Department of Neurology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA.
Hugo W. Moser Research Institute at Kennedy Krieger Institute, 707 North Broadway, Baltimore, MD, 21205, USA.
Neurogenetics. 2018 Jan;19(1):41-47. doi: 10.1007/s10048-017-0535-3. Epub 2018 Jan 10.
Rett syndrome (RTT) is caused by mutations in methyl-CpG-binding protein 2 (MECP2), but defects in a handful of other genes (e.g., CDKL5, FOXG1, MEF2C) can lead to presentations that resemble, but do not completely mirror, classical RTT. In this study, we attempted to identify other monogenic disorders that share features with RTT. We performed a retrospective chart review on n = 319 patients who had undergone clinical whole exome sequencing (WES) for further etiological evaluation of neurodevelopmental diagnoses that remained unexplained despite extensive prior workup. From this group, we characterized those who (1) possessed features that were compatible with RTT based on clinical judgment, (2) subsequently underwent MECP2 sequencing and/or MECP2 deletion/duplication analysis with negative results, and (3) ultimately arrived at a diagnosis other than RTT with WES. n = 7 patients had clinical features overlapping RTT with negative MECP2 analysis but positive WES providing a diagnosis. These seven patients collectively possessed pathogenic variants in six different genes: two in KCNB1 and one each in FOXG1, IQSEC2, MEIS2, TCF4, and WDR45. n = 2 (both with KCNB1 variants) fulfilled criteria for atypical RTT. RTT-associated features included the following: loss of hand or language skills (n = 3; IQSEC2, KCNB1 x 2); disrupted sleep (n = 4; KNCB1, MEIS2, TCF4, WDR45); stereotyped hand movements (n = 5; FOXG1, KNCB1 x 2, MEIS2, TCF4); bruxism (n = 3; KCNB1 x 2; TCF4); and hypotonia (n = 7). Clinically based diagnoses can be misleading, evident by the increasing number of genetic conditions associated with features of RTT with negative MECP2 mutations.
雷特综合征(RTT)是由甲基-CpG 结合蛋白 2(MECP2)突变引起的,但少数其他基因(如 CDKL5、FOXG1、MEF2C)的缺陷也可导致与经典 RTT 相似但不完全相同的表现。在这项研究中,我们试图确定其他具有 RTT 特征的单基因疾病。我们对 n=319 名接受临床全外显子组测序(WES)以进一步确定神经发育诊断病因的患者进行了回顾性图表审查,这些患者尽管进行了广泛的前期检查,但仍无法解释诊断。从这组患者中,我们确定了以下特征的患者:(1)根据临床判断,具有与 RTT 相符的特征;(2)随后进行 MECP2 测序和/或 MECP2 缺失/重复分析结果为阴性;(3)最终通过 WES 诊断为非 RTT。n=7 名患者的临床特征与 RTT 重叠,MECP2 分析结果为阴性,但 WES 检测结果为阳性。这 7 名患者的共有的致病性变异位于 6 个不同的基因中:2 个在 KCNB1,1 个在 FOXG1、IQSEC2、MEIS2、TCF4 和 WDR45。n=2 名(均为 KCNB1 变异)符合非典型 RTT 的标准。与 RTT 相关的特征包括以下:丧失手或语言技能(n=3;IQSEC2,KCNB1 x 2);睡眠障碍(n=4;KNCB1、MEIS2、TCF4、WDR45);刻板手运动(n=5;FOXG1、KNCB1 x 2、MEIS2、TCF4);磨牙(n=3;KCNB1 x 2;TCF4);以及张力减退(n=7)。基于临床的诊断可能会产生误导,这可以从越来越多的与 MECP2 突变阴性的 RTT 相关特征的遗传条件中看出。