Bernstein J M, Doyle W J
Department of Otolaryngology, State University of New York at Buffalo.
Ann Otol Rhinol Laryngol Suppl. 1994 May;163:15-9. doi: 10.1177/00034894941030s505.
A pathophysiologic model of otitis media with effusion secondary to IgE-mediated hypersensitivity is described. Specific mediators of inflammation are released by mucosal mast cells in the nasal mucosa following the interaction of antigen and specific IgE antibody. These mediators increase vascular permeability, mucosal blood flow, and, most important, mucus production. Furthermore, accessory cell types are recruited by colony-stimulating factors that in turn provide an autocrine-positive feedback for the influx of further inflammatory cells. The eustachian tube is then effectively obstructed by both intrinsic venous engorgement and extrinsic mucus plugs, isolating the middle ear space from the ambient environment. The net result is the increased exchange of nitrogen into the middle ear mucosa from the middle ear cavity. This causes the development of a significant middle ear underpressure that disrupts tight junctions and allows for transudation of fluids into the middle ear space. The prolonged obstruction of the eustachian tube with mucus results in middle ear inflammation, mucosal metaplasia, and increased glandular activities, all of which are hallmarks of chronic otitis media with effusion.
本文描述了一种由IgE介导的超敏反应继发的分泌性中耳炎的病理生理模型。抗原与特异性IgE抗体相互作用后，鼻黏膜中的黏膜肥大细胞释放特定的炎症介质。这些介质增加血管通透性、黏膜血流量，最重要的是增加黏液分泌。此外，集落刺激因子募集辅助细胞类型，进而为更多炎症细胞的流入提供自分泌正反馈。然后，咽鼓管因内在静脉充血和外在黏液栓而有效阻塞，使中耳腔与周围环境隔离。最终结果是中耳腔内氮气向中耳黏膜的交换增加。这导致中耳显著负压的形成，破坏紧密连接并使液体渗入中耳腔。咽鼓管被黏液长期阻塞会导致中耳炎症、黏膜化生和腺体活动增加，所有这些都是慢性分泌性中耳炎的特征。
