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May 1994

Sudden Sensorineural Hearing Loss and Hemostatic Mechanisms

Author Affiliations

From the Departments of Otolaryngology—Head and Neck Surgery (Drs Einer, Axelsson, and Edström) and Internal Medicine (Dr Tengborn), Sahlgrenska Hospital, University of Göteborg (Sweden).

Arch Otolaryngol Head Neck Surg. 1994;120(5):536-540. doi:10.1001/archotol.1994.01880290046008

Objective:  To evaluate the possible causal role of pathologic hemostatic mechanisms in sudden hearing loss.

Design:  The study was prospective.

Setting:  The patients were hospitalized, and all tests were performed at the hospital.

Patients:  Thirty-two consecutive patients with sudden hearing loss participated, as well as a control group of 28 healthy individuals. The control group was matched with regard to body mass index.

Main Outcome Measures:  Venous blood analyses were made regarding general blood parameters, as well as specific hemostatic parameters.

Results:  Twenty-five of the patients had some kind of aberration of specific hemostasis parameters; seven patients had an increase in the activity of the plasminogen activator inhibitor 1 (ie, a glycoprotein associated with diminished fibrinolysis) compared with that in the control group (P<.05). Increased plasminogen activator inhibitor levels were most frequently observed among the patients who were overweight. Seven of the oldest patients had an increase of D-dimers, ie, a degradation product of fibrin, and most of these patients had a history of cardiovascular disease.

Conclusion:  Although isolated aberrations in the hemostatic pathway were observed, we concluded that pathologic hemostasis does not seem to have a decisive importance for the pathogenesis of sudden deafness.(Arch Otolaryngol Head Neck Surg. 1994;120:536-540)