CAJ | 학술논문

目的探讨脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)Val66Met功能基因多态性和环境因素及其相互作用对抗抑郁剂治疗抑郁症临床疗效的影响.方法按照美国诊断和统计手册第4版(DSM-Ⅳ)入组340例抑郁症患者,其中280例完成12周抗抑郁剂治疗.治疗前后采用汉密尔顿抑郁量表(HDRS)评定抑郁严重程度和治疗疗效,采用儿童期创伤问卷(CTQ-SF)及生活事件量表(LES)分别评定早期负性生活事件及发病前应激事件刺激量,采用Illumina GoldenGate定制芯片分析患者BDNFVal66Met基因多态性并进行基因分型.结果抑郁症未痊愈组患者中男性比例显著高于痊愈组(P=0.008).痊愈组BDNF Val66Met基因型分布(AA:AG:GG=28:79:40),等位基因分布(A:G=135:159)与未痊愈组中基因型分布(AA:AG:GG=29:81:23)和等位基因分布(A:G=139:127),经性别校正后差异无统计学意义(P＞0.05).将患者分为首发患者和复发患者,均未发现BDNF Val66Met基因型和等位基因分布频率在2组间差异有显著性(均P＞0.05).儿童期创伤问卷及生活事件量表分值2组间差异无统计学意义(P＞0.05);多元回归分析显示患者年龄和LES社交问题分值进入回归方程,是影响抑郁严重程度的主要因素,而Logistic回归分析显示患者性别、HDRS基线分值及精神疾病家族史进入回归方程,是抗抑郁剂近期疗效的影响因素(均P＜0.05).多因素Logistic回归模型分析显示BDNF Val66Met基因型及各量表赋值交互作用对抗抑郁剂疗效影响并无统计学意义(均P＞0.05).结论伴有精神疾病家族史、抑郁症状严重、年龄较大的男性抑郁症患者近期疗效差,但BDNF Val66Met功能基因多态性、早期负性生活事件及其相互作用不是抗抑郁剂疗效的主要影响因素.
목적 탐토뇌원성신경영양인자(brain-derived neurotrophic factor,BDNF)Val66Met공능기인다태성화배경인소급기상호작용대항억욱제치료억욱증림상료효적영향.방법 안조미국진단화통계수책제4판(DSM-Ⅳ)입조340례억욱증환자,기중280례완성12주항억욱제치료.치료전후채용한밀이돈억욱량표(HDRS)평정억욱엄중정도화치료료효,채용인동기창상문권(CTQ-SF)급생활사건량표(LES)분별평정조기부성생활사건급발병전응격사건자격량,채용Illumina GoldenGate정제심편분석환자BDNFVal66Met기인다태성병진행기인분형.결과 억욱증미전유조환자중남성비례현저고우전유조(P=0.008).전유조BDNF Val66Met기인형분포(AA:AG:GG=28:79:40),등위기인분포(A:G=135:159)여미전유조중기인형분포(AA:AG:GG=29:81:23)화등위기인분포(A:G=139:127),경성별교정후차이무통계학의의(P＞0.05).장환자분위수발환자화복발환자,균미발현BDNF Val66Met기인형화등위기인분포빈솔재2조간차이유현저성(균P＞0.05).인동기창상문권급생활사건량표분치2조간차이무통계학의의(P＞0.05);다원회귀분석현시환자년령화LES사교문제분치진입회귀방정,시영향억욱엄중정도적주요인소,이Logistic회귀분석현시환자성별、HDRS기선분치급정신질병가족사진입회귀방정,시항억욱제근기료효적영향인소(균P＜0.05).다인소Logistic회귀모형분석현시BDNF Val66Met기인형급각량표부치교호작용대항억욱제료효영향병무통계학의의(균P＞0.05).결론 반유정신질병가족사、억욱증상엄중、년령교대적남성억욱증환자근기료효차,단BDNF Val66Met공능기인다태성、조기부성생활사건급기상호작용불시항억욱제료효적주요영향인소.
Objective To explore the effect of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism,environmental factor and their interactions on antidepressant treatment.Methods 340 patients of major depressive disorder (MDD) who met the diagnosis criteria of MDD ( DSM-Ⅳ Axis Ⅰ) were recruited.280 patients of them were finished 12 weeks antidepressant treatment.The severity of depression was measured with the Hamilton Depression Rating Scale (HDRS) before and after 12 weeks antidepressant treatment.Childhood Trauma Questionnaire,28-item Short Form (CTQ-SF) and Life Events Scale (LES) were used to evaluate childhood adverse and life stress before onset.Genotyping of BDNF Val66Met polymorphism was detected by Illumina GoldenGate assays.Results Male patients proportion were significantly higher in non-remitters than remitters (P =0.008 ).After adjusting by gender, the frequencies of genotype and allele for the BDNF Val66Met polymorphism were no significant difference between remitters (AA: AG: GG = 28: 79: 40, A:G = 135:159 ) and non-remitters (AA: AG: GG = 29:81:23 ,A: G = 139:127 ) (P ＞0.05 ).There was no significant difference of CTQ scores and LES scores between the two groups (P＞0.05 ).The regression analysis showed that social intercourse problem and age were the risk factor for the severity of depression.The gender, HDRS baseline scores and mental disorder family history were associated with the efficacy of 12 weeks antidepressant.However,there was no significantly relationship between the interaction of BDNF Val66Met polymorphism and environment with the antidepressant treatment.Conclusion The older men with the mental disorder family history, severe depression symptom would be less-response to antidepressant treatment.However, BDNF Val66Met polymorphism, childhood trauma, life events stress and the interaction of BDNF Val66Met polymorphism and environment have no significantly effect on the 12 weeks antidepressant treatment.