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<p><b>BACKGROUND</b>Bilateral sudden sensorineural hearing loss (BSSHL) is rare and assumed to be a different clinical entity compared to unilateral SSHL (USSHL). This study examined the differences between the idiopathic BSSHL and USSHL.</p><p><b>METHODS</b>Forty-six sequential BSSHL patients (Se-BSSHL) and 68 simultaneous BSSHL (Si-BSSHL) were consecutively admitted between June 2008 and December 2015. Two sets of patients served as control groups: (1) USSHL patients with healthy contralateral ear and (2) USSHL patients with contralateral preexisting hearing loss (USSHLwCHL). We retrospectively analyzed differences among four cohorts using analysis of variance, Kruskal-Wallis test, Welch's t-test, and Chi-square test as appropriate before and after propensity score matching (PSM) based on age, gender, and body mass index (BMI).</p><p><b>RESULTS</b>The prevalence of idiopathic BSSHL was 8.6% (114/1329) among the total SSHL patients. In the total cohort, USSHL patients tended to be younger, female, and tended to have lower BMI, renal parameters, and total cholesterol in addition to higher high-density lipoprotein compared to the other three groups. Most routine blood indicators, some coagulation markers, and immunoglobulin M (H = 13.4, P = 0.004) were significantly different among the study groups. After PSM, the major significant differences were found in audiometric characteristics. Si-BSSHL and Se-BSSHL patients demonstrated similar hearing thresholds as USSHL but were significantly better than the USSHLwCHL patients across most frequencies before and after treatment (H = 30.0, P < 0.001 for initial hearing and H = 12.0, P = 0.007 for final hearing). Moreover, the BSSHL patients showed different hearing loss distribution patterns (more descending type, χ2 = 33.8, P = 0.001) with less hearing gain (H = 17.5, P < 0.001) compared to the USSHL patients.</p><p><b>CONCLUSIONS</b>Idiopathic BSSHL is a relatively rare subtype of SSHL with a higher rate of descending audiogram type and inferior hearing outcome rather than being classified as a completely different disease entity compared to USSHL.</p>
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Background Glycogen synthase kinase-3β (GSK-3β)plays an important role in glucose metabolism,and it may be affect the occurrence of diabetic retinopathy(DR).ObjectiveThe present study was to investigate the effect of valsartan and fluvastatin on the expression of GSK-3β in retina of diabetes rat model.MethodsDiabetes mellitus models were induced by intrapenetoneal injection of streptozotocin(STZ) in 47 clean Sprague-Dawley(SD) rats and were then randomedly divided into 4 groups.Ten other normal rats were served as normal control group.Sodium carboxy methyl cellulose solution,valsartan,fluvastatin,valsartan+fluvastatin and sodium carboxy methyl cellulose solution was given by oral once per day for 12 weeks respectively in diabetes control group ( n =12),valsartan group ( n =12 ),fluvastatin group ( n =11 ),valsartau + fluvastatin group ( n =12 ) and normal control group.Twelve weeks after administration of drugs,blood glucose was measured and compared among various groups,and the expression of p-GSK-3β ( Ser-9 ) protein in retina was quantified and located by Western blot and immunohistochemistry,respectively.Results Twelve weeks after use of drugs,the level of blood glucose was(5.28±0.30),(26.08±3.33 ),(26.03 ±2.66 ),(25.90± 2.86 ),(25.99 ± 2.14 ) mmol/L in the normal control group,diabetes control group,valsartan,fluvastatin,valsartan + fluvastatin group,respectively,showing a significant difference among the 5 groups ( F =110.74,P＜0.01 ).Western blot showed that the grey value of p-GSK-3β ( Ser-9 ) /β-actin in retina in the diabetic control group was significant higher than the normal group(2.774±0.139 vs 1.927±0.111,q =15.79,P＜0.01 ),and that in valsartan,fluvastatin,valsartan+fluvastatin group was lower than the diabetic control group ( 1.895 ±0.090,2.051 ± 0.113,1.537 ± 0.071 vs 2.774 ± 0.139 ) ( q =1 3.69,13.48,23.06,P ＜ 0.01 ).The grey value of p-GSK-3β (Ser-9)/β-actin in the valsartan+fluvastatin group was declined in comparison with the valsartan group and fluvastatin group ( q =6.67,9.58,P＜0.01 ).Immunohistochemistry showed that the p-GSK-3β(Ser-9) protein was expressed all over the retinal layers and obviously in retinal ganglion cell layer(GCL) in normal control group.But the p-GSK-3β(Ser-9) protein was expressed significantly in diabetic control group.The expression of p-GSK-3β (Ser-9)protein was attenuated both in valsartan and fluvastatin groups and further attenuated in valsartan + fluvastatin group. Conclusions p-GSK-3β (Ser-9) protein is overexpressed in GCL of retina of diabetes rat.Both valsartan and fluvastatin can inhibit the expression of p-GSK-3β (Ser-9) and even getting stronger when they combined.