Tryptophan Hydroxylase 2 유전자다형성과 항정신병약물로 유발된 지연성운동장애의 연관성

Abstract

Objectives : Tardive dyskinesia (TD) is a serious and sometimes irreversible adverse effect that may develop during long-term antipsychotics treatment. Previous studies have suggested that brain serotonergic systems are related to TD vulnerability and tryptophan hydroxylase (TPH) is the rate limiting enzyme in the biosynthesis of serotonin. This study aimed to investigate the association between TPH2 gene -703G/T polymorphism (rs4570625) and antipsychotic-induced TD in the Korean schizophrenia patients. Methods : We investigated whether TPH2 gene -703G/T polymorphism is associated with antipsychotic-induced TD in 280 Korean schizophrenia patients. The subjects with TD (n=105) and without TD (n=175) were matched for antipsychotic drug exposure and other relevant variables. Results : There was no significant difference in the distribution of genotypic (χ2=3.00, p=0.223) and allelic (χ2=0.19, p=0.661) frequencies between patients group with TD and without TD. There was no significant difference in total Abnormal Involuntary Movement Scale score (F=1.95, p=0.362) among the genotype groups, either. Conclusions : The present study does not support that TPH2 gene -703G/T polymorphism is involved in TD of the Korean schizophrenia subjects.