Little F B, Koufman J A, Kohut R I, Marshall R B
Ann Otol Rhinol Laryngol. 1985 Sep-Oct;94(5 Pt 1):516-9. doi: 10.1177/000348948509400521.
A case of subglottic stenosis, recalcitrant to conventional therapy, was associated with asymptomatic aspiration of gastric acid into the larynx. Once the reflux was controlled by use of an antacid regimen and an H2 blocker, the subglottic stenosis resolved and the patient could be decannulated. This case led to the use of an experimental canine model of subglottic stenosis to examine gastric acid as a pathogenic factor in the development of subglottic stenosis. In control animals, mucosal lesions healed without development of stenosis. In experimental animals with mucosal lesions painted with gastric acid, subglottic stenosis developed. When perichondrium and cartilage were violated and gastric acid applied, stenosis was even more severe and developed more rapidly.
一例声门下狭窄患者,常规治疗无效,其与胃酸无症状反流至喉部有关。一旦通过使用抗酸方案和H2阻滞剂控制了反流,声门下狭窄得以缓解,患者可以拔除气管套管。该病例促使使用声门下狭窄的实验性犬模型来研究胃酸作为声门下狭窄发展中的致病因素。在对照动物中,黏膜病变愈合且未发生狭窄。在用胃酸涂抹黏膜病变的实验动物中,出现了声门下狭窄。当软骨膜和软骨受到侵犯并应用胃酸时,狭窄更严重且发展更快。