首页> 外文期刊>Journal of clinical gastroenterology >Detrimental impact of acid and pepsin on the rate of luminal release of transforming growth factor alpha. Its potential pathogenetic role in the development of reflux esophagitis.
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Detrimental impact of acid and pepsin on the rate of luminal release of transforming growth factor alpha. Its potential pathogenetic role in the development of reflux esophagitis.

机译:酸和胃蛋白酶对转化生长因子α的腔释放速率的有害影响。其在反流性食管炎发展中的潜在致病作用。

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摘要

The impact of intraluminal acid and pepsin on the rate of esophageal luminal release of transforming growth factor alpha (TGF alpha), measured by RIA, in 21 asymptomatic volunteers and 26 patients with reflux esophagitis (RE) was investigated. Esophageal secretion was collected, using an esophageal perfusion catheter, during mucosal exposure to NaCl, HCl or HCl/Pepsin and final saline. The basal rate of luminal TGF alpha release in controls was steady throughout the entire four perfusion periods with saline. This rate declined by 71% during mucosal exposure to HCl (p = 0.002) and by 74% during esophageal perfusion with HCl/pepsin (p = 0.011). The basal rate of luminal TGF alpha release in patients with RE was 27% higher than the corresponding value in controls (1.076 +/- 0.140 vs. 0.850 +/- 0.180 ng/min, p = 0.050). Mucosal exposure to acid and acid/pepsin solutions in RE patients also resulted in a significant decline in the luminal release of TGF alpha by 43% (p < 0.001) and by 42% (p < 0.001) respectively. Despite this decline, TGF alpha in patients with RE was significantly higher (p < 0.001) than in controls. The decline in esophageal TGF alpha release during HCl and HCl/pepsin exposure may facilitate the development of mucosal damage. The increase in esophageal TGF alpha release in patients with RE may represent a compensatory mechanism developed by the mucosal inflammatory changes.
机译:通过RIA测定了21名无症状志愿者和26例反流性食管炎患者中的腔内酸和胃蛋白酶对转化生长因子α(TGFα)食管腔腔释放速率的影响。在食管粘膜暴露于NaCl,HCl或HCl /胃蛋白酶和最终生理盐水期间,使用食管灌注导管收集食管分泌物。在整个四个充满盐水的灌注期中,对照组中管腔TGFα释放的基础速率稳定。在粘膜接触HCl时,该比率下降了71%(p = 0.002),在食管中用HCl /胃蛋白酶灌注时,该比率下降了74%(p = 0.011)。 RE患者的管腔TGFα释放基础率比对照组的相应值高27%(1.076 +/- 0.140 ng .. 0.850 +/- 0.180 ng / min,p = 0.050)。 RE患者酸和胃酸/胃蛋白酶溶液的粘膜暴露也导致TGFα的腔内释放分别显着下降43%(p <0.001)和42%(p <0.001)。尽管有这种下降,RE患者的TGFα仍显着高于对照组(p <0.001)。在HCl和HCl /胃蛋白酶接触过程中,食管TGFα释放的下降可能促进粘膜损伤的发展。 RE患者食管TGFα释放的增加可能代表由粘膜炎性变化引起的代偿机制。

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