Vascular risk factors in sudden hearing loss
Vascular risk factors in sudden hearing loss
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DOI：
10.1160/th05-08-0554
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发表时间：
2006-03-01
影响因子：
6.7
通讯作者：
Walter, M
中科院分区：
文献类型：
--
作者：
Rudack, C;Langer, C;Walter, M
低密度脂蛋白（LDL）和纤维蛋白原分离术最近被报道为治疗突发性听力损失（SHL）的有效方法。在这项研究中，我们调查了脂蛋白和/或纤维蛋白原血浆浓度、相关基因多态性和其他心血管危险因素是否也是SHL的危险因素。采用常规实验室方法和PCR分析，对142例连续患者和84例年龄和性别匹配的相同种族背景的对照组进行了总胆固醇、高密度脂蛋白和低密度脂蛋白血浆浓度、纤维蛋白原水平和两种功能相关的纤维蛋白原多态性检测。此外，我们检测了血小板糖蛋白Ia (GPIa) C807T多态性，这是最近提出的SHL的遗传危险因素，我们比较了患者和对照组的临床特征。总胆固醇和低密度脂蛋白胆固醇浓度在患者和对照组之间没有差异。SHL患者血浆纤维蛋白原水平显著升高（260 57 vs 239 110 mg/dl, p=0.002）。然而，在多变量分析中，纤维蛋白原与SHL无关，所研究的纤维蛋白原多态性均与SHL无关。相比之下，gpia807多态性位点的T等位基因携带者发生SHL的风险增加（OR为1.81），与C等位基因携带者相比（OR为3.0），更有可能无法从SHL中恢复。此外，SHL患者中吸烟者的比例显著高于对照组（56.3% vs. 19.3%, p < 0.0001）。总之，经典冠状动脉危险因素与SHL危险因素之间存在部分重叠。高胆固醇血症和低脂蛋白血症（低高密度脂蛋白胆固醇水平）显然不是SHL的主要危险因素，而GPIa C807T多态性、纤维蛋白原水平升高和吸烟与SHL的风险增加有关。总之，这些发现表明血管参与了SHL的发病机制，并可能对治疗和预防策略的发展具有重要意义。
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.