The majority of effusion samples contained pepsin/pepsinogen protein; only 29% were active. The pepsin level in effusion samples based on activity is substantially lower than levels based on antibody detection; however, the pH present would irreversibly inhibit pepsin, which would explain the low levels of active enzyme. Pepsin/pepsinogen levels in the effusion samples were up to 1000 times higher than serum levels, whereas albumin and fibrinogen levels were of the same magnitude. The pepsin in middle ear effusions is almost certainly due to reflux of gastric contents, and there may be a role for antireflux therapy in the treatment of otitis media with effusion.

Otitis media with effusion (OME) is the most common cause of deafness in children in the developed world. In this article we aim to present an overview of current research developments on the aetiology of OME and the resulting implications for treatment. In the model we describe, the primary event is inflammation of the middle ear mucosa, usually due to the presence of bacteria. This leads to the release of inflammatory mediators, which cause secretion of a mucin-rich effusion by up-regulating mucin genes. Prolonged stimulation of the inflammatory response and poor mucociliary clearance lead to persistence of the middle ear fluid, giving rise to the clinical presentation of OME. We describe OME in the following sequence: the initial production of the effusion, the composition of the effusion produced, and factors impairing clearance of the effusion.

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Middle ear effusions from children undergoing myringotomy were classified into thick (mucoid) and thin (serous) on the basis of their flow properties. Their composition was analysed and their rheological properties measured. The viscosity of the effusions was measured using a Contraves low shear viscometer and expressed as specific viscosity per mg/ml of non-dialysable solids present. In order to measure the effusion viscosity it was necessary to solubilize the effusion by mild homogenisation in a phosphate buffer pH 6.7 containing a cocktail of proteolytic inhibitors. The viscosity of mucoid effusions was significantly greater than that of the serous effusions. There was a small but measurable amount of proteolytic activity in the effusions, range 0.05-1.79 micrograms/mg of non-dialysable solids. This proteolytic activity was not significantly different between the thick and thin effusions and was therefore unlikely to explain the difference in viscosity. Analysis of the constituents of the effusions showed that glycoprotein and DNA but not protein nor lipid were significantly higher in the mucoid effusions compared to the serous effusions. The viscosity of the effusions correlated with the glycoprotein concentration but not with the protein or lipid concentration. Under certain circumstances the DNA concentration did correlate with the viscosity of the effusion. However, digestion with a proteinase free DNase did not reduce the viscosity of the effusion. These results demonstrate that classifying effusions as thick and thin based on visual inspection and flow properties is valid and that the only constituent present in the effusions that determines viscosity is mucin.