scholarly journals The association of genetic polymorphisms in interleukin-1 receptors type 1 and type 2 with sudden sensorineural hearing loss in a Taiwanese population: a case control study

Author(s):  
Chen-Yu Chien ◽  
Shu-Yu Tai ◽  
Kuan-Hui Li ◽  
Hua-Ling Yang ◽  
Leong-Perng Chan ◽  
...  

Abstract Background Sudden sensorineural hearing loss (SSNHL) is a disease with an unknown etiology; damage to the auditory nerve from inflammation due to viral infection or vascular incidents has been implicated. According to several studies, cytokines, including interleukins, are associated with SSNHL in terms of serum expression and genetic polymorphisms. Interleukin-1 (IL-1) plays a key role in inflammation and may be associated with SSNHL. This study analyzed the association of single nucleotide polymorphisms (SNPs) of IL-1 receptor (IL-1R) genes with SSNHL in Taiwan. Methods We conducted a case–control study involving 401 patients with SSNHL and 730 healthy controls. Four SNPs (IL-1R type 1 gene [IL1R1] [rs3917225 and rs2234650] and IL-1R type 2 gene [IL1R2] [rs4141134 and rs2071008]) were selected. The genotypes were determined using the TaqMan assay. The Hardy–Weinberg equilibrium (HWE) was tested for each SNP, and genetic effects were evaluated. Results The TT genotype of rs2234650 had an adjusted odds ratio (OR) of 2.988 (95% confidence interval [95% CI] 1.27–6.82) (P = 0.012) compared with the CC genotype in patients with SSNHL. The SNP rs2234650 was associated with SSNHL in the recessive model (TT vs. CC + CT, P = 0.0206, OR = 2.681). The CT genotype of rs4141134 had an adjusted OR of 3.860 (95% CI 2.01–7.44; P < 0.0001) compared with the TT genotype, in patients with SSNHL. The SNP rs4141134 was associated with SSNHL under the dominant model (CC + CT vs. TT, P < 0.0001, OR = 4.087). Conclusion These findings suggest that IL1R1 and IL1R2 gene polymorphisms may contribute to an increased risk of SSNHL in Taiwan.

2014 ◽  
Vol 125 (1) ◽  
pp. E28-E32 ◽  
Author(s):  
Gabriella Cadoni ◽  
Eleonora Gaetani ◽  
Pasqualina M. Picciotti ◽  
Dario Arzani ◽  
Miriam Quarta ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Alessandro Castiglione ◽  
Andrea Ciorba ◽  
Claudia Aimoni ◽  
Elisa Orioli ◽  
Giulia Zeri ◽  
...  

Background. Even if various pathophysiological events have been proposed as explanations, the putative cause of sudden hearing loss remains unclear.Objectives. To investigate and to reveal associations (if any) between the main iron-related gene variants and idiopathic sudden sensorineural hearing loss.Study Design. Case-control study.Materials and Methods. A total of 200 sudden sensorineural hearing loss patients (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 (FPN1;SLC40A1), the two isoforms C1 and C2 (p.P570S) of the transferrin protein (TF), the amino acidic substitutions p.H63D and p.C282Y in the hereditary hemochromatosis protein (HFE), and the polymorphism c.–582AG in the promoter of theHEPCgene, which encodes the protein hepcidin (HAMP).Results. The homozygous genotype c.−8GG of theSLC40A1gene 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 genotypeFPN1−8GG was significantly associated with increased risk of developing sudden hearing loss. These findings suggest new research should be conducted in the field of iron homeostasis in the inner ear.


2010 ◽  
Vol 119 (2) ◽  
pp. 82-88 ◽  
Author(s):  
Gabriella Cadoni ◽  
Alessandro Scorpecci ◽  
Francesca Cianfrone ◽  
Sara Giannantonio ◽  
Gaetano Paludetti ◽  
...  

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