TRPM8 genetic variant is associated with chronic migraine and allodynia.
Adult
Case-Control Studies
Cohort Studies
Female
Genetic Predisposition to Disease
/ epidemiology
Genetic Variation
/ genetics
Genome-Wide Association Study
/ methods
Humans
Hyperalgesia
/ diagnosis
Male
Middle Aged
Migraine Disorders
/ diagnosis
Polymorphism, Single Nucleotide
/ genetics
TRPM Cation Channels
/ genetics
Taiwan
/ epidemiology
Pain sensitisation
Single nucleotide polymorphism
rs10166942
Journal
The journal of headache and pain
ISSN: 1129-2377
Titre abrégé: J Headache Pain
Pays: England
ID NLM: 100940562
Informations de publication
Date de publication:
16 Dec 2019
16 Dec 2019
Historique:
received:
08
10
2019
accepted:
02
12
2019
entrez:
18
12
2019
pubmed:
18
12
2019
medline:
5
3
2020
Statut:
epublish
Résumé
Many single nucleotide polymorphisms (SNPs) have been reported to be associated with migraine susceptibility. However, evidences for their associations with migraine endophenotypes or subtypes are scarce. We aimed to investigate the associations of pre-identified migraine susceptibility loci in Taiwanese with migraine endophenotypes or subtypes, including chronic migraine and allodynia. The associations of six SNPs identified from our previous study, including TRPM8 rs10166942, LRP1 rs1172113, DLG2 rs655484, GFRA1 rs3781545, UPP2 rs7565931, and GPR39 rs10803531, and migraine endophenotypes, including chronic migraine and allodynia were tested. Significant associations in the discovery cohort were validated in the replication cohort. The adjusted odds ratios (aOR) were calculated after controlling for confounders. In total, 1904 patients (mean age 37.5 ± 12.2 years old, female ratio: 77.7%) including 1077 in the discovery cohort and 827 in the replication cohort were recruited. Of them, 584 (30.7%) had chronic migraine. Of the 6 investigated SNPs, TRPM8 rs10166942 T allele-carrying patients were more likely to have chronic migraine than non-T allele carriers in both discovery and replication cohorts and combined samples (33.7% vs. 25.8%, p = 0.004, aOR = 1.62). In addition, T allele carriers reported more allodynic symptoms than non-T allele carriers (3.5 ± 3.7 vs. 2.6 ± 2.8, p < 0.001). However, allodynia severity did not differ between episodic and chronic migraine patients. No further correlations between genetic variants and endophenotypes were noted for the other SNPs. TRPM8 may contribute to the pathogenesis of chronic migraine. However, our study did not support allodynia as a link between them. The underlying mechanisms deserve further investigations.
Sections du résumé
BACKGROUND
BACKGROUND
Many single nucleotide polymorphisms (SNPs) have been reported to be associated with migraine susceptibility. However, evidences for their associations with migraine endophenotypes or subtypes are scarce. We aimed to investigate the associations of pre-identified migraine susceptibility loci in Taiwanese with migraine endophenotypes or subtypes, including chronic migraine and allodynia.
METHODS
METHODS
The associations of six SNPs identified from our previous study, including TRPM8 rs10166942, LRP1 rs1172113, DLG2 rs655484, GFRA1 rs3781545, UPP2 rs7565931, and GPR39 rs10803531, and migraine endophenotypes, including chronic migraine and allodynia were tested. Significant associations in the discovery cohort were validated in the replication cohort. The adjusted odds ratios (aOR) were calculated after controlling for confounders.
RESULTS
RESULTS
In total, 1904 patients (mean age 37.5 ± 12.2 years old, female ratio: 77.7%) including 1077 in the discovery cohort and 827 in the replication cohort were recruited. Of them, 584 (30.7%) had chronic migraine. Of the 6 investigated SNPs, TRPM8 rs10166942 T allele-carrying patients were more likely to have chronic migraine than non-T allele carriers in both discovery and replication cohorts and combined samples (33.7% vs. 25.8%, p = 0.004, aOR = 1.62). In addition, T allele carriers reported more allodynic symptoms than non-T allele carriers (3.5 ± 3.7 vs. 2.6 ± 2.8, p < 0.001). However, allodynia severity did not differ between episodic and chronic migraine patients. No further correlations between genetic variants and endophenotypes were noted for the other SNPs.
CONCLUSIONS
CONCLUSIONS
TRPM8 may contribute to the pathogenesis of chronic migraine. However, our study did not support allodynia as a link between them. The underlying mechanisms deserve further investigations.
Identifiants
pubmed: 31842742
doi: 10.1186/s10194-019-1064-2
pii: 10.1186/s10194-019-1064-2
pmc: PMC6916225
doi:
Substances chimiques
TRPM Cation Channels
0
TRPM8 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
115Subventions
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST 108-2321-B-010 -014 -MY2 and 108-2321-B-010 001
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST-107-2314-B-010-021
Organisme : Ministry of Health and Welfare
ID : MOHW108-TDU-B-211-133001
Organisme : Ministry of Education
ID : The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project
Organisme : Ministry of Education
ID : The Featured Areas Research Center Program within the framework of the Higher Education Sprout Project
Organisme : Taipei Veterans General Hospital
ID : VGH-108-C-105
Organisme : Taipei Veterans General Hospital
ID : VGH-108-C-066
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