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晚期恰加斯病贲门失弛缓症的胃分泌和激素模式。

Gastric secretory and hormonal patterns in end-stage chagasic achalasia.

机构信息

Digestive Surgery Division, Department of Gastroenterology, University of São Paulo School of Medicine, São Paulo, Brazil.

出版信息

Dis Esophagus. 2009;22(7):606-10. doi: 10.1111/j.1442-2050.2009.00961.x. Epub 2009 Mar 17.

Abstract

Achalasia surgical treatment alters the esophagogastric junction anatomy (cardiomyotomy plus fundoplication or esophagectomy and gastric pull-up), thus favoring a certain degree of gastroesophageal reflux. Gastric secretory and hormonal functioning is not completely known in chagasic patients. The aim of this study was to evaluate the gastric secretory and hormonal response in patients with end-stage chagasic achalasia compared with normal subjects. Gastric secretion and hormonal response were assessed by estimation of gastric acid secretion (GAS) in basal condition and after pentagastrin stimulation, basal serum gastrin, and serum pepsinogen (SP) in basal condition and after betazole hydrochloride (Histalog; Eli Lilly and Company, Indianapolis, IN, USA) stimulation in 27 patients with chagasic achalasia. The results were then compared with those of 24 normal subjects. In the chagasic group, the mean basal and stimulated GAS were significantly lower than in the control group (basal: 1.277 vs. 3.13, P = 0.002; stimulated: 15.9 vs. 35.8, P = 0.0001). Chagasic patients' SG levels showed a significantly higher basal value than the control group (83.3 vs. 36.8, P = 0.0001). There was a significant increase of SP after stimulation compared with the basal levels in both chagasic and control groups. Although the chagasic patients' SP values were higher than the controls, this difference was not statistically significant, either in basal and stimulated conditions (basal: 122.0 vs. 108.9, stimulated 120 min: 177.1 vs. 158.9). In patients with chronic Chagas' disease (ChD), although autonomic denervation does not suppress the strength of the gastric mucosal cells' secretory response to stimulation, it reduces GAS (parietal cell) without, however, affecting SP production (chief cells). On the other hand, the gastrin-producing cells have continuously been stimulated by low GAS.

摘要

贲门失弛缓症的手术治疗改变了食管胃结合部的解剖结构(心肌切开加胃底折叠术或食管切除术和胃上提术),从而导致一定程度的胃食管反流。恰加斯病患者的胃分泌和激素功能尚不完全清楚。本研究旨在评估晚期恰加斯病贲门失弛缓症患者与正常对照者的胃分泌和激素反应。通过估计基础状态和五肽胃泌素刺激后的胃酸分泌(GAS)、基础血清胃泌素和基础贝拉唑盐酸(Histalog;印第安纳波利斯 Eli Lilly and Company,IN,USA)刺激后的血清胃蛋白酶原(SP)来评估胃分泌和激素反应,共 27 例恰加斯病贲门失弛缓症患者。然后将结果与 24 例正常对照者进行比较。在恰加斯组中,基础和刺激后的 GAS 均显著低于对照组(基础:1.277 比 3.13,P=0.002;刺激:15.9 比 35.8,P=0.0001)。恰加斯病患者的 SG 水平基础值明显高于对照组(83.3 比 36.8,P=0.0001)。两组患者刺激后 SP 均较基础值显著升高。尽管恰加斯病患者的 SP 值高于对照组,但无论是基础值还是刺激值,差异均无统计学意义(基础:122.0 比 108.9,刺激 120 分钟:177.1 比 158.9)。在慢性恰加斯病(ChD)患者中,尽管自主神经去神经支配不会抑制胃黏膜细胞对刺激的分泌反应强度,但它会降低 GAS(壁细胞),而不会影响 SP 产生(主细胞)。另一方面,胃泌素产生细胞一直受到低 GAS 的刺激。

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