RESUMEN
PURPOSE: We investigated whether tryptophan hydroxylase 2 (TPH2) gene polymorphisms were involved in the aggravation of migraines due to the overuse of medication. METHODS: Forty-seven migraine patients (6 males and 41 females; 36.4 10.3 years) and 22 MOH patients (1 male and 21 females; 39.6 9.9 years) who had migraines participated in this study. The genotypes for the TPH2 gene polymorphisms (rs4565946, rs4570625, and rs4341581) were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. RESULTS: The rs4565946, rs4570625, and rs4341581 genotypes were similarly distributed between migraine patients and MOH patients. CONCLUSION: The results of this study showed no association between tryptophan TPH2 gene polymorphisms and the complication of MOH in patients with migraines.
Asunto(s)
Pueblo Asiatico/genética , Cefaleas Secundarias/genética , Trastornos Migrañosos/genética , Polimorfismo de Longitud del Fragmento de Restricción , Triptófano Hidroxilasa/genética , Adulto , Femenino , Predisposición Genética a la Enfermedad , Genotipo , Cefaleas Secundarias/tratamiento farmacológico , Humanos , Masculino , Persona de Mediana Edad , Trastornos Migrañosos/tratamiento farmacológicoRESUMEN
BACKGROUND AND PURPOSE: Migraine patients are particularly prone to the complication of medication-overuse headache (MOH). Although it has been shown that A allele carriers for the tumor necrosis factor (TNF)-ß gene G252A polymorphism are at high risk of the development of migraine without aura, the relationship between the TNF-ß gene G252A polymorphism and MOH is unknown. We investigated whether the TNF-ß gene G252A polymorphism is involved in the aggravation of migraine by overuse of medications. METHODS: Forty-seven migraine patients (6 males and 41 females; age 36.4±10.3 years, mean±SD) and 22 MOH patients (1 male and 21 females; age 39.6±9.9 years) who had migraine were included in this study. The genotype for the TNF-ß gene G252A polymorphism was determined by polymerase-chain-reaction restriction-fragment-length polymorphism analysis. RESULTS: The distribution of TNF-ß gene G252A genotype frequency differed significantly between migraine and MOH patients (p=0.013). The G/G genotype was carried by 23% of the migraine patients but it was absent in MOH patients. CONCLUSIONS: G/G genotype carriers appear to be less susceptible to the aggravation of migraine by overuse of medications. The G252A TNF-ß gene polymorphism may be one of the factors contributing to the complications of MOH in patients with migraine.
RESUMEN
Migraine is a multifactorial disease with various factors, such as genetic polymorphisms and personality traits, but the contribution of those factors is not clear. To clarify the pathogenesis of migraine, the contributions of genetic polymorphisms and personality traits were simultaneously investigated using multivariate analysis. Ninety-one migraine patients and 119 non-headache healthy volunteers were enrolled. The 12 gene polymorphisms analysis and NEO-FFI personality test were performed. At first, the univariate analysis was performed to extract the contributing factors to pathogenesis of migraine. We then extracted the factors that independently contributed to the pathogenesis of migraine using multivariate stepwise logistic regression analysis. Using the multivariate analysis, three gene polymorphisms including monoamine oxidase A (MAOA) T941G, methylenetetrahydrofolate reductase (MTHFR) C677T, and tumor necrosis factor beta (TNF-ß) G252Α, and the neuroticism and conscientiousness scores in NEO-FFI were selected as significant factors that independently contributed to the pathogenesis of migraine. Their odds ratios were 1.099 (per point of neuroticism score), 1.080 (per point of conscientiousness score), 2.272 (T and T/T or T/G vs G and G/G genotype of MAOA), 1.939 (C/T or T/T vs C/C genotype of MTHFR), and 2.748 (G/A or A/A vs G/G genotype of TNF-ß), respectively. We suggested that multiple factors, such as gene polymorphisms and personality traits, contribute to the pathogenesis of migraine. The contribution of polymorphisms, such as MAOA T941G, MTHFR C677T, and TNF-ß G252A, were more important than personality traits in the pathogenesis of migraine, a multifactorial disorder.
