素敏感性增加的现象，在很大程度上仍无法解释。关于这些参数在非消化性溃疡病（PUD）患者中如何受H. pylori感染影响以及它们与H. pylori诱导的胃炎之间的关系，现有证据不足。本研究的目的是比较未患PUD的H. pylori阳性和H. pylori阴性患者的基础胃酸分泌（BAO）、MAO以及壁细胞对胃泌素的敏感性，并研究其与个体餐后胃泌素释放以及胃窦和胃体胃炎程度的关系。
通过CLO试验和组织学检查（分别从胃窦和胃体各取两块活检组织）评估了14名年龄、体重和性别相当的H. pylori阳性和16名H. pylori阴性的非溃疡患者的H. pylori状态。由一位不了解胃酸分泌数据的病理学家评估胃炎评分。在测定BAO之后，通过0.03 - 6.0μg/kg⁻¹ h⁻¹剂量范围内的累积五肽胃泌素剂量反应曲线确定五肽胃泌素与胃酸分泌的关系，并测定MAO（Vmax）和五肽胃泌素敏感性（ED50）。通过放射免疫分析法测定基础和餐后胃泌素释放。
与H. pylori阴性受试者相比，H. pylori阳性受试者的胃炎评分显著更高。H. pylori阳性和H. pylori阴性组之间五肽胃泌素刺激胃酸分泌的剂量反应曲线没有差异。胃炎评分、基础酸分泌量（BAO）、峰值酸分泌量（PAO）、最大酸分泌量（MAO）、ED50值与血浆胃泌素值之间均未发现相关性。然而，H. pylori感染受试者的PAO和MAO数据变化相当大，各自超过50%的数据高于或低于未感染受试者相应值的相对较低范围。
H. pylori诱导的胃炎并不会规律性地增强非溃疡患者的最大胃酸分泌量，也不会改变壁细胞对胃泌素的敏感性。因此，H. pylori感染不太可能直接导致DU病中这些参数的增加。然而，我们的数据支持这样一种观点，即慢性H. pylori感染在某些患者亚组中可能增强或减弱最大胃酸分泌能力。
