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Nav1.7 或神经生长因子受体基因多态性与三叉神经痛无关。

No Association of Polymorphisms in Nav1.7 or Nerve Growth Factor Receptor Genes with Trigeminal Neuralgia.

机构信息

Programa de Pós-Graduação em Patologia, Faculdade de Medicina, Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil.

Programa de Pós-Graduação em Biologia Celular, Instituto de Ciências Biológicas (ICB), UFMG, Belo Horizonte, MG, Brazil.

出版信息

Pain Med. 2019 Jul 1;20(7):1362-1369. doi: 10.1093/pm/pny191.

DOI:10.1093/pm/pny191
PMID:30307573
Abstract

OBJECTIVE

Trigeminal neuralgia is defined as a sudden severe shock-like pain within the distribution of the trigeminal nerve. Pain is a subjective experience that is influenced by gender, culture, environment, psychological traits, and genes. Sodium channels and nerve growth factor play important roles in the transmission of nociceptive signals and pain. The aim of this study was to investigate the occurrence of Nav1.7 sodium channel and nerve growth factor receptor TrkA gene polymorphisms (SCN9A/rs6746030 and NTRK1/rs633, respectively) in trigeminal neuralgia patients.

METHODS

Ninety-six subjects from pain specialty centers in the southeastern region of Brazil were divided into 2 groups: 48 with classical trigeminal neuralgia diagnosis and 48 controls. Pain was evaluated using the visual analog scale and multidimensional McGill Pain Questionnaire. Genomic DNA was obtained from oral swabs in all individuals and was analyzed by real-time polymerase chain reaction.

RESULTS

No association was observed between evaluated polymorphisms and trigeminal neuralgia. For allele analyses, patients and controls had similar frequencies for both genes. Genotype distribution or allele frequencies of polymorphisms analyzed here did not correlate to pain scores.

CONCLUSIONS

Although no association of evaluated polymorphisms and trigeminal neuralgia diagnosis or pain severity was observed, our data do not exclude the possibility that other genotypes affecting the expression of Nav1.7 or TrkA are associated with the disease. Further studies should investigate distinct genetic polymorphisms and epigenetic factors that may be important in expression of these molecules.

摘要

目的

三叉神经痛被定义为三叉神经分布区域内突然出现的剧烈电击样疼痛。疼痛是一种主观体验,受性别、文化、环境、心理特征和基因的影响。钠通道和神经生长因子在伤害性信号和疼痛的传递中发挥着重要作用。本研究旨在探讨 Nav1.7 钠通道和神经生长因子受体 TrkA 基因多态性(SCN9A/rs6746030 和 NTRK1/rs633)在三叉神经痛患者中的发生情况。

方法

从巴西东南部的疼痛专科中心招募了 96 名受试者,分为 2 组:48 名经典三叉神经痛诊断患者和 48 名对照组。使用视觉模拟评分法和多维 McGill 疼痛问卷评估疼痛。从所有个体的口腔拭子中提取基因组 DNA,并通过实时聚合酶链反应进行分析。

结果

未观察到评估的多态性与三叉神经痛之间存在关联。对于等位基因分析,患者和对照组在两个基因中均具有相似的频率。分析的多态性的基因型分布或等位基因频率与疼痛评分无关。

结论

尽管未观察到评估的多态性与三叉神经痛诊断或疼痛严重程度相关,但我们的数据不能排除其他影响 Nav1.7 或 TrkA 表达的基因型与该疾病相关的可能性。进一步的研究应调查可能对这些分子表达重要的不同遗传多态性和表观遗传因素。

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