Risk Factor For Sudden Sensorineural Hearing Loss Research Articles

Associations of Blood Lipids with the Risk and Prognosis of Sudden Sensorineural Hearing Loss: A Meta-analysis.

Patients with sudden sensorineural hearing loss (SSNHL) may lose their hearing. The relationship between SSNHL and total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels is still unclear. The association of TC, TG, HDL-C, and LDL-C levels with the risk and prognosis of SSNHL was explored in this study. After searching for literature in different databases, 13 researches were used to summarize the risk and prognosis of SSNHL associations with TC, TG, HDL-C, and LDL-C using meta-analysis. Total cholesterol had a significant association with the risk of SSNHL (95% CI, 1.34-2.91). Adjustment for confounding factors and grouping criteria of TG were all significant sources of heterogeneity. One of the significant sources of heterogeneity in the LDL-C subgroup analyses was an adjustment for confounders. Sensitivity analysis revealed a robust association between TC and the risk of SSNHL. There was a significant publication bias in the association between TC and SSNHL prognosis High TC level is a risk factor for SSNHL.

Causal associations of thyroid function and sudden sensorineural hearing loss: a bidirectional and multivariable Mendelian randomization study

BackgroundObservational studies have indicated a potential association between thyroid dysfunction and the risk of sudden sensorineural hearing loss (SSNHL). However, the precise causal relationship between the two remains uncertain. The objective of our study was to assess the causal influence of thyroid function on SSNHL by employing a bidirectional and multivariable Mendelian randomization (MR) approach.MethodsSingle-nucleotide polymorphisms (SNPs) associated with free thyroid (FT4) and thyroid stimulating hormone (TSH) were selected from the summary data of a large genome-wide association study (GWAS) conducted on European individuals. The summary-level data of SSNHL were also obtained from a GWAS, which included 196,592 participants (1,491 cases and 195,101 controls). The MR analysis primarily utilized the inverse variance weighted (IVW) method, with sensitivity analyses performed using the weighted median, MR-Egger, and MR-PRESSO approaches.ResultsIn the IVW method, an elevated genetically predicted FT4 level was found to effectively reduce the risk of SSNHL (OR = 0.747, 95% CI = 0.565–0.987, P = 0.04). These findings were consistent when conducting multivariate MR analysis, which adjusted for TSH levels (OR = 0.929, 95% CI = 0.867–0.995, P = 0.036). However, genetically predicted TSH levels did not emerge as a risk factor for SSNHL (OR = 1.409, 95% CI = 0.895–1.230, P = 0.547). Furthermore, even after adjusting for FT4 levels in the multivariate MR analysis, no evidence of a direct causal relationship between TSH levels and the risk of SSNHL was observed (OR = 1.011, 95% CI = 0.880–1.161, P = 0.867). The reverse MR analysis showed that there was no evidence of a direct causal relationship between SSNHL and the risk of FT4 level (OR = 1.026, 95% CI = 0.999–1.054, P = 0.056) or TSH level (OR = 1.002, 95% CI = 0.989–1.015, P = 0.702).ConclusionWithin the normal range, genetic variants associated with higher FT4 levels demonstrate a potential protective effect against SSNHL, whereas there is no direct causal relationship between TSH levels and the risk of SSNHL.

Comorbidities and laboratory changes of sudden sensorineural hearing loss: a review.

Sudden sensorineural hearing loss (SSNHL) is defined as an abrupt hearing loss of more than 30 dB in three contiguous frequencies within 72 h. It is an emergency disease requiring immediate diagnosis and treatment. The incidence of SSNHL in Western countries' population is estimated between 5 and 20 per 1,00,000 inhabitants. The etiology of SSNHL remains unknown. Due to the uncertainty of the cause of SSNHL, at present, no specific treatment targets the cause of SSNHL, resulting in poor efficacy. Previous studies have reported that some comorbidities are risk factors for SSNHL, and some laboratory results may provide some clues for the etiology of SSNHL. Atherosclerosis, microthrombosis, inflammation, and the immune system may be the main etiological factors for SSNHL. This study confirms that SSNHL is a multifactorial disease. Some comorbidities, such as virus infections, are suggested to be the causes of SSNHL. In summary, by analyzing the etiology of SSNHL, more targeting treatments should be used to achieve a better effect.

