李树林, 王泽, 王茜. 糖皮质激素受体基因、工作紧张水平的交互作用与创伤后应激障碍易感性的关系[J]. 环境与职业医学, 2016, 33(11): 1076-1079. DOI: 10.13213/j.cnki.jeom.2016.15708
引用本文: 李树林, 王泽, 王茜. 糖皮质激素受体基因、工作紧张水平的交互作用与创伤后应激障碍易感性的关系[J]. 环境与职业医学, 2016, 33(11): 1076-1079. DOI: 10.13213/j.cnki.jeom.2016.15708
LI Shu-lin, WANG Ze, WANG Qian. Association Between Interaction of Glucocorticoid Receptor Genes and Work Stress Levels and Susceptibility of Post-Traumatic Stress Disorder[J]. Journal of Environmental and Occupational Medicine, 2016, 33(11): 1076-1079. DOI: 10.13213/j.cnki.jeom.2016.15708
Citation: LI Shu-lin, WANG Ze, WANG Qian. Association Between Interaction of Glucocorticoid Receptor Genes and Work Stress Levels and Susceptibility of Post-Traumatic Stress Disorder[J]. Journal of Environmental and Occupational Medicine, 2016, 33(11): 1076-1079. DOI: 10.13213/j.cnki.jeom.2016.15708

糖皮质激素受体基因、工作紧张水平的交互作用与创伤后应激障碍易感性的关系

Association Between Interaction of Glucocorticoid Receptor Genes and Work Stress Levels and Susceptibility of Post-Traumatic Stress Disorder

  • 摘要: 目的

    分析创伤后应激障碍(PTSD)的主要危险因素,探讨糖皮质激素受体(GR)基因rs17209237、rs41423247 位点与紧张水平的交互作用,为筛选PTSD敏感人群提供依据。

    方法

    采用病例对照研究方法,以新疆某三甲医院确诊治疗的PTSD患者(60 例)作为病例组,以同期经三甲医院确诊遭受过创伤性事件,但没有发展为PTSD的120 例为对照组,进行量表调查(工作紧张测量问卷)和血样采集(经知情同意,早晨空腹采集静脉血样5 mL),用于分析GR基因与紧张水平的交互作用。

    结果

    工作紧张中,子项工作紧张强度病例组高于对照组(P<0.05),OR值为6.122;工作压力在病例组和对照组差异有统计学意义,病例组的工作压力高于对照组(P<0.05),OR值为10.543。GR基因rs41423247 位点C/G基因型的频率分布病例组高于对照组(P<0.05),C等位基因携带者GC可能是PTSD 的危险因素(OR=2.14,95%CI:1.10~4.16)。GR基因rs41423247 位点突变型与工作压力正相乘交互作用(P<0.05),OR值为3.256。

    结论

    工作紧张强度和工作压力大者PTSD 的患病风险高。GR基因rs41423247 位点C等位基因携带者GCPTSD 发病风险高。GR基因是PTSD 的遗传易感基因,GR基因rs41423247 位点与工作压力共同作用可能增加PTSD 的患病风险。

     

    Abstract: Objective

    To examine the major risk factors of post-traumatic stress disorder (PTSD), assess the interaction of glucocorticoid receptor (GR) gene rs17209237 and rs41423247 and work stress levels, and provide evidence for screening sensitive populations of PTSD.

    Method

    The study adopted a case-control design. Patients from tertiary grade A hospitals in Xinjiang diagnosed with PTSD (n=60) were enrolled as the case group, and those who suffered a traumatic event diagnosed in the same period but did not develop to PTSD (n=120) were enrolled as the control group. They were investigated with Job Stress Survey (JSS) and gave informed consent to collect morning fasting venous blood samples (5 mL). GR gene-stress interaction was assessed.

    Result

    Job stress intensity in the case group was higher than that in the control group (P<0.05) (OR=6.122), so was the job pressure (P<0.05) (OR=10.543). The frequency of GR gene rs41423247 C/G genotype in the case group was higher than that in the control group (P<0.05), and C allele carrier (GC) was a risk factor for PTSD (OR=2.14, 95%CI: 1.10-4.16). There was a positive multiplication interaction between GR gene rs41423247 mutant type and job pressure (P<0.05) (OR=3.256).

    Conclusion

    Job stress intensity and job pressure increase the possibility of suffering from PTSD. GR gene rs41423247 locus C allele (GC) increases the possibility of suffering from PTSD. GR gene is a genetic risk factor for PTSD, and the joint action of GR gene rs41423247 and job pressure increases the risk of PTSD.

     

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