The analyses of middle ear effusion (MEE) in otitis media may prove important information for better understanding of etiology, evaluation of inflammatory stages of the middle ear cavity, and evaluation of the efficacy of the treatment. Biochemical composition of serous and mucoid effusion has been characterized in terms of enzymes (lactate dehydrogenase, (LDH), lysozyme, alkaline and acid phosphates), and hexosamine content of MEE. In addition to immunoglobulin (IgA, G, and M) content, several new immunochemical parameters (immune complexes, complements, secretory IgA) and histamines have been determined in various types of MEE. Bacteriological findings of MEE, age of patients, viscosity of MEE, and clinical course (fresh or recurrent) have been correlated with the results of biochemical and immunochemical analyses of MEE. Parallel studies of animal models (serous otitis media by eustachian tube obstruction, purulent otitis media by direct innoculation of pneumococcus) showed sequential changes of mucoperiosteum and alteration of enzyme levels (LDH, lysozyme) at various times after the induction of experimental otitis media. It was found that LDH and lysozyme levels were higher in the purulent otitis media group than in the serous otitis media group and that enzyme levels decreased with clearing of the bacteria along with the resorption of inflammatory changes evidenced by histology. Human MEE studies showed that lysozyme levels were higher in the culture positive group than in the negative group, substantiating the animal findings. Strong indications have been shown that biochemical and immunochemical characteristics of MEE can reflect the degree of inflammatory changes in the middle ear cavity. Thus, baseline information necessary to specify the factors responsible for chronicity or the tendency of recurrence of otitis media has been established. Further longitudinal studies are necessary to evaluate the efficacy of presently available treatment on the management of the disease process in otitis media.
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|Published - Mar 1982