Rolla G, Colagrande P, Magnano M, Debernardi V, Dutto L, Delpiano L, Cassolino P, Bucca C
Department of Biomedical Sciences and Human Oncology, University of Torino, Italy.
J Allergy Clin Immunol. 1998 Aug;102(2):204-9. doi: 10.1016/s0091-6749(98)70087-9.
Cough associated with gastroesophageal reflux (GER) may originate in extrathoracic airway receptors made hypersensitive by acid-induced mucosal injury.
We investigated the role of laryngeal disease and dysfunction in the pathogenesis of GER-associated cough in nonasthmatic patients.
Seven patients with GER-associated cough were compared with 7 patients with GER but no cough. The patients underwent fiberoptic endoscopy for assessment of laryngitis and esophagitis (expressed by scores); esophageal manometry; 24-hour pH monitoring; lung function tests; and histamine inhalation challenge with assessment of bronchial threshold (concentration provoking 10% fall in FEV1 [PC10]), extrathoracic airway threshold (concentration provoking 25% fall in the maximal midinspiratory flow [PC25MIF50]), and cough threshold (concentration provoking 5 or more coughs PCcough). The patients were reevaluated after 3 months of medical treatment for GER.
Patients with cough, compared with those without cough, had significantly higher laryngitis scores (P = .002), lower esophageal sphincter pressures, longer time with pH below 4 (P = .003), greater number of episodes of reflux longer than 5 minutes (P = .016), longer esophageal clearance time (P = .048), and significantly lower PC25MIF50 (P = .005) and PCcough (P = .008) values. Laryngitis score was significantly inversely related to either PCcough (P < .001) or PC25MIF50 (P <.01) but not to PC10. Laryngitis score, PC25MIF50, and PCcough were all closely related to GER severity. After GER treatment, laryngitis, PC25MIF50, and PCcough were all significantly improved.
These findings suggest that GER-associated cough is strongly associated with laryngeal disease and dysfunction consequent to acid reflux injury in nonasthmatic patients.
与胃食管反流(GER)相关的咳嗽可能起源于因酸诱导的黏膜损伤而变得超敏的胸外气道感受器。
我们研究了喉部疾病和功能障碍在非哮喘患者GER相关性咳嗽发病机制中的作用。
将7例GER相关性咳嗽患者与7例有GER但无咳嗽的患者进行比较。患者接受纤维内镜检查以评估喉炎和食管炎(以评分表示);食管测压;24小时pH监测;肺功能测试;以及组胺吸入激发试验,评估支气管阈值(引起第一秒用力呼气容积[FEV1]下降10%的浓度[PC10])、胸外气道阈值(引起最大吸气中期流速下降25%的浓度[PC25MIF50])和咳嗽阈值(引起5次或更多次咳嗽的浓度[PC咳嗽])。在对GER进行3个月药物治疗后对患者进行重新评估。
与无咳嗽的患者相比,有咳嗽的患者喉炎评分显著更高(P = 0.002),食管下括约肌压力更低,pH低于4的时间更长(P = 0.003),反流持续超过5分钟的发作次数更多(P = 0.016),食管清除时间更长(P = 0.048),并且PC25MIF50(P = 0.005)和PC咳嗽(P = 0.008)值显著更低。喉炎评分与PC咳嗽(P < 0.001)或PC25MIF50(P < 0.01)显著负相关,但与PC10无关。喉炎评分、PC25MIF50和PC咳嗽均与GER严重程度密切相关。GER治疗后,喉炎、PC25MIF50和PC咳嗽均有显著改善。
这些发现表明,在非哮喘患者中,GER相关性咳嗽与酸反流损伤导致的喉部疾病和功能障碍密切相关。