Aviv J E, Liu H, Parides M, Kaplan S T, Close L G
Department of Otolaryngology-Head and Neck Surgery, New York-Presbyterian Hospital and College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
Ann Otol Rhinol Laryngol. 2000 Nov;109(11):1000-6. doi: 10.1177/000348940010901103.
There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity in these patients by endoscopic administration of air pulses to the laryngeal mucosa in order to elicit the laryngeal adductor reflex. The purpose of this study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proton pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 25 healthy controls. The laryngopharyngeal sensory level, posterior laryngeal edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LPR were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on H2 blockers for 3 months and then retested. In the dysphagia group, 48 of 54 patients (89%) had edema of the posterior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) had edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, chi2 test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edema in 14 of the 21 (67%) who had pretreatment edema and resolution of sensory deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non-LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvement in laryngeal edema in none of the 11 and improvement in sensory deficits in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI group were significant (p < .01, Fisher's exact test). We conclude that patients with dysphagia and edema of the posterior larynx as a result of LPR have sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and improvement of sensory deficits, both subjectively and objectively.
对于喉咽反流（LPR）患者，目前尚无可靠方法来量化因酸暴露于喉后部而导致的水肿。然而，通过在内镜下向喉黏膜施加气脉冲以引发喉内收肌反射，从而量化这些患者的喉咽敏感性是可行的。本研究的目的是确定LPR患者在喉咽是否存在感觉缺陷，以及用质子泵抑制剂（PPI）治疗这些患者是否能使感觉缺陷得到缓解。对54例无神经系统疾病的吞咽困难患者和25名健康对照者进行了前瞻性的伴有感觉测试的吞咽功能灵活内镜评估。评估了喉咽感觉水平、喉后部水肿和LPR情况。我们将LPR定义为食物从食管入口逆行进入下咽。LPR患者接受3个月的奥美拉唑或兰索拉唑治疗，然后再次进行测试。无LPR的患者接受3个月的H2阻滞剂治疗，然后再次进行测试。在吞咽困难组中，54例患者中有48例（89%）存在喉后部水肿，54例中有42例（78%）存在喉咽感觉缺陷。我们发现54例中有38例（70%）存在LPR。在对照组中，25名受试者中有1例（4%）存在水肿、感觉缺陷和LPR。吞咽困难组与对照组在水肿、感觉缺陷和LPR发生率方面的差异具有统计学意义（p <.001，卡方检验）。23例接受PPI治疗的LPR患者前来复诊，21例治疗前有水肿的患者中有14例（67%）喉水肿得到改善，19例治疗前有感觉缺陷的患者中有15例（79%）感觉缺陷得到缓解。在非LPR、非PPI组中，16例患者中有11例前来复诊，11例患者中无一例喉水肿得到改善，11例中有1例（9.1%）感觉缺陷得到改善。LPR、PPI组与非LPR、非PPI组在喉水肿和感觉缺陷改善情况方面的差异具有统计学意义（p <.01，Fisher精确检验）。我们得出结论，因LPR导致吞咽困难和喉后部水肿的患者在喉咽存在感觉缺陷。用PPI治疗这些患者似乎能使喉咽水肿得到缓解，并在主观和客观上改善感觉缺陷。
