Vascular risk factors in sudden hearing loss
Claudia Rudack1 , Claus Langer2 , Wolfgang Stoll1 , Stephan Rust 3 , Michael Walter2,3
1 Department of Otorhinolaryngology, Head and Neck Surgery, 2 Institute of Clinical Chemistry and Laboratory Medicine, 3 Leibniz Institute for Arteriosclerosis Research, University Münster, Münster, Germany
Summary
Low density lipoprotein (LDL) and fibrinogen apheresis was recentlyreported to be an effective therapy in sudden hearing loss(SHL). In this study, we investigated whether lipoprotein and/orfibrinogen plasma concentrations, related gene polymorphismsand other cardiovascular risk factors are also risk factors forSHL.Total cholesterol, HDL and LDL cholesterol plasma concentrations,fibrinogen levels, and two functionally relevant fibrinogenpolymorphisms were determined in 142 consecutive patientsand in 84 age- and sex-matched control subjects of thesame ethnic background, using routine laboratory methods andPCR analysis. In addition, we determined the platelet glycoproteinIa (GPIa) C807T polymorphism, which was recently proposedto be a genetic risk factor for SHL, and we compared thepatients’ and controls’ clinical characteristics.Total and LDL cholesterol concentrations were not different betweenpatients and controls. Fibrinogen plasma levels were significantlyincreased in SHL patients (260±57 vs. 239±110 mg/dl, p=0.002). However, fibrinogen was not related to SHL in multivariateanalysis,and none of the investigated fibrinogen polymorphismswas associated with SHL. By contrast,T allele carriers ofthe GPIa 807 polymorphic site had an increased risk to developSHL (OR 1.81) and were more likely not to recover from SHL,compared to C allele carriers (OR 3.0). Moreover, significantlymore SHL patients were current smokers (56.3% vs. 19.3% inthe control group, p<0.0001).In conclusion, there is a partial overlap between classical coronaryrisk factors and risk factors for SHL. Hypercholesterolemiaand hypoalphalipoproteinemia (low HDL cholesterol levels) areapparently no major risk factors for SHL, whereas the GPIaC807T polymorphism, elevated fibrinogen levels, and smokingare associated with an increased risk for SHL.Altogether thesefindings suggest a vascular involvement in the pathogenesis ofSHL and may have important implications for the developmentof therapeutic and preventive s Keywords
thrombophilia, gene mutations, platelet physiology, fibrinogen / fibrin, lipid mediators
DOI
http://dx.doi.org/10.1160/TH05-08-0554