Atrial Fibrillation Is Not Associated With Sudden Sensorineural Hearing Loss.

The aim of this study is to assess the association between atrial fibrillation (AF) and sudden sensorineural hearing loss (SSNHL). This study was conducted by searching the longitudinal health insurance database of the Taiwan National Health Insurance Program for relevant information from January 1, 2000, to December 31, 2011. Patients with AF were matched with non-AF controls with a 1:1 strategy according to propensity scores. Multiple logistic regression analyses were performed to determine the risk of SSNHL. In total, 14 698 patients with AF were matched with the same number of non-AF patients as controls. After propensity score matching, the use of antiplatelet or anticoagulation medications and the occurrence of SSNHL were found to have a significant difference between AF and non-AF patients. The occurrence of SSNHL was found to be higher in men, those of 45 to 74 years old, and patients with hypertension in both AF and non-AF groups. Multiple logistic regression analyses revealed that male gender, age between 45 and 74 years, hyperlipidemia, and hypertension are risk factors for SSNHL. The use of aspirin was found to reduce the rate of SSNHL (odds ratio [OR]: 0.67, 95% CI: 0.49-0.94, P = .019), but AF was not found to be a risk factor for SSNHL (OR: 0.89, 95% CI: 0.64-1.23, P = .467). The association between AF and SSNHL is not significant.

ENOS gene Glu298Asp variant confer risk in sudden sensorineural hearing loss

Background: Sudden sensorineural hearing loss (SSNHL) causes the loss of hearing of 30 dB or greater on at least three contiguous frequencies. It is known to be a multifactorial disease which the exact cause is unknown, rendering it as an idiopathic disorder of patients.Aims/objectives: This study aims to shed further light on pathogenesis of this disease by studying the association between eNOS gene Glu298Asp polymorphism and VDR gene FokI polymorphism with SSNHL in Iranian population.Material and methods: This study involves a total of 77 cases and 100 controls, with patients inflicted with SSNHL categorized in case group and healthy subjects as control group. Genotyping of the VDR and eNOS genes was conducted by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) method.Results: Our results showed a statistically significant association between genotype frequencies of eNOS gene Glu298Asp polymorphism in case group compared to healthy individuals in the control group (p = .01). Also, TT genotype was significantly the most prevalent genotype in case group in comparison to control group (TT vs GT + GG, OR = 3.5; 95% CI = 1.18–11.79). On the other hand, analysis of VDR gene FokI polymorphism frequencies showed no statistically significant association with SSNHL.Conclusions and significance: Our findings showed a significant association between the eNOS gene Glu298Asp polymorphism and SSNHL in the Iranian population; and “TT” genotype might be considered as a risk factor for SSNHL.

The Role of Autoimmunity in the Pathogenesis of Sudden Sensorineural Hearing Loss.

Sudden sensorineural hearing loss (SSHL) is a clinically common acute symptom in otolaryngology. Although the incidence of SSHL has increased around the world in recent years, the etiology of the disease is still unclear. It has been reported that infections, ototoxic drugs, membrane labyrinth rupture, carcinomas, circulatory system diseases, autoimmune diseases, brain lesions, mental diseases, congenital or inherited diseases, and so on, are all risk factors for SSHL. Here, we discuss the autoimmune mechanisms behind SSHL, which might be induced by type II–IV allergic reactions. We also introduce the main immunosuppressive medications that have been used to treat SSHL, which will help us to identify potential targets for immune therapy.

Risk of sudden sensorineural hearing loss in patients with common preexisting sensorineural hearing impairment: a population-based study in Taiwan.

