Vascular risk factors in sudden hearing loss

Abstract

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.

Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio in Patients with Sudden Sensorineural Hearing Loss

“…It has been believed that bacteria- or virus-induced chronic inflammation could cause microvascular injury, vascular endothelial dysfunction, and atherosclerosis, leading to an increased risk of cochlear ischemia [7, 12, 13]. Furthermore, susceptibility to genetic thrombosis or cardiovascular risk factors would further aggravate the risk of cochlear ischemia [14, 15]. The NLR in peripheral blood has not only been proved to be one of the definitive markers of chronic inflammation in the cardiovascular system, it is also a reliable predictor of functional recovery after vascular disease.…”

Status of Lipid Profile and Uric Acid in Sudden Sensorineural Hearing Loss

“…Also, Kazmierczak H and Doroszeweska G 23 concluded that disturbance of glucose metabolism and hyperinsulinemia may be responsible for inner ear diseases, whereas role of disturbance of lipid metabolism remains vague. Likewise, Claudia Rudack et al 24 found correlation between HDL-CH and LDL-CH and SSNHL. Our study shows higher blood uric acid level in SSNHL group compared to control group.…”

The Significance of Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio as Markers for Prognosis in Idiopathic Sudden Sensorineural Hearing Loss

“…Interestingly, ISSNHL could also be the result of an ear microcirculation alteration due to genetic prothrombotic susceptibility or cardiovascular risk factors such as hypertension and diabetes [14,15]. A higher blood viscosity may determine damage in ear microcirculation that can produce hearing loss [16,17].…”