中耳腔貯留液

抄録

In the past decade interest in the pathogenesis of otitis media with effusion (OME) has been renewed along with striking advances in immunology and widespread use of electron microscopy. The clinical aspect of OME seems unlike that of middle ear infection. However, recent immunologic and microbiologic studies have found evidence that the main causative agent of OME is bacterial infection. Many morphologic studies have proved that the mucosa lining the tympanic cavity is a respiratory type, suggesting that the accumulation of effusion can be attributed to the enhanced secretory activity and dysfunction of mucociliary clearance of the mucosa of the tympanic cavity and eustachian tube as well.
Secretory IgA is the main immunoglobulin component in certain external secretions. This immunoglobulin is produced locally in the mucous membrane and secreted to the lumen upon antigenic stimuli. This mechanism is called a local immunologic defense system. The results of several immunochemical and immunobiological studies have demonstrated the presence of a local immune defense system in the middle ear.
Although it is hard to make a definite classification of middle ear effusions, an acceptable proposal came from the Second International Symposium on Recent Advances in Otitis Media with Effusion (Columbus, Ohio, 1979). Any single laboratory criterion could not differentiate an effusion from one belonging to another category. Nevertheless, mucoid, purulent, and even serous effusions each has secretory IgA. It is generally accepted that mucoid effusions come mainly from secretion, while serous effusions come mainly from serum transudation. Thus, middle ear effusion is a mixture of secretion and serum transudation.
On the basis of clinical observations it has been shown that allergy is one of the major causes in the production of middle ear effusion. However, cytologic studies and IgE studies on middle ear effusions failed to find evidence that supports an atopic allergic etiology of this entity. The demonstration of T lymphocytes and elevated C₃ proactivator in middle ear effusions suggests that types III and IV allergic reactions injure the middle ear mucosa, resulting in the formation of middle ear effusion. However, it is still not proven.