Kalayasiri Rasmon, Verachai Viroj, Gelernter Joel, Mutirangura Apiwat, Malison Robert T
Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Addiction. 2014 Jun;109(6):965-76. doi: 10.1111/add.12512. Epub 2014 Mar 17.
To explore the clinical features of methamphetamine-induced paranoia (MIP) and associations between MIP and a genetic polymorphism in dopamine β-hydroxylase (DBH-1021C→T).
Retrospective analysis of clinical presentation and genetic association by χ(2) test and logistic regression analysis.
A Thai substance abuse treatment center.
A total of 727 methamphetamine-dependent (MD) individuals.
Clinical: Semi-Structured Assessment for Drug Dependence and Alcoholism (SSADDA) and the Methamphetamine Experience Questionnaire (MEQ). Genetic: DBH-1021C→T.
Forty per cent of individuals (289 of 727; 39.8%) with MD had MIP. Within-binge latency to MIP onset occurred more rapidly in the most recent compared with initial MIP episode (P = 0.02), despite unchanging intake (P = 0.89). Individuals with MIP were significantly less likely to carry lower (TT/CT) compared with higher (CC) activity genotypes (34.3 versus 43.3%; χ(2) 1 = 5, P = 0.03). DBH effects were confirmed [odds ratio (OR) = 0.7, P = 0.04] after controlling for associated clinical variables (MD severity, OR = 3.4, P < 0.001; antisocial personality disorder, OR = 2.2, P < 0.001; alcohol dependence, OR = 1.4, P = 0.05; and nicotine dependence, OR = 1.4, P = 0.06). TT/CT carriers were more likely to initiate cigarette smoking (OR = 3.9, P = 0.003) and probably less likely to be dependent on alcohol (OR = 0.6, P = 0.05).
Among methamphetamine-dependent individuals, paranoia appears to occur increasingly rapidly in the course of a session of methamphetamine use. Severity of methamphetamine dependence and antisocial personality disorder predicts methamphetamine-induced paranoia. The genetic polymorphism in dopamine β-hydroxylase is associated with methamphetamine-induced paranoia and influences smoking initiation.
探讨甲基苯丙胺所致偏执（MIP）的临床特征以及MIP与多巴胺β-羟化酶基因多态性（DBH-1021C→T）之间的关联。
通过χ²检验和逻辑回归分析对临床表现及基因关联进行回顾性分析。
泰国一家药物滥用治疗中心。
共727名甲基苯丙胺依赖（MD）个体。
临床方面：药物依赖与酒精中毒半结构化评估（SSADDA）及甲基苯丙胺体验问卷（MEQ）。基因方面：DBH-1021C→T。
40%的MD个体（727名中的289名，占39.8%）患有MIP。与首次MIP发作相比，在最近一次发作中，MIP发作的 binge 内潜伏期更快出现（P = 0.02），尽管摄入量不变（P = 0.89）。与高活性基因型（CC）相比，MIP个体携带低活性（TT/CT）基因型的可能性显著降低（34.3%对43.3%；χ² = 5，P = 0.03）。在控制相关临床变量（MD严重程度，比值比（OR）= 3.4，P < 0.001；反社会人格障碍，OR = 2.2，P < 0.001；酒精依赖，OR = 1.4，P = 0.05；尼古丁依赖，OR = 1.4，P = 0.06）后，DBH的影响得到证实（OR = 0.7，P = 0.04）。TT/CT携带者更有可能开始吸烟（OR = 3.9，P = 0.003），且可能较少依赖酒精（OR = 0.6，P = 0.05）。
在甲基苯丙胺依赖个体中，偏执在甲基苯丙胺使用过程中似乎越来越迅速地出现。甲基苯丙胺依赖的严重程度和反社会人格障碍可预测甲基苯丙胺所致偏执。多巴胺β-羟化酶基因多态性与甲基苯丙胺所致偏执相关，并影响吸烟起始。
