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辣椒素受体(TRPV1)与非糜烂性反流病

Capsaicin receptor (TRPV1) and non-erosive reflux disease.

作者信息

Bhat Yasser M, Bielefeldt Klaus

机构信息

Division of Gastroenterology, Hepatology & Nutrition, University of Pittsburgh School of Medicine, PA 15213, USA.

出版信息

Eur J Gastroenterol Hepatol. 2006 Mar;18(3):263-70. doi: 10.1097/00042737-200603000-00006.

Abstract

BACKGROUND/AIM: Non-erosive reflux disease (NERD) is a common and heterogeneous disorder. We hypothesized that changes in peripheral innervation may lead to hyperalgesia and contribute to the development of the disorder.

METHODS

Patients referred for evaluation of reflux symptoms with wireless pH monitoring were asked to provide demographic and clinical data and complete a survey related to severity of reflux symptoms. Endoscopies were performed to rule out macroscopic abnormalities of the esophageal mucosa. Biopsies obtained 2 cm above the gastroesophageal junction were stained for protein gene product 9.5 (PGP 9.5; general neuronal marker) and TRPV1 (capsaicin receptor) immunoreactivity. The density of immunoreactive fibers in the esophageal mucosa was determined morphometrically.

RESULTS

A total of 39 patients without evidence of Barrett's metaplasia, erosive or ulcerative esophagitis were enrolled. Most patients had daily symptoms. The total esophageal acid exposure time was 5.6+/-0.6%, with 16 patients (41%) having increased acid reflux. Immunoreactivity for PGP 9.5 or TRPV1 was detected in papillary structures as well as within the epithelium (free intra-epithelial endings). Total acid-exposure time, but not symptom score or duration correlated significantly with density of PGP 9.5 immunoreactivity and TRPV1 positive fibers.

CONCLUSION

Even in the absence of macroscopic injury, esophageal acid exposure is associated with changes in mucosal innervation of the esophagus, thus potentially further enhancing symptoms in patients with gastroesophageal reflux.

摘要

背景/目的:非糜烂性反流病(NERD)是一种常见的异质性疾病。我们推测外周神经支配的改变可能导致痛觉过敏,并促成该疾病的发展。

方法

对因反流症状接受无线pH监测评估的患者,要求其提供人口统计学和临床数据,并完成一项与反流症状严重程度相关的调查。进行内镜检查以排除食管黏膜的宏观异常。在胃食管交界处上方2 cm处获取的活检组织进行蛋白基因产物9.5(PGP 9.5;一般神经元标志物)和瞬时受体电位香草酸亚型1(TRPV1;辣椒素受体)免疫反应性染色。通过形态计量学确定食管黏膜中免疫反应性纤维的密度。

结果

共纳入39例无巴雷特化生、糜烂性或溃疡性食管炎证据的患者。大多数患者有日常症状。食管总酸暴露时间为5.6±0.6%,16例患者(41%)有酸反流增加。在乳头结构以及上皮内(游离上皮内末梢)检测到PGP 9.5或TRPV1的免疫反应性。总酸暴露时间与PGP 9.5免疫反应性和TRPV1阳性纤维的密度显著相关,而症状评分或持续时间与之无关。

结论

即使在没有宏观损伤的情况下,食管酸暴露也与食管黏膜神经支配的改变有关,从而可能进一步加重胃食管反流患者的症状。

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