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Changes in gastric ECL cells and parietal cells after long-term administration of high-dose omeprazole to patients with Barrett's esophagus

机译:长期给巴雷特食管患者服用大剂量奥美拉唑后胃ECL细胞和壁细胞的变化

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[Purpose] Long-term administration of PPI causes hyperplastic changes of the gastric parietal cells; however, the detailed mechanism remains to be clarified. We administered high-dose omeprazole to patients with Barrett's esophagus for 2 years, and investigated changes in gastric ECL (Enterochromafiin-like) cells using endoscopic biopsy specimens to clarify the etiology of hyperplasia of the parietal cells. [Methods] The subjects were 69 patients who were diagnosed as having Barrett's esophagus (39 males, 30 females). We established two groups, an omeprazole-treated group and a ranitidine-treated group. Upper digestive tract endoscopy was performed before administration, and 12 and 24 months after the start of administration. Biopsy was performed in the greater curvature of the gastric body. The ECL/parietal cell counts and the grade of hyperplasia of the gastric mucosa were determined under a microscope. In addition, the fasting serum gastrin level was measured, and statistical analysis was performed. [Results] In the omeprazole-treated group, the ECL cell count was markedly increased 12 months after the start of administration, but was lower than the pretreatment value 24 months after the start of administration. The parietal and ECL cell counts significantly increased. Furthermore, there were no changes in mucosa thickness. The fasting serum gastrin level significantly increased. In the ranitidine-treated group, there was no increase in the ECL cell count, and the parietal cell count was decreased. There was no significant increase in mucosa thickness. The fasting serum gastrin level increased, although the rate of increase was markedly smaller than that in the omeprazole-treated group. [Conclusion] Not the direct pharmacological actions of PPI but hypergastrinemia-associated secondary changes may be etiologically involved in hyperplasia of the parietal cells related to long-term administration of PPI.
机译:[目的]长期服用PPI会引起胃壁细胞增生性改变;但是,具体机制还有待澄清。我们对巴雷特食管患者服用了大剂量的奥美拉唑2年,并使用内窥镜活检标本调查了胃ECL(肠嗜铬蛋白样)细胞的变化,以阐明壁细胞增生的病因。方法对69例确诊为巴雷特食管的患者进行治疗,其中男39例,女30例。我们建立了两组,奥美拉唑治疗组和雷尼替丁治疗组。上消化道内镜检查在给药前以及给药开始后12和24个月进行。在胃体较大的弯曲处进行活检。在显微镜下测定ECL /壁细胞计数和胃粘膜增生的等级。另外,测定空腹血清胃泌素水平,并进行统计分析。 [结果]在奥美拉唑治疗组中,ECL细胞计数在开始给药后12个月显着增加,但低于开始给药后24个月的治疗前值。壁细胞和ECL细胞计数显着增加。此外,粘膜厚度没有变化。空腹血清胃泌素水平显着升高。在雷尼替丁治疗组中,ECL细胞计数没有增加,而壁细胞计数却减少了。粘膜厚度没有明显增加。空腹血清胃泌素水平增加,尽管增加的速度明显小于奥美拉唑治疗组。 [结论]与长期服用PPI有关的壁细胞增生可能与病原学有关,不是PPI的直接药理作用,而是高胃泌素血症相关的继发变化。

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