Sudden Sensorineural Hearing Loss Group Research Articles

Different prognostic characteristics between profound sudden sensorineural hearing loss and total sudden hearing loss

To clarify the different prognostic characteristics between profound sudden sensorineural hearing loss (SSNHL) and total SSNHL. The patients with SSNHL who visited Eye Ear Nose and Throat Hospital from June 2007 to September 2008 were reviewed retrospectively. All the 204 patients, with pure tone average (PTA) threshold more than 90 dB, were enrolled and divided into two groups, including total SSNHL and profound SSNHL groups. The relationship between recovery rate and prognostic factors including the age, complications, time period between onset and therapy was analyzed. There were 57 cases of total SSNHL and 147 cases of profound SSNHL in this series. Tinnitus was complained in more than 90% of the patients in both groups, which was higher than that of dizziness and ear fullness. Dizziness was present in 64.9% (37/57) patient with total SSNHL group and 45.6% (67/147) patients with profound SSNHL, which had significant difference between the two groups (χ(2) = 5.72, P = 0.017). The PTA threshold improvement in total SSNHL group and profound SSNHL group was (36.4 ± 19.3) dB and (40.2 ± 21.3) dB respectively, which was no significant difference between the two groups (t = 1.165, P = 0.245). The cured patients were all those received therapy within 1 week following the onset of SSNHL, which was of 2.6% (1/38) patients in the total SSNHL group and 14.3% (14/98) patients in the profound SSNHL group (P = 0.045). Furthermore, 3.5% (2/57) patients in total SSNHL group as well as 29.9% (44/147) patients in profound SSNHL group obtained a good result with PTA threshold ≤ 50 dB after therapy (χ(2) = 15.92, P = 0.001). In addition, the favorable prognosis was related with the onset-therapy time point(P = 0.001), but not related to the patients' age. Profound SSNHL and total SSNHL though both with PTA threshold > 90 dB had significant differences recovery rate and need to be studied separately.

Determination of serum adiponectin and high-sensitivity C-reative protein in patients with idiopathic sudden sensorineural hearing loss and its clinical significance

Objective To study the role and clinical significance of serum adiponectin and high-sensitivity C-reative protein(Hs-CRP)in idiopathic sudden sensorineural hearing loss by measuring the change of their levels in the patients with idiopathic sudden sensorineural hearing loss.Methods Adiponectin Was determined by ELISA method,Hs-CBP was determined by rate nephelometry immunoassuy.The levels adiponectin and Hs-CRP were determined in the 102 idiopathic sudden sensorineural hearing loss patients who were observed at two different time points:before and after treatment,and thirty-five patients with other neurologic diseases(20with sciatica,16withtrigeminal neuralgia)and thirty healthy people were used as control.Results The levels of Hs-CRP in serum of patients with idiopathic sudden sensorineural hearing loss were markedly higher than those in the two control groups(P<0.01);the levels of Hs-CRP in the idiopathic sudden sensorineural hearing loss group after treatment were significantly less than that before treatment(P<0.01).The levels adiponectin in serum of pailents with idiopathic sudden sensorineural hearing loss were markedly lower than those in the two control groups(P<0.01);the levels of adiponectin in the idiopathic sudden sensorineural hearing loss group after treatment were significantly higher than that before treatment(P<0.01).There was negatively correlation between adiponectin and Hs-CRP in patients with idiopathic sudden sensorineural hearing loss(r=-0.63,P<0.01).Conclusion The levels of serum adiponectin and Hs-CRP have instructive significance in idiopathic sudden sensorineural hearing loss treating and prognosis estimating. Key words: Adiponectin; Idiopathic sudden sensorineural hearing loss; High-sensitivity C-reactive protein(Hs-CRP)

Impact of Methionine Synthase Gene and Methylenetetrahydrofolate Reductase Gene Polymorphisms on the Risk of Sudden Sensorineural Hearing Loss

Idiopathic sudden sensorineural hearing loss (SSNHL) represents a frequently encountered otological disease of unknown etiology. In recent years, several inherited risk factors have been found in the pathogenesis of vascular diseases. In the present study, we determined whether specific polymorphism or the combination of polymorphisms in folate-dependent homocysteine metabolism genes can act as predisposing inherited vascular risk factors in the development of SSNHL. We conducted a prospective case-control study using DNA samples extracted from 81 patients diagnosed as suffering from SSNHL and 264 healthy control subjects. Three functional polymorphisms were analyzed by polymerase chain reaction amplification, restriction enzyme digestion, and DNA fragment separation by electrophoresis: methylenetetrahydrofolate reductase (MTHFR) C677T, MTHFR A1298C, and methionine synthase (MTR) A2756G polymorphisms. The prevalence of the homozygous genotype of MTR 2756GG in the SSNHL patients (9%) was significantly higher than in the control group (4%) (p = 0.011). The allelic frequency of the G allele of the MTR A2756G polymorphism among SSNHL patients (12.5%) was also significantly higher than in the control group (5%) (p = 0.033). The prevalence of patients possessing two polymorphisms (31%) and three polymorphisms (17%) in the SSNHL group was significantly higher than in the control group (23 and 9%, respectively; p = 0.019). The frequency of patients with a very high rank risk (double homozygous) was significantly higher in the SSNHL group, MTHFR 677TT/MTR 2675GG – 7%, than the frequency of patients in the control group, MTHFR 677TT/MTR 2675GG – 3% (p = 0.030). Certain polymorphisms in genes encoding enzymes in the folate-dependent homocysteine metabolism are associated with SSNHL. In our case-control study, a significant association between MTR 2756GG genotype and SSNHL was found which may represent an inherited vascular risk factor in the pathogenesis of SSNHL.