Vascular risk factors in sudden hearing loss

Claudia Rudack; Claus Langer; Wolfgang Stoll; Stephan Rust; Michael Walter

doi:10.1160/TH05-08-0554

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2006; 95(03): 454-461
DOI: 10.1160/TH05-08-0554

Blood Coagulation, Fibrinolysis and Cellular Haemostasis

Schattauer GmbH

Vascular risk factors in sudden hearing loss

Claudia Rudack

¹Department of Otorhinolaryngology, Head and Neck Surgery, University Münster, Münster, Germany

,

Claus Langer

²Institute of Clinical Chemistry and Laboratory Medicine, University Münster, Münster, Germany

,

Wolfgang Stoll

¹Department of Otorhinolaryngology, Head and Neck Surgery, University Münster, Münster, Germany

,

Stephan Rust

³Leibniz Institute for Arteriosclerosis Research, University Münster, Münster, Germany

,

Michael Walter

²Institute of Clinical Chemistry and Laboratory Medicine, University Münster, Münster, Germany

³Leibniz Institute for Arteriosclerosis Research, University Münster, Münster, Germany

› Author Affiliations

Abstract

Summary

Low density lipoprotein (LDL) and fibrinogen apheresis was recently reported to be an effective therapy in sudden hearing loss (SHL). In this study, we investigated whether lipoprotein and/or fibrinogen plasma concentrations, related gene polymorphisms and other cardiovascular risk factors are also risk factors for SHL.

Total cholesterol, HDL and LDL cholesterol plasma concentrations, fibrinogen levels, and two functionally relevant fibrinogen polymorphisms were determined in 142 consecutive patients and in 84 age- and sex-matched control subjects of the same ethnic background, using routine laboratory methods and PCR analysis. In addition, we determined the platelet glycoprotein Ia (GPIa) C807T polymorphism, which was recently proposed to be a genetic risk factor for SHL, and we compared the patients’ and controls’ clinical characteristics.

Total and LDL cholesterol concentrations were not different between patients and controls. Fibrinogen plasma levels were significantly increased in SHL patients (260±57 vs. 239±110 mg/dl, p=0.002). However, fibrinogen was not related to SHL in multivariate analysis,and none of the investigated fibrinogen polymorphisms was associated with SHL. By contrast,T allele carriers of the GPIa 807 polymorphic site had an increased risk to develop SHL (OR 1.81) and were more likely not to recover from SHL, compared to C allele carriers (OR 3.0). Moreover, significantly more SHL patients were current smokers (56.3% vs. 19.3% in the control group, p<0.0001).

In conclusion, there is a partial overlap between classical coronary risk factors and risk factors for SHL. Hypercholesterolemia and hypoalphalipoproteinemia (low HDL cholesterol levels) are apparently no major risk factors for SHL, whereas the GPIa C807T polymorphism, elevated fibrinogen levels, and smoking are associated with an increased risk for SHL.Altogether these findings suggest a vascular involvement in the pathogenesis of SHL and may have important implications for the development of therapeutic and preventive strategies.

Keywords

Gene mutations - platelet physiology - fibrinogen / fibrin - lipid mediators - thrombophilia

Full Text

References

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