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载脂蛋白 E 基因多态性与儿童和青少年注意缺陷多动障碍患者接受哌甲酯治疗后食欲下降的相关性。

Association of a carboxylesterase 1 polymorphism with appetite reduction in children and adolescents with attention-deficit/hyperactivity disorder treated with methylphenidate.

机构信息

Department of Genetics, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.

出版信息

Pharmacogenomics J. 2013 Oct;13(5):476-80. doi: 10.1038/tpj.2012.25. Epub 2012 Jun 12.

DOI:10.1038/tpj.2012.25
PMID:22688218
Abstract

Carboxylesterase 1 is the enzyme involved in methylphenidate (MPH) metabolism. The aim of this study was to evaluate the association between a -75 T>G polymorphism and appetite reduction in children with attention-deficit/hyperactivity disorder (ADHD). A sample of 213 children with ADHD was investigated. The primary outcome was appetite reduction measured by the Barkley Stimulant Side Effect Rating Scale applied at baseline, at 1 and 3 months of treatment. MPH doses were augmented until no further clinical improvement or significant adverse events occurred. The G allele presented a trend for association with appetite reduction scores (P=0.05). A significant interaction between the G allele and treatment over time for appetite reduction scores was also observed (P=0.03). The G allele carriers presented a higher risk for appetite reduction worsening when compared with T allele homozygotes (odds ratio=3.47, P=0.01). The present results suggest an influence of carboxylesterase 1 -75 T>G polymorphism on the worsening of appetite reduction with MPH treatment in youths with ADHD.

摘要

羧基酯酶 1 是参与哌醋甲酯(MPH)代谢的酶。本研究旨在评估-75T>G 多态性与注意缺陷多动障碍(ADHD)儿童食欲减退之间的关联。对 213 名患有 ADHD 的儿童进行了调查。主要结果是通过基线、治疗 1 个月和 3 个月时应用 Barkley 兴奋剂副作用评定量表测量的食欲减退。增加 MPH 剂量,直到不再出现临床改善或出现明显不良反应。G 等位基因与食欲减退评分呈关联趋势(P=0.05)。还观察到 G 等位基因与治疗时间之间对食欲减退评分的显著交互作用(P=0.03)。与 T 等位基因纯合子相比,G 等位基因携带者食欲减退恶化的风险更高(比值比=3.47,P=0.01)。本研究结果提示羧基酯酶 1-75T>G 多态性可能影响 MPH 治疗青少年 ADHD 时食欲减退的恶化。

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