Rolla G, Colagrande P, Scappaticci E, Bottomicca F, Magnano M, Brussino L, Dutto L, Bucca C
Department of Biomedical Sciences and Human Oncology, University of Torino, Italy.
J Allergy Clin Immunol. 1997 Jul;100(1):52-7. doi: 10.1016/s0091-6749(97)70194-5.
In sinusitis bronchoconstriction is supposed to originate from pharyngobronchial reflexes triggered by seeding of the inflammatory process into the pharynx.
Our aim was to evaluate whether in sinusitis bronchial and extrathoracic airway (EA) dysfunction correlate with morphologic abnormalities of the pharyngeal mucosa.
We performed histamine inhalation challenge, nasal lavage, and nasopharyngeal biopsies in 24 nonasthmatic patients with exacerbation of chronic sinusitis. The histamine PC20 was the threshold of bronchial responsiveness, and that causing 25% fall in maximal midinspiratory flow was the threshold of EA responsiveness (PC25MIF50). Thresholds of 8 mg/ml or less were assumed to indicate bronchial hyperresponsiveness (BHR) or EA hyperresponsiveness (EAHR). PC20 and PC25MIF50 values were related to clinical data, nasal lavage fluid eosinophils, pharyngeal epithelium and basement membrane thickness, and density of submucosal vessels and nervous fibers.
The PC20 was closely related to PC25MIF50 (p = 0.0004). Ten patients had EAHR, 9 had combined EAHR and BHR, and 5 had neither EAHR nor BHR. EAHR was strongly associated with epithelial thinning, and BHR with long-standing sinusitis, a lower PC25MIF50, increased submucosal nerve density and increased nasal lavage fluid eosinophils.
Our findings suggest that in nonasthmatic patients with sinusitis, pharyngeal damage may contribute to airway dysfunction by favoring the access of irritants to submucosal nerve endings, with activation of constrictive reflexes to the EA. Proliferation of sensory neurons, consequent to long-lasting pharyngeal inflammation, may cause more severe EA narrowing and activate pharyngobronchial reflexes.
在鼻窦炎中，支气管收缩被认为源于炎症过程蔓延至咽部所触发的咽支气管反射。
我们的目的是评估在鼻窦炎中，支气管和胸外气道（EA）功能障碍是否与咽黏膜的形态学异常相关。
我们对24例慢性鼻窦炎急性加重期的非哮喘患者进行了组胺吸入激发试验、鼻腔灌洗和鼻咽活检。组胺PC20是支气管反应性的阈值，导致最大吸气中期流速下降25%的组胺浓度是EA反应性的阈值（PC25MIF50）。8mg/ml或更低的阈值被认为表明支气管高反应性（BHR）或EA高反应性（EAHR）。PC20和PC25MIF50值与临床数据、鼻腔灌洗液嗜酸性粒细胞、咽上皮和基底膜厚度以及黏膜下血管和神经纤维密度相关。
PC20与PC25MIF50密切相关（p = 0.0004）。10例患者有EAHR，9例患者同时有EAHR和BHR，5例患者既无EAHR也无BHR。EAHR与上皮变薄密切相关，BHR与长期鼻窦炎、较低的PC25MIF50、黏膜下神经密度增加和鼻腔灌洗液嗜酸性粒细胞增加有关。
我们的研究结果表明，在鼻窦炎非哮喘患者中，咽部损伤可能通过促使刺激物接触黏膜下神经末梢，激活对EA的收缩反射，从而导致气道功能障碍。长期咽部炎症导致的感觉神经元增殖，可能会导致更严重的EA狭窄并激活咽支气管反射。
