H Einer1, L Tengborn, A Axelsson, S Edström. 1. Department of Otolaryngology--Head and Neck Surgery, Sahlgrenska Hospital, University of Göteborg, Sweden.
Abstract
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.
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.