Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
BMC Med Genet. 2014 Feb 25;15:24. doi: 10.1186/1471-2350-15-24.
Mutations in the cyclin-dependent kinase-like 5 (CDKL5) (NM_003159.2) gene have been associated with early-onset epileptic encephalopathies or Hanefeld variants of RTT(Rett syndrome). In order to clarify the CDKL5 genotype-phenotype correlations in Chinese patients, CDKL5 mutational screening in cases with early-onset epileptic encephalopathies and RTT without MECP2 mutation were performed.
The detailed clinical information including clinical manifestation, electroencephalogram (EEG), magnetic resonance imaging (MRI), blood, urine amino acid and organic acid screening of 102 Chinese patients with early-onset epileptic encephalopathies and RTT were collected. CDKL5 gene mutations were analyzed by PCR, direct sequencing and multiplex ligation-dependent probe amplification (MLPA). The patterns of X-chromosome inactivation (XCI) were studied in the female patients with CDKL5 gene mutation.
De novo CDKL5 gene mutations were found in ten patients including one missense mutation (c.533G > A, p.R178Q) which had been reported, two splicing mutations (ISV6 + 1A > G, ISV13 + 1A > G), three micro-deletions (c.1111delC, c.2360delA, c.234delA), two insertions (c.1791 ins G, c.891_892 ins TT in a pair of twins) and one nonsense mutation (c.1375C > T, p.Q459X). Out of ten patients, 7 of 9 females with Hanefeld variants of RTT and the remaining 2 females with early onset epileptic encephalopathy, were detected while only one male with infantile spasms was detected. The common features of all female patients with CDKL5 gene mutations included refractory seizures starting before 4 months of age, severe psychomotor retardation, Rett-like features such as hand stereotypies, deceleration of head growth after birth and poor prognosis. In contrast, the only one male patient with CDKL5 mutation showed no obvious Rett-like features as females in our cohort. The X-chromosome inactivation patterns of all the female patients were random.
Mutations in CDKL5 gene are responsible for 7 with Hanefeld variants of RTT and 2 with early-onset epileptic encephalopathy in 71 girls as well as for 1 infantile spasms in 31 males. There are some differences in the phenotypes among genders with CDKL5 gene mutations and CDKL5 gene mutation analysis should be considered in both genders.
细胞周期蛋白依赖性激酶样 5 (CDKL5) 基因 (NM_003159.2) 的突变与早发性癫痫性脑病或 Hanefeld 变异型 RTT(雷特综合征)有关。为了阐明中国患者中 CDKL5 基因型-表型相关性,对无 MECP2 突变的早发性癫痫性脑病和 RTT 患者进行了 CDKL5 基因突变筛查。
收集 102 例早发性癫痫性脑病和 RTT 患者的详细临床资料,包括临床表现、脑电图(EEG)、磁共振成像(MRI)、血液、尿液氨基酸和有机酸筛查。通过 PCR、直接测序和多重连接依赖性探针扩增(MLPA)分析 CDKL5 基因突变。对 CDKL5 基因突变的女性患者进行 X 染色体失活(XCI)模式研究。
在 10 例患者中发现了新生 CDKL5 基因突变,包括 1 例已报道的错义突变(c.533G > A,p.R178Q)、2 例剪接突变(ISV6 + 1A > G,ISV13 + 1A > G)、3 例微缺失(c.1111delC、c.2360delA、c.234delA)、2 例插入(c.1791 ins G、c.891_892 ins TT 在一对双胞胎中)和 1 例无义突变(c.1375C > T,p.Q459X)。9 例 Hanefeld 变异型 RTT 的女性患者中有 7 例,2 例早发性癫痫性脑病的女性患者中有 7 例,1 例婴儿痉挛症的男性患者中有 1 例。所有 CDKL5 基因突变女性患者的共同特征包括 4 个月前开始的难治性癫痫发作、严重精神运动发育迟缓、手刻板动作等雷特样特征、出生后头围生长减速和预后不良。相比之下,我们队列中唯一的一名 CDKL5 突变男性患者没有明显的雷特样特征。所有女性患者的 X 染色体失活模式均为随机。
CDKL5 基因突变导致 7 例 Hanefeld 变异型 RTT 和 2 例早发性癫痫性脑病的 71 名女孩以及 31 名男性中的 1 例婴儿痉挛症。CDKL5 基因突变的男女患者表型存在差异,应考虑在男女两性中进行 CDKL5 基因突变分析。