胃食管反流病发病及症状感知机制

Mechanism of gastroesophageal refl ux disease pathogenesis and its symptom perception

胃食管反流病(GERD)的症状和并发症可能是由多种因素的机制产生的,其中包括了胃酸和胃蛋白酶等重要的致病因素。食管黏膜与反流的食物长期接触可能是由一个有缺陷的抗反流屏障和腔隙清除机制所导致的,也可能是食管上皮肉眼可观察到损伤产生的。对酸敏感的神经末梢受体可能在食管疼痛与食管感觉过敏的发生过程中发挥着作用。同时,特定细胞因子和趋化因子的分布似乎决定了GERD的不同表型。其部分解释了一部分患者的食管炎发生机制。尽管这些研究结果显示在GERD发病机制中有额外的炎症介质和神经递质产生,但食管过敏与食管炎症之间的关系仍然不明确。此外,胃食管反流病患者绝大多数(70%)不发展食为管糜烂,被称为非糜烂性反流病。探讨GERD发病机制中炎症的激活途径,以更好地了解的侵蚀性和非糜烂性反流病患者,并提供新的治疗方法。

The pathogenesis of GERD symptoms may have a multifactorial mechanism, in which noxious factors, including acid-pepsin and acid, are involved. The interaction ofrefluxed content and esophageal mucosa probably caused by a defective luminal clearance and mucosa barrier mechanisms, would be responsible for visual detectable lesion of esophageal mucosa. The researches of animal models with long time contact of acid content demonstrated that receptors on nerve endings may be involved in esophageal sensitivity and nociception. At the meantime, specific chemokine and cytokine may explain the different esophageal subtypes of GERD, partly illuminating the genesis of esophagitis in a subtype. Researches indicate that there are additional neurotransmitters and inflammatory mediators in GERD patients, the relationship of the esophageal inflammation and hypersensitivity is still not clear. Moreover, over 70% of GERD patients don＇t to be erosive, a subset called non-erosive reflux disease. This summary aims to elucidate the pathogenesis of inflammatory in GERD to differentiate erosive and non-erosive reflux disease and provide new therapeutic approaches.