Bernstein J M
Department of Otolaryngology, State University of New York, Buffalo.
Otolaryngol Clin North Am. 1992 Feb;25(1):197-211.
The potential mechanisms of IgE-mediated hypersensitivity in OME have been reviewed. Two important questions were addressed at the beginning of this manuscript: (1) is OME an allergic disease, or (2) is OME a complication of an allergic disease in another part of the respiratory system? In regard to the first question, recurrent OME is associated with allergic rhinitis in about one-third of the studied population. However, of the patients who do have allergic rhinitis, in the great majority of children the middle ear mucosa is not the target organ. Rather, there appears to be increasing evidence that with both nasal provocation and natural antigen provocation in children during a normal allergen season, eustachian tube function is altered by nasal allergy. Whether this is truly physiologic or an artificial phenomenon cannot be determined at this time, as it is not absolutely clear whether the nine-step eustachian tube function test currently performed is really a measure of eustachian tube dysfunction, despite its forming the basis of all studies published so far, although one must conclude from current data that allergic rhinitis can produce eustachian tube dysfunction; there have been no cases in these studies in which allergic rhinitis produced otitis media. However, eustachian tube dysfunction is one of the major precursors in the development of OME. We believe that the anatomic part of the upper respiratory tract involved in the IgE-mediated hypersensitivity is most likely the mucosa of the nasopharyngeal portion of the eustachian tube. Inasmuch as total nasal obstruction, at least in adults, does not produce eustachian tube dysfunction in the great majority of cases, it is proposed that eustachian tube dysfunction that follows nasal provocation and occurs during the normal allergy season does so as a result of the transport of mediators of inflammation from inflammatory cells in the nasal mucosa via the nasal mucociliary system to the nasopharyngeal orifice of the eustachian tube. The role of food allergy is still problematic, but this author suggests that there is some supportive evidence that food immune complexes, particularly with dairy products, may play a role, especially in the otitis-prone child under the age of 2 years.(ABSTRACT TRUNCATED AT 400 WORDS)
关于分泌性中耳炎(OME)中IgE介导的超敏反应的潜在机制已进行了综述。在本手稿开头提出了两个重要问题:(1)OME是一种过敏性疾病,还是(2)OME是呼吸系统另一部位过敏性疾病的并发症?关于第一个问题,在约三分之一的研究人群中,复发性OME与过敏性鼻炎相关。然而,在患有过敏性鼻炎的患者中,绝大多数儿童的中耳黏膜并非靶器官。相反,越来越多的证据表明,在正常过敏原季节,儿童经鼻腔激发试验和天然抗原激发试验后,鼻过敏会改变咽鼓管功能。目前尚无法确定这是真正的生理现象还是人为现象,因为目前尚不完全清楚当前进行的九步咽鼓管功能测试是否真的能衡量咽鼓管功能障碍,尽管它是迄今为止所有已发表研究的基础,不过从现有数据可以得出结论,过敏性鼻炎可导致咽鼓管功能障碍;在这些研究中,尚无过敏性鼻炎导致中耳炎的病例。然而,咽鼓管功能障碍是OME发生发展的主要先兆之一。我们认为,上呼吸道中参与IgE介导的超敏反应的解剖部位很可能是咽鼓管鼻咽部的黏膜。由于至少在成年人中,完全性鼻阻塞在大多数情况下不会导致咽鼓管功能障碍,因此有人提出,在正常过敏季节经鼻腔激发试验后出现的咽鼓管功能障碍,是由于炎症介质从鼻黏膜中的炎性细胞经鼻黏液纤毛系统转运至咽鼓管的鼻咽部开口所致。食物过敏的作用仍存在问题,但本文作者认为,有一些支持性证据表明食物免疫复合物,尤其是乳制品中的免疫复合物,可能起作用,特别是在2岁以下易患中耳炎的儿童中。(摘要截选至400字)