Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1983 Mar-Apr;95(3-4):341-9.
doi: 10.3109/00016488309130952.

Granulocyte protease inhibition in acute and chronic middle ear effusion

Granulocyte protease inhibition in acute and chronic middle ear effusion

B Carlsson et al. Acta Otolaryngol. 1983 Mar-Apr.

Abstract

A comparative study was made of granulocyte proteases and protease inhibitors in middle ear effusions (MEE) from patients with acute otitis media (OMA) and serous otitis media (SOM). The mean concentrations of the granulocyte proteases, neutral protease and elastase were three- to fourfold higher in OMA as compared to SOM effusions. The mean concentration of granulocyte elastase in SOM effusions was approximately 1 400, and in OMA effusions 5 500 times higher than the corresponding plasma concentrations. In OMA patients the individual MEE/plasma ratios of the main plasma protease inhibitors, alpha 1-antitrypsin, antichymotrypsin and alpha 2-macroglobulin, showed a positive uniform correlation with corresponding albumin MEE/plasma ratios. In SOM effusions, the concentration of alpha 2-macroglobulin was low, indicating a restricted membrane passage in SOM. In SOM effusions both alpha 1-antitrypsin and the locally produced antileukoprotease showed a residual inhibitory capacity. In OMA effusions the inhibitory capacity of anti-leukoprotease was saturated, whereas there was a residual inhibitory capacity of alpha 1-antitrypsin. However, in those OMA effusions, where large amounts of alpha 1-antitrypsin complexes with granulocyte proteases were found, most of the remaining free alpha 1-antitrypsin was inactive.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources