FORMI-Oslo University Hospital, Oslo, Norway.
Department of Research, Innovation and Education, Division of Clinical Neuroscience, Oslo University Hospital, Oslo, Norway.
Scand J Pain. 2020 Oct 28;21(1):163-173. doi: 10.1515/sjpain-2020-0091. Print 2021 Jan 27.
The underlying mechanisms for individual differences in experimental pain are not fully understood, but genetic susceptibility is hypothesized to explain some of these differences. In the present study we focus on three genetic variants important for modulating experimental pain related to serotonin (SLC6A4 5-HTTLPR/rs25531 A>G), catecholamine (COMT rs4680 Val158Met) and opioid (OPRM1 rs1799971 A118G) signaling. We aimed to investigate associations between each of the selected genetic variants and individual differences in experimental pain.
In total 356 subjects (232 low back pain patients and 124 healthy volunteers) were genotyped and assessed with tests of heat pain threshold, pressure pain thresholds, heat pain tolerance, conditioned pain modulation (CPM), offset analgesia, temporal summation and secondary hyperalgesia. Low back pain patients and healthy volunteers did not differ in regards to experimental test results or allelic frequencies, and were therefore analyzed as one group. The associations were tested using analysis of variance and the Kruskal-Wallis test.
No significant associations were observed between the genetic variants (SLC6A4 5-HTTLPR/rs25531 A>G, COMT rs4680 Val158Met and OPRM1 rs1799971 A118G) and individual differences in experimental pain (heat pain threshold, pressure pain threshold, heat pain tolerance, CPM, offset analgesia, temporal summation and secondary hyperalgesia).
The selected pain-associated genetic variants were not associated with individual differences in experimental pain. Genetic variants well known for playing central roles in pain perception failed to explain individual differences in experimental pain in 356 subjects. The finding is an important contribution to the literature, which often consists of studies with lower sample size and one or few experimental pain assessments.
个体在实验性疼痛方面的差异的潜在机制尚不完全清楚，但遗传易感性被假设可以解释其中的一些差异。在本研究中，我们重点关注三个与与血清素（SLC6A4 5-HTTLPR/rs25531 A>G）、儿茶酚胺（COMT rs4680 Val158Met）和阿片类（OPRM1 rs1799971 A118G）信号有关的实验性疼痛相关的遗传变异体。我们旨在研究所选遗传变异体与实验性疼痛个体差异之间的关系。
共 356 名受试者（232 名腰痛患者和 124 名健康志愿者）进行基因分型，并进行热痛阈、压痛阈、热痛耐受、条件性疼痛调制（CPM）、偏侧镇痛、时间总和和继发性痛觉过敏的测试。腰痛患者和健康志愿者在实验测试结果或等位基因频率方面没有差异，因此将其作为一个组进行分析。使用方差分析和 Kruskal-Wallis 检验测试关联。
未观察到遗传变异体（SLC6A4 5-HTTLPR/rs25531 A>G、COMT rs4680 Val158Met 和 OPRM1 rs1799971 A118G）与实验性疼痛个体差异（热痛阈、压痛阈、热痛耐受、CPM、偏侧镇痛、时间总和和继发性痛觉过敏）之间存在显著关联。
所选与疼痛相关的遗传变异体与实验性疼痛个体差异无关。在 356 名受试者中，已知在疼痛感知中起核心作用的遗传变异体未能解释实验性疼痛的个体差异。这一发现是对文献的重要贡献，文献中经常包含样本量较小且仅有一项或几项实验性疼痛评估的研究。
