CBCL pediatric bipolar disorder profile and ADHD: Comorbidity and quantitative trait loci analysis
CBCL pediatric bipolar disorder profile and ADHD: Comorbidity and quantitative trait loci analysis
复制标题
DOI：
10.1097/chi.0b013e3181825a68
复制
发表时间：
2008-10-01
影响因子：
13.3
通讯作者：
Smalley, Susan L.
中科院分区：
文献类型：
--
作者：
McGough, James J.;Loo, Sandra K.;Smalley, Susan L.
目的：儿童行为检查表（CBCL-PBD）的儿童双相情感障碍特征，是一种避免临床医生意识形态偏见的家长完成的测量，已被证明对区分注意缺陷/多动障碍（ADHD）患者有用。我们使用CBCL-PBD谱来区分合并症的模式，并在多个受影响的ADHD兄弟姐妹样本的全基因组扫描中寻找数量性状位点。方法：采用《学龄期儿童情感障碍与精神分裂症量表-现在版和终生版》和CBCL对540例5 ~ 18岁ADHD患者进行评估。父母被评估为情感性障碍和精神分裂症终生版，并辅以情感性障碍和学龄儿童精神分裂症破坏性行为障碍。根据CBCL-PBD档案对比精神共病的模式。数量性状位点方差成分分析用于鉴定可能携带CBCL-PBD数量表型易感基因的潜在基因组区域。结果：双相情感障碍占总样本的不到2%。CBCL-PBD分类与广泛性焦虑障碍（p = 0.001）、对立违抗性障碍（p = 0.008）、行为障碍（p = 0.003）和父母药物滥用（p = 0.005）增加相关。在2q染色体上发现中度显著的连锁信号（多点最大负荷评分= 2.5）。结论：CBCL-PBD特征区分了ADHD患者中具有显著合并症的子集。对CBCL-PBD表型的连锁分析表明，某些基因组区域值得进一步研究导致严重精神病理的基因。
Objective: The pediatric bipolar disorder profilme of the Child Behavior Checklist (CBCL-PBD), a parent-completed measure that avoids clinician ideological bias, has proven useful in differentiating patients with attention-deficit/hyperactivity disorder (ADHD). We used CBCL-PBD profiles to distinguish patterns of comorbidity and to search for quantitative trait loci in a genomewide scan in a sample of multiple affected ADHD sibling pairs. Method: A total of 540 ADHD subjects ages 5 to 18 years were assessed with the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime version and CBCL. Parents were assessed with the Schedule for Affective Disorders and Schizophrenia-Lifetime version supplemented by the Schedule for Affective Disorders and Schizophrenia for School-Age Children for disruptive behavioral disorders. Patterns of psychiatric comorbidity were contrasted based on the CBCL-PBD profile. A quantitative trait loci variance component analysis was used to identify potential genomic regions that may harbor susceptibility genes for the CBCL-PBD quantitative phenotype. Results: Bipolar spectrum disorders represented less than 2% of the overall sample. The CBCL-PBD classification was associated with increased generalized anxiety disorder (p = .001), oppositional defiant disorder (p = .008), conduct disorder (p = .003), and parental substance abuse (p = .005). A moderately significant linkage signal (multipoint maximum lod score = 2.5) was found on chromosome 2q. Conclusions: The CBCL-PBD profile distinguishes a subset of ADHD patients with significant comorbidity. Linkage analysis of the CBCL-PBD phenotype suggests certain genomic regions that merit further investigation for genes predisposing to severe psychopathology.