Genetic and Acquired Prothrombotic Risk Factors and Sudden Hearing Loss

2007 ◽  
Vol 117 (3) ◽  
pp. 547-551 ◽  
Author(s):  
Pasquale Capaccio ◽  
Francesco Ottaviani ◽  
Valeria Cuccarini ◽  
Alessandro Bottero ◽  
Antonio Schindler ◽  
...  
2012 ◽  
Vol 51 (11) ◽  
pp. 800-805 ◽  
Author(s):  
Massimo Fusconi ◽  
Antonio Chistolini ◽  
Armando de Virgilio ◽  
Antonio Greco ◽  
Fulvio Massaro ◽  
...  

2005 ◽  
Vol 26 (6) ◽  
pp. 383-387 ◽  
Author(s):  
Pasquale Capaccio ◽  
Francesco Ottaviani ◽  
Valeria Cuccarini ◽  
Umberto Ambrosetti ◽  
Enrico Fagnani ◽  
...  

2011 ◽  
Vol 16 (3) ◽  
pp. 185-190 ◽  
Author(s):  
Massimo Fusconi ◽  
Antonio Chistolini ◽  
Noemi Angelosanto ◽  
Patrizia Pignoloni ◽  
Mario Tombolini ◽  
...  

2006 ◽  
Vol 95 (03) ◽  
pp. 454-461 ◽  
Author(s):  
Claudia Rudack ◽  
Claus Langer ◽  
Wolfgang Stoll ◽  
Stephan Rust ◽  
Michael Walter

SummaryLow 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.


Author(s):  
Jin Wook Kwak ◽  
Su Jin Lim ◽  
Young-Ho Hong ◽  
Seog-Kyun Mun

Author(s):  
Yoon Seok Choi ◽  
Si-Youn Song ◽  
Yong-Dae Kim ◽  
Chang Hoon Bae

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