The etiology of SSNHL is not well understood at present. There are different theories about its etiology and risk factors of SSNHL are a topic of debate across the literature [14
]. Some clinical research indicates that risk factors of SSNHL overlap those of cardiovascular disease, such as hyperfibrinogenemia and smoking [14
]. As far as the correlation between dyslipidemia and SSNHL, opinions vary. A clinical study of 86 subjects in China showed that the levels of total cholesterol (TC), triglyceride (TG), and lipoprotein A (Lp(a)) were significantly higher in patients with SSNHL than in control subjects [15
]. This study indicated plasma viscosity, ratio viscosity of whole blood, reduced viscosity of whole blood, high and low shear relative viscosity of whole blood, index of red blood cells transmutation, and fibrinogen level in the plasma of patients with SSNHL were also significantly elevated in comparison with those in control subjects. In a retrospective study, Oreskovic reported that patients with SSNHL had significantly higher plasma concentrations of cholesterol and low-density lipoprotein cholesterol, compared with controls [7
]. However, their test group was on average 15 years older than the control group, which may have influenced the results. In addition, it is suggested that fibrinogen/LDL apheresis may improve cochlear blood flow by acutely decreasing plasma cholesterol and fibrinogen [11
]. However, it is hard to say whether the therapeutic effect is gained from lowing fibrinogen or LDL. There are also some negative reports of the relationship between dyslipidemia and SSNHL [14
]. In order to add to the clinical evidence of this problem and to avoid selection bias, we carried out this retrospective study with the data of SSNHL patients in a medium-sized clinical hospital of Nantong, China, which is a moderately developed medium-sized city, instead of major medical institutions.
It is generally accepted that serum lipid level is correlated with age and body mass index (BMI) [16
]. Therefore, we matched our disordered group with normal subjects who have the same age, gender and similar weight to avoid these confounding factors. It is also believed hypertension, diabetes and smoking habits could impair vascular tone and integrity in the vascular bed of the ears, thus could promoting SSNHL [4
]. We compared the prevalence of hypertension, diabetes and smoking habits between the SSNHL and control groups, and no significant difference was found. The average of serum lipid data of both groups is in the normal range. Similar results have been reported in previous studies [7
Approximately 40% of LDL particles are enriched with cholesterol, so serum LDL-C levels are related to TC level. A batch of clinical and epidemiological studies demonstrate a continuous, graded relationship of serum LDL level to long-term risk of coronary heart disease and cardiovascular disease (CVD) [5
]. LDL enters the vascular wall through endothelial cells and is detained in subendothelial tissue and converted to the oxidized form(Ox-LDL). Macrophages are engulfed by Ox-LDLs and converted into xanthoma cells. The proliferation and coalescing of xanthoma cell then turns into the lipid core of an atherosclerotic plaque. Therefore, serum level of TC and LDL-C are closely related with thrombotic diseases and some scholars believe cardiovascular risk also has a significant impact on the onset of SSNHL [20
]. Meanwhile, high cholesterol not only affects the inner ear blood supply [21
], but can also affect the activities of outer hair cells by damaging their structure [22
]. Apo B is an elementary composition of LDL-C, which is essential for the binding of LDL particles to the LDL receptor, allowing cells to internalize LDL and thus absorb cholesterol. A considerable amount of data exists to indicate that apo B is a strong predictor of CVD risk [23
]. Our study has shown that TC, LDL-C, and apo B of SSNHL group are significantly higher than those of the control group, which correlates well with the mechanism of these serum lipid parameters leading to CVD. On the other hand, HDL-C and apo AI are considered to be protective factors of CVD [24
]. In this study, SSNHL patients also showed lower HDL-C and apo AI level than controls but this trend was not statistically significant.
As far as mechanism is concerned, there are a lot of studies indicating that dyslipidemia can cause SSNHL by affecting the inner ear blood supply. An animal experiment shows endothelial dysfunction in cerebral arterioles were significantly increased in apoE(-/-) mice on the high-fat diet >6 months compared with the control group [25
]. Another animal experiment found that blood flow in the cochleas was reduced significantly in hypertensive rats exposed to an atherogenic diet compared to that of normotensive or hypertensive control animals [26
]. It is generally accepted that Nitric oxide, a potent vasodilator plays an extremely important role in the blood supply of inner ear [27
]. LDL cholesterol can impair NO release, influencing the blood supply of inner ear, while dyslipidemia [28
]. On the other hand, dyslipidemia can cause SSNHL by damaging the inner ear structure. After the administration of a hyperlipid diet for 3 months, histochemical study of the guinea pigs’ inner ear revealed variations in lipid metabolism and partial disorders of the outer hair cells while electron microscopic observations showed vacuolar and parenchymal protrusions on the surfaces of the striavascularis and Corti’s organ [29
]. It has also been reported that cholesterol has different distributions among outer hair cell membranes, and when water-soluble cholesterol is incorporated into the cells, the outer hair cell lateral wall stiffness parameter increases, which impairs the activity of outer hair cell [22
One of the major limitations of this study is the observational design. In order to avoid bias, we tried to collect as much patient data as possible. Since dyslipidemia may cause SSNHL by affecting the inner ear blood supply with the forming of atherosclerosis plaque, which is also the pathogeny of cardiovascular disease, we did not exclude the patients with CVD. However, no other vascular studies were done in all patients.