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Sudden sensorineural hearing loss (SSNHL) is frequently classified as ‘idiopathic’ since the causative factor responsible for its onset is not identified in most cases. In the present study, we determined whether SSNHL is clinically associated with serum anti-heat shock protein-70 (anti-HSP70) and antiphospholipids (anti-PLs) autoantibodies and whether these autoantibodies have an impact on the prognosis of SSNHL. Sera from 63 patients with SSNHL were screened prospectively for the presence of anti-HSP70 and anti-PLs autoantibodies by an enzyme-linked immunosorbent assay test. Anti-PLs antibodies in this study consisted of anticardiolipin, and anti-β2-glycoprotein-1 antibodies. Serum was assayed for anti-HSP70 IgG antibodies using recombinant human HSP70. Demographic, clinical, and audiometric variables were analyzed to find the possible role of serum autoantibodies in SSNHL patients. Sixteen patients (25.4%) had demonstrable anti-HSP70 antibodies in serum. Twenty-one patients (33.3%) showed a positive result for at least one isotype (IgM or IgG) of anti-PLs. In 19% of the patients, anti-HSP70 and anti-PLs antibodies were positive in two combinations. A statistically significant association was found between anti-HSP70 antibodies and the Siegel recovery grade subgroup. SSNHL patients who were positive for anti-HSP70 antibodies showed a significantly higher rate of complete recovery and incomplete but partial recovery than SSNHL patients without anti-HSP70 antibodies (p = 0.0496). Statistically significant association was found between total anticardiolipin, total anti-β2-glycoprotein-1, total anti-PLs, and anti-PLs in combination with anti-HSP70 antibodies and age (p = 0.0229). The detection of autoantibodies to HSP70 and PLs offers a pliable explanation for the immune-mediated mechanism of SSNHL. The present study confirms and supports previous studies regarding the association between anti-HSP70 and anti-PLs antibodies with SSNHL, and is the first to identify a positive association between anti-HSP70 antibodies and a positive outcome of SSNHL. Further studies are necessary in order to identify and further clarify the immunologic role of the presence of autoantibodies and their impact on the prognosis of SSNHL. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Sudden sensorineural hearing loss (SSNHL) is frequently classified as ‘idiopathic’ since the causative factor is not identified in most cases. In the present study we determined whether SSNHL is associated with common viral infections, namely enterovirus, cytomegalovirus (CMV) and Epstein-Barr virus (EBV). Between April 2004 and March 2005, we conducted a prospective cohort study on 48 unselected patients with unilateral idiopathic SSNHL. Plasma samples obtained at presentation were analyzed for the presence of enterovirus RNA by reverse-transcription polymerase chain reaction (RT-PCR). Recent occurrence of CMV and EBV infection was determined by serological tests. Among 23 men and 25 women aged 18–84 years (mean age 51.67 years), none presented with clinical symptoms of a viral infection compatible with preceding or concurrent viral infection. One patient (2.08%) had evidence of enterovirus infection by RT-PCR, 3 patients (6.25%) had EBV IgM, and none were positive for CMV IgM. The majority of SSNHL patients (91.67%) did not have evidence of any of the three common viral infections upon presentation. The present study failed to identify recent or concurrent systemic viral infections among SSNHL patients, except for a small proportion who demonstrated recent viral infection. Therefore the theory that viral infection is a factor in SSNHL pathogenesis is not supported by this study. Further studies in larger patient populations and different epidemiological settings are required in order to verify the true role of viral infections in SSNHL. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

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. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]