ObjectiveThe role of preexisting sensorineural hearing impairment on the risk for sudden sensorineural hearing loss (SSHL) is still unclear. In this study, we aimed to assess the risk of SSHL in patients with common preexisting sensorineural hearing impairment using population-based data.MethodsA population-based case-control study design was used to analyze claims data between January 2001 and December 2011 obtained from the Taiwan National Health Insurance Research Database. The cases consisted of 514 patients with SSHL and the controls were frequency matched to 2,570 cases by sex, 10-year age group, and year of index date. Common sensorineural hearing impairments were retrospectively assessed in the cases and controls. Associations between sensorineural hearing impairment and risk of SSHL were evaluated using unconditional univariate and multivariate logistic regression analyses.ResultsThe mean age for the 3,084 study subjects was 53.1 years (standard deviation, S.D. = 15.6). Of the 514 cases, 49 (9.5%) had sensorineural hearing impairment while only 44 (1.7%) of the 2,570 controls had the same condition. Univariate logistic regression analyses indicated that preexisting sensorineural hearing impairment was significantly associated with SSHL (odds ratio, OR = 6.05, p < 0.001). Other comorbidities including hypertension, diabetes mellitus, and hyperlipidemia also showed significant associations with SSHL. Similar results were obtained when the association between SSHL and sensorineural hearing impairment was adjusted with either all the covariates (adjusted OR = 6.22, p < 0.001) or with only those selected using a backward elimination procedure (adjusted OR = 6.20, p < 0.001).ConclusionsResults from this population-based case-control study revealed that common sensorineural hearing impairment might be a novel risk factor for SSHL.

Migraine a risk factor for SSNHL

Among patterns of hearing loss, sudden sensorineural hearing loss (SSNHL) ranks as one of the least common, accounting for 1% of all cases of hearing loss with approximately 4000 new cases reported each year (1). However, the inability to prepare for the sudden loss of function, the lack of a satisfying explanation for its cause, and the limited treatment options also make it a particularly devastating disorder. A specific cause for the hearing loss is found in less than 15% of cases and guidelines for management of SSNHL have only recently been published (2,3). Prior association studies have shown that traditional vascular risk factors such as smoking, hypertension, dyslipidemia, and diabetes can be risk factors for SSNHL, with one study even showing a higher risk of subsequent stroke in patients with SSNHL (4). However, meta-analyses have shown that these associations are also inconsistent (5). Although a history of migraine is not generally considered to be a risk factor for SSNHL, it has also not been systematically investigated. Case reports have indicated that some patients who experience SSNHL also experience other symptoms attributable to migraine and that sudden hearing loss associated with a severe migraine headache can be associated with ischemic changes in the inner ear (6,7). In this volume, Chu et al. report on the association between migraine and the incidence of SSNHL over a 10-year period using the National Health Insurance Research Database in Taiwan, which is based on a universal health care system with centralized information on all diagnostic codes and prescriptions. The study was designed as a retrospective case-control study, with the incidence of SSNHL in migraine patients and controls in the year 2000 used as the baseline. Migraine and SSNHL were both diagnosed by ICD9-CM codes, as were major vascular risk factors such as diabetes, hypertension, dyslipidemia, and atrial fibrillation. After exclusion of a history of SSNHL at baseline, Meniere’s disease, and acoustic neuromas, 10,280 migraine patients were compared to 41,120 controls. These subjects were followed for a median of five years until one of three outcomes was obtained: 1) development of SSNHL, 2) subject death, or 3) end of the study in 2009. The study required that the diagnosis of migraine be coded by a neurologist and that the diagnosis of SSNHL be coded by an otolaryngologist. The authors report a 1.8-fold increased risk of SSNHL in patients with migraine with a very small but detectable cumulative risk of SSNHL each year throughout the 10 years of observation. This cumulative risk amounted to 0.4% in migraine patients and 0.2% in controls. In a multivariate analysis, comorbidity with hypertension increased the risk to 1.92 in migraine patients, but this was not statistically significant. The role of hypertension in the risk of SSNHL in controls was not reported, however. The study provides a global perspective on the incidence of SSNHL. The authors calculated an incidence of 81.6 cases in 100,000 person-years in migraine subjects and 45.7 cases per 100,000 person-years in controls. The relative risk increased to 118.6 per 100,000 person-years in migraine subjects over the age of 40 years. These estimates are much higher than the often-reported incidence of five to 20 cases in 100,000 person-years for SSNHL (2,3,5). However, some widely cited incidence data in the current literature are extrapolated from as few as 18 patients cared for in one health care system or are reported frompersonal communications (8,9). Older studies also did not use the current, more generally accepted criteria for SSNHL that require a loss of 30 dBof hearing in three consecutive frequencies occurring over less than 72 hours. Conversely, the reported incidence in the study was lower than the 160 per 100,000 person-years reported in 2004 from a German population (10). One challenge to making an accurate assessment of the incidence of SSNHL in any setting is that acuity can often be difficult to determine, especially if the patient recovers quickly. Between one-third and two-thirds of

