Linking laryngopharyngeal reflux to otitis media with effusion: pepsinogen study of adenoid tissue and middle ear fluid

Abstract

Hypothesis/objectives: Laryngopharyngeal reflux (LPR) was recently implicated in the etiology of otitis media with effusion (OME). To study the hypothesis that gastric juice reaches the middle ear through the nasopharynx and eustachian tube, we evaluated the presence of pepsinogen in the adenoid tissues of children with otitis media with effusion (OME) and compared them with the tissues of a control group of children without OME.

Methods: In the study group, middle ear effusions (MEEs) and adenoidal tissue biopsies were obtained from patients undergoing simultaneous tympanostomy tube placement and adenoidectomy. In the control group, adenoid specimens were taken during adenoidectomy (+/- tonsillectomy) from children with no history of OME. The adenoid tissues were analyzed immunohistochemically to confirm the presence of pepsinogen. Normal gastric tissue was used as a positive control and lymphatic tissue as a negative control. Total pepsinogen levels of MEE were measured with enzyme-linked immunosorbent assay.

Results: Adenoid tissue of the OME group (n = 25) demonstrated significantly higher pepsinogen immunoreactivity when compared with the adenoid tissue of the control group (n = 29), specifically in staining of both the epithelia (p < .0001) and the subepithelia, (p < .001). The presence of pepsinogen was detected in 84% of MEEs from the OME group, at concentrations 1.86 to 12.5 times higher than that of serum. Pepsinogen messenger ribonucleic acid was not demonstrated in any of the adenoid tissues of the OME group.

Conclusion: LPR plays an important role in the pathogenesis of OME as gastric reflux reaches the middle ear through the nasopharynx and eustachian tube to cause OME.