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Clinical and Applied Thrombosis/Hemostasis
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Candidate Genes of Cerebrovascular Disease and Sudden Sensorineural Hearing Loss

Jae-Young Um, Chul-Ho Jang, Kyu-Yeop Kim, Su-Jin Kim, Na-Hyung Kim, Phil-Dong Moon, In-Young Choi, Noh-Yil Myung, Hyun-Ja Jeong, Seung-Heon Hong, and Hyung-Min Kim, PhD*

* To whom correspondence should be addressed. E-mail: hmkim{at}khu.ac.kr.


   Abstract
Auditory dysfunction is related to large/small vessel occlusions and hemorrhage. Sudden sensorineural hearing loss (SSNHL) frequently occurs with anterior inferior cerebellar artery occlusion proximal to the internal auditory artery. Moreover, SSNHL has various pathogenetic mechanisms, the main proposed mechanisms being vascular disease, membrane ruptures, infection, and autoimmunity. Tumor necrosis factor (TNF) is an important cytokine in the inflammation process of cerebrovascular diseases. In the current study, the possible effects of polymorphisms in TNF-{alpha} and TNF-{beta} genes on SSNHL are evaluated. Two genetic polymorphisms in the TNF locus (TNF-{alpha} –308 G -->A and TNF-{beta} +252 A -->G) were investigated as risk factors for SSNHL by determining their prevalence in 97 SSNHL patients and in 587 controls. A significant increase was found for the TNF-{beta} allele 1 in SSNHL patients compared with the controls ({chi}2 = 7.251, P = .007, odds ratio [OR] = 1.534, confidence interval [CI] = 1.12-2.10). These findings suggest that the TNF-{beta} +252 locus plays an important role in the etiopathogenesis of SSNHL.

First published on October 14, 2009
Clinical and Applied Thrombosis/Hemostasis 2009, doi:10.1177/1076029609348313


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