Steroid Combination Therapy and Detoxification Enzyme Gene Polymorphisms in Sudden Sensorineural Hearing Loss Patients

The purpose of this study was to evaluate the relations among the combined therapy with steroid and the detoxification enzyme gene polymorphisms in patients with sudden sensorineural hearing loss (SSNHL). The pathogenetic mechanism of inner ear dysfunction could involve an increase in lipid peroxidation and a decrease in cellular antioxidant defense. Glutathione S-transferases (GSTs) and cytochrome P450 (CYP) belong to a system of detoxification and antioxidant enzymes that have been demonstrated in the inner ear. A prospective study in patients with SSNHL. All 441 subjects were genotyped for GSTM1, GSTT1, and CYP1A1 polymorphisms. The polymorphisms were analyzed by polymerase chain reaction amplification, restriction enzyme digestion, and deoxyribonucleic acid fragment separation by electrophoresis. No significant difference was observed between SSNHL patients and controls in 3 polymorphisms. However, the prevalence of the partial recovery group in patients with the CC genotype of CYP1A1 (22%) was higher than that in the complete recovery (7.4%) or no recovery group (12.5%) for the subjects classified according to modified Siegel's criteria but were not statistically significant. This is the first approach to analyze gene polymorphism and efficacy of clinical treatment of patients with SSNHL, although the observations do not confirm the effect of the GSTM1/T1 and CYP1A1 genotypes as a risk factor for SSNHL.

Candidate Genes of Cerebrovascular Disease and Sudden Sensorineural Hearing Loss

Auditory dysfunction is related to large/small vessel occlusions and hemorrhage. Sudden sensorineural hearing loss (SSNHL) frequently occurs with anterior inferior cerebellar artery occlusion proximal to the internal auditory artery. Moreover, SSNHL has various pathogenetic mechanisms, the main proposed mechanisms being vascular disease, membrane ruptures, infection, and autoimmunity. Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of cerebrovascular diseases. In the current study, the possible effects of polymorphisms in TNF-alpha and TNF-beta genes on SSNHL are evaluated. Two genetic polymorphisms in the TNF locus (TNF-alpha -308 G - ->A and TNF-beta +252 A - ->G) were investigated as risk factors for SSNHL by determining their prevalence in 97 SSNHL patients and in 587 controls. A significant increase was found for the TNF-beta allele 1 in SSNHL patients compared with the controls (chi( 2) = 7.251, P = .007, odds ratio [OR] = 1.534, confidence interval [CI] = 1.12-2.10). These findings suggest that the TNF-beta +252 locus plays an important role in the etiopathogenesis of SSNHL.

Lack of Association between Inherited Thrombophilic Risk Factors and Idiopathic Sudden Sensorineural Hearing Loss in Italian Patients

We investigated the presence of congenital thrombophilic risk factors in a population of consecutive Italian patients affected by idiopathic sudden sensorineural hearing loss (SSNHL). We investigated 48 patients with idiopathic SSNHL for the presence of congenital thrombophilic risk factors. The factor V Leiden G1691A, the prothrombin G20210A allele, and methylenetetrahydrofolate reductase (MTHFR) C677T genotypes were investigated. Allele frequencies and genotype distribution of all factors found in patients were compared to those of 48 healthy subjects of the same ethnic background by Chi2 and odds-ratio analysis. Odds ratios and 95% confidence intervals were calculated for allele and genotype frequencies of all thrombophilia variants. Statistical significance was accepted with a p value of less than .05. We also performed the following blood tests: hemacytometric analysis including platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, erythrocyte sedimentation rate, C-reactive protein, protein S, protein C, antithrombin III, and activated protein C resistance. In our series, we did not find an association between SSNHL and abnormal levels of antithrombin III, protein C, protein S, D-dimer, or fibrinogen; activated protein C resistance; or factor V G1691A, prothrombin G20210A, or MTHFR C677T mutations. At present, the few studies regarding genetic polymorphisms of congenital thrombophilic factors in SSNHL are not conclusive. According to our data, factor V G1691A, prothrombin G20210A, and MTHFR C677T variants should be not considered risk factors for SSNHL. Further large prospective studies are needed to provide currently lacking information and to improve our knowledge in the field before we recommend the determination of genetic polymorphism in SSNHL as routine practice.