POU4F3基因多态性与噪声性高频听力损失易感性的关系
Association Between Genetic Variations in POU4F3 and Susceptibility of Noise-Induced High Frequency Hearing Loss
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摘要:
目的 探讨
POU4F3 基因单核苷酸多态性（SNPs）与中国人群中噪声性高频听力损失易感性之间的关系。方法 采用1:1配对病例对照研究方法，依据听力测试结果，将双耳高频平均听阈≥40 dB定义为病例组，双耳语频的任意频段和高频平均听阈均 < 25 dB定义为对照组，共248对。对噪声暴露作业工人进行健康检查、问卷调查和纯音听力测试。利用SNPscanTM多重SNP分型试剂盒检测rs1368402和rs891969位点的基因型。分别采用配对
t 检验和配对χ 2检验比较两组间计量资料和计数资料的分布差异，利用条件logistic回归模型分析2个SNP位点与噪声性高频听力损失易感性之间的关联。结果 经吸烟、饮酒、高血压和累计噪声暴露量（
CNE ）校正后，POU4F3 基因rs1368402和rs891969位点的基因型和等位基因分布在病例组与对照组之间的差异无统计学意义（P >0.05）。按CNE 分层后发现，当CNE >95 dB（A）时，与rs1368402位点CC/CA 基因型相比，携带AA 基因型的个体发生噪声性高频听力损失的风险增加（校正OR =1.547，95%CI =1.002~2.389，P < 0.05）；与rs891969位点AA/GA 基因型相比，携带GG 基因型的个体发生噪声性高频听力损失的风险增加（校正OR =1.650，95%CI =1.032~2.639，P < 0.05）。并按噪声暴露水平、吸烟、饮酒和高血压进行分层分析，未见有统计学意义的结果（P >0.05）。单体型分析中也未见病例组与对照组单体型频率差异有统计学意义（P >0.05）。结论 POU4F3 基因单个位点多态性可能不是影响噪声性高频听力损失的遗传易感性因素，但rs1368402和rs891969位点多态性与噪声之间的交互作用可能对其具有重要影响。经Bonferroni检验校正后，上述相关性不再具有统计学意义，研究结果还需进一步验证。Abstract:Objective To investigate whether
POU4F3 single nucleotide polymorphisms (SNPs) are associated with susceptibility to the development of noise-induced high frequency hearing loss in a Chinese population.Methods A 1:1 matched case-control study was performed, including 248 cases whose average hearing threshold was more than or equal to 40 dB in high frequency and 248 controls whose average hearing threshold was less than 25 dB in high frequency and vocal speech frequency. Information of the subjects was gathered by questionnaire, physical tests, and pure-tone audiometry. Rs1368402 and rs891969 were genotyped using SNPscanTM multiplex SNP genotyping kit. Continuous variables and categorical variables were analyzed by t-test and chi-square test respectively. Conditional logistic regression models were used to assess the associations between the genotypes and noise-induced high frequency hearing loss.
Results After adjusting for smoking, drinking, hypertension, and cumulative noise exposure (CNE), there were no significant differences in the distribution of genotypes and alleles frequencies of
POU4F3 rs1368402 and rs891969 between the case and control groups (P >0.05). After stratified by CNE, when CNE>95 dB(A), compared with rs1368402CC/CA genotypes, those carryingAA genotype had a significantly increased risk of noise-induced high frequency hearing loss (adjustedOR =1.547, 95%CI =1.002-2.389,P < 0.05); compared with rs891969AA/GA genotypes, those carryingGG genotype had a significantly increased risk of noise-induced high frequency hearing loss (adjustedOR =1.650, 95%CI =1.032-2.639,P < 0.05). After stratified by noise exposure levels, smoking, drinking, and hypertension, there were no significant differences between the two groups (P >0.05). According to haplotype analysis, no statistical difference was found between the case and control subjects (P >0.05).Conclusion The results suggest that
POU4F3 genetic variants may not modify the susceptibility to noiseinduced high frequency hearing loss. But interactions are found between SNPs and noise, which may affect the susceptibility to noise-induced high frequency hearing loss. However, the differences are not significant after Bonferroni correction.
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