Murayama Y, Miyagawa J, Shinomura Y, Kanayama S, Yasunaga Y, Nishibayashi H, Yamamori K, Higashimoto Y, Matsuzawa Y
Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Gut. 1999 Nov;45(5):653-61. doi: 10.1136/gut.45.5.653.
BACKGROUND/AIM: Helicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H pylori associated enlarged fold gastritis, suggesting that H pylori infection affects parietal cell function in the gastric body. The aim of this study was to evaluate the effects of H pylori infection on parietal cell morphology and function in hypochlorhydric patients.
PATIENTS/METHODS: The presence of H pylori infection, mucosal length, and inflammatory infiltration were investigated in six patients with enlarged fold gastritis and 12 patients without enlarged folds. Parietal cell morphology was examined by immunohistochemistry using an antibody against the alpha subunit of H(+),K(+)-ATPase and electron microscopy. In addition, gastric acid secretion and fasting serum gastrin concentration were determined before and after the eradication of H pylori.
In the H pylori positive patients with enlarged fold gastritis, fold width, foveolar length, and inflammatory infiltration were increased. In addition, the immunostaining pattern of H(+), K(+)-ATPase was less uniform, and the percentage of altered parietal cells showing dilated canaliculi with vacuole-like structures and few short microvilli was greatly increased compared with that in H pylori positive patients without enlarged folds. After eradication, fold width, foveolar length, and inflammatory infiltrates decreased and nearly all parietal cells were restored to normal morphology. On the other hand, altered parietal cells were negligible in H pylori negative patients. In addition, the basal acid output and tetragastrin stimulated maximal acid output increased significantly from 0.5 (0.5) to 4.1 (1.5) mmol/h and from 2.5 (1.2) to 13.8 (0.7) mmol/h (p<0.01), and fasting serum gastrin concentrations decreased significantly from 213.5 (31.6) to 70.2 (7.5) pg/ml (p<0.01) after eradication in patients with enlarged fold gastritis.
The morphological changes in parietal cells associated with H pylori infection may be functionally associated with the inhibition of acid secretion seen in patients with enlarged fold gastritis.
背景/目的：幽门螺杆菌感染与全胃炎患者胃酸过少有关。此前已有研究表明，根除幽门螺杆菌会导致幽门螺杆菌相关性肥厚性胃炎患者的胃酸分泌增加，这表明幽门螺杆菌感染会影响胃体壁细胞的功能。本研究的目的是评估幽门螺杆菌感染对胃酸过少患者壁细胞形态和功能的影响。
患者/方法：对6例肥厚性胃炎患者和12例无胃皱襞增厚的患者进行幽门螺杆菌感染、黏膜长度和炎症浸润情况的调查。使用抗H(+)，K(+)-ATP酶α亚基的抗体通过免疫组织化学和电子显微镜检查壁细胞形态。此外，在根除幽门螺杆菌前后测定胃酸分泌和空腹血清胃泌素浓度。
在幽门螺杆菌阳性的肥厚性胃炎患者中，皱襞宽度、小凹长度和炎症浸润增加。此外，H(+)，K(+)-ATP酶的免疫染色模式不太均匀，与无胃皱襞增厚的幽门螺杆菌阳性患者相比，显示有扩张的小管和空泡样结构且微绒毛短少的壁细胞改变百分比大大增加。根除后，皱襞宽度、小凹长度和炎症浸润减少，几乎所有壁细胞都恢复到正常形态。另一方面，幽门螺杆菌阴性患者中改变的壁细胞可忽略不计。此外，肥厚性胃炎患者根除幽门螺杆菌后，基础胃酸分泌量和四肽胃泌素刺激的最大胃酸分泌量显著增加，分别从0.5(0.5)mmol/h增至4.1(1.5)mmol/h以及从2.5(1.2)mmol/h增至13.8(0.7)mmol/h(p<0.01)，空腹血清胃泌素浓度从213.5(31.6)pg/ml显著降至70.2(7.5)pg/ml(p<0.01)。
与幽门螺杆菌感染相关的壁细胞形态变化可能在功能上与肥厚性胃炎患者胃酸分泌受抑制有关。
