贲门失弛缓症(achalasia,AC)的病因和发病机制尚未完全阐明,有学者认为下食管括约肌(LES)不能松弛的机制是肠肌丛内抑制性神经元的选择性丧失,导致乙酰胆碱引起肌缩神经的无对抗性兴奋。LES持续性收缩,引起咽下困难、食物反流和胸骨后疼痛等症状。曾有人将本病分为典型(classic)型和高动力(vigorous)型,前者食管明显扩张且缺乏蠕动,后者食管扩张较轻,有高振幅的同步收缩,胸痛症状较突出,但后来Goldenbarg et al证实两者并无明显差别,认为以食管的收缩振幅作为AC分类的标准是不可靠的。我院曾收治1例17岁的男性患者,病程12~+ mo,1a前因急性上呼吸道感染,在输液抗炎治疗的过程中出现咽下困难等AC的症状,推测本病的发生是否与病毒感染或某些药物有关,尚待进一步探讨。 The etiology and pathogenesis of achalasia (AC) have not yet been fully elucidated. Some scholars think that the mechanism by which the lower esophageal sphincter (LES) can not relax is the selective loss of inhibitory neurons in the myenteric plexus, resulting in the contraction of acetylcholine Nervous non-antagonistic excitement. LES persistent contraction, causing swallowing difficulties, food reflux and sternal pain and other symptoms. The disease was divided into classic and vigorous type. The former had significant esophageal expansion and lack of peristalsis. The latter had mild esophageal dilatation and high-amplitude systolic contraction with prominent chest pain. However, Goldenbarg et al confirmed that there was no significant difference between the two, that the esophageal contraction amplitude as AC classification criteria is not reliable. In our hospital, a 17-year-old man was admitted to the hospital for a course of 12 to + mo. The acute upper respiratory tract infection was caused in 1a. Symptoms such as dysphagia caused by AC were observed during the infusion anti-inflammatory treatment. Virus infection or certain drugs, remains to be further explored.