Sudden XXXX and polymorphisms in iron homeostasis genes: new insights from a case-control study.

@entity1 @entity14398 @entity25341 @entity31392 @entity69 @entity65483 @entity1274 @entity14397 @entity14399 @entity6350 @entity9595 @entity2459
Background. Even if various pathophysiological events have been proposed as explanations, the putative cause of @entity2459 remains unclear. Objectives. To investigate and to reveal associations (if any) between the main iron-related gene variants and @entity1274 . Study Design. Case-control study. Materials and Methods. A total of 200 sudden @entity1274 @entity1 (median age 63.65 years; range 10-92) were compared with 400 healthy control subjects. The following genetic variants were investigated: the polymorphism c.-8CG in the promoter of the ferroportin gene ( @entity25341 ; @entity25341 ), the two isoforms @entity6350 ( @entity65483 ) of the @entity69 protein (TF), the amino acidic substitutions @entity14397 and @entity14399 in the @entity9595 protein ( @entity14398 ), and the polymorphism c.-582AG in the promoter of the @entity31392 gene, which encodes the protein hepcidin ( @entity31392 ). Results. The homozygous genotype c.-8GG of the @entity25341 gene revealed an OR for ISSNHL risk of 4.27 (CI 95%, 2.65-6.89; P = 0.001), being overrepresented among cases. Conclusions. Our study indicates that the homozygous genotype @entity25341 -8GG was significantly associated with increased risk of developing @entity2459 . These findings suggest new research should be conducted in the field of iron homeostasis in the inner ear.
