Linnstaedt Sarah D, Bortsov Andrey V, Soward April C, Swor Robert, Peak David A, Jones Jeffrey, Rathlev Niels, Lee David C, Domeier Robert, Hendry Phyllis L, McLean Samuel A
TRYUMPH Research Program, University of North Carolina, Chapel Hill, NC, USA Anesthesiology, University of North Carolina, Chapel Hill, NC, USA Emergency Medicine, William Beaumont Hospital, Royal Oak, MI, USA Emergency Medicine, Massachusetts General Hospital, Boston, MA, USA Emergency Medicine, Spectrum Health System, Grand Rapids, MI, USA Emergency Medicine, Baystate Medical Center, Springfield, MA, USA Emergency Medicine, North Shore University Hospital, Manhasset, NY, USA Emergency Medicine, Saint Joseph Mercy Health System, Ypsilanti, MI, USA Emergency Medicine, University of Florida College of Medicine, Jacksonville, FL, USA Emergency Medicine, University of North Carolina, Chapel Hill, NC, USA.
Pain. 2016 Jan;157(1):273-279. doi: 10.1097/j.pain.0000000000000374.
Musculoskeletal pain (MSP) is a common sequela of traumatic stress exposure. While biological factors contributing to chronic MSP after motor vehicle collision (MVC) have traditionally focused on tissue injury, increasing evidence suggests that neuro/stress/immune processes mediated by stress system activation may play a more dominant role. In a previous study, we found that genetic variants in the hypothalamic-pituitary-adrenal (HPA) axis-related gene FKBP5 influence vulnerability to persistent MSP 6 weeks after MVC. In the present cohort study (n = 855), we evaluated whether genetic variants in several other important HPA axis-related genes, including the glucocorticoid receptor (NR3C1), corticotropin-releasing hormone receptor R1 (CRHR1), and corticotropin-releasing hormone-binding protein (CRHBP), influence risk of chronic MSP over time after MVC. Genetic polymorphism rs7718461 in the CRHBP gene showed significant association (P = 0.0012) with overall pain severity during the year after MVC in regression models controlling for multiple comparisons. Two additional CRHBP alleles in high linkage disequilibrium with rs7718461 also showed trend-level significance. In secondary analyses, a significant interaction between this CRHBP locus (minor allele frequency = 0.33) and time was observed (P = 0.015), with increasing effect observed over time following trauma. A significant CRHBP × FKBP5 interaction was also observed, with substantially increased MSP after MVC in those with a risk allele in both genes compared with either gene alone. The results of this study indicate that genetic variants in 2 different HPA axis genes predict chronic MSP severity following MVC and support the hypothesis that the HPA axis is involved in chronic post-MVC MSP pathogenesis.
肌肉骨骼疼痛(MSP)是创伤性应激暴露后的常见后遗症。虽然传统上认为机动车碰撞(MVC)后导致慢性MSP的生物学因素主要集中在组织损伤上,但越来越多的证据表明,应激系统激活介导的神经/应激/免疫过程可能发挥更主要的作用。在先前的一项研究中,我们发现下丘脑 - 垂体 - 肾上腺(HPA)轴相关基因FKBP5中的基因变异会影响MVC后6周持续性MSP的易感性。在本队列研究(n = 855)中,我们评估了其他几个重要的HPA轴相关基因中的基因变异,包括糖皮质激素受体(NR3C1)、促肾上腺皮质激素释放激素受体R1(CRHR1)和促肾上腺皮质激素释放激素结合蛋白(CRHBP),是否会影响MVC后慢性MSP的长期风险。在控制多重比较的回归模型中,CRHBP基因中的基因多态性rs7718461与MVC后一年内的总体疼痛严重程度显示出显著关联(P = 0.0012)。与rs7718461处于高连锁不平衡状态的另外两个CRHBP等位基因也显示出趋势水平的显著性。在二次分析中,观察到该CRHBP基因座(次要等位基因频率 = 0.33)与时间之间存在显著交互作用(P = 0.015),创伤后随时间推移效应增强。还观察到显著的CRHBP×FKBP5交互作用,与单一基因具有风险等位基因的个体相比,两个基因均具有风险等位基因的个体在MVC后MSP显著增加。本研究结果表明,2个不同的HPA轴基因中的基因变异可预测MVC后的慢性MSP严重程度,并支持HPA轴参与MVC后慢性MSP发病机制的假说。