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两名患有严重智力障碍和自闭症患者的X连锁肌酸转运体缺乏症

X-Linked creatine transporter deficiency in two patients with severe mental retardation and autism.

作者信息

Póo-Argüelles P, Arias A, Vilaseca M A, Ribes A, Artuch R, Sans-Fito A, Moreno A, Jakobs C, Salomons G

机构信息

Department of Neuropediatrics, Hospital Sant Joan de Déu, Barcelona, Spain.

出版信息

J Inherit Metab Dis. 2006 Feb;29(1):220-3. doi: 10.1007/s10545-006-0212-4.

Abstract

We describe the first two unrelated Spanish patients with creatine transporter deficiency initially identified by brain proton magnetic resonance spectroscopy (MRS). The clinical phenotype was characterized by severe mental retardation, epilepsy, autism, severe speech delay and absence of brain creatine by MRS. Urine creatine/creatinine ratio was increased and creatine uptake in fibroblasts was impaired in both patients. On DNA sequence analysis of the SLC6A8/creatine transporter gene, one hemizygous mutation was found in each patient: one mutation was novel and consisted of a deletion of two nucleotides c.878-879delTC in exon 5, resulting in a frameshift (p.Lys293fsX3), and in the other patient a known deletion of three nucleotides 1222-1224delTTC in exon 8 resulting in p.Phe408del. Creatine treatment for one year failed to improve the neurological symptoms and was associated with a striking increase in body weight in both patients (13 and 16 kg, respectively).

摘要

我们描述了首例最初通过脑质子磁共振波谱(MRS)鉴定的两名无血缘关系的西班牙肌酸转运蛋白缺乏症患者。临床表型的特征为严重智力发育迟缓、癫痫、自闭症、严重语言发育迟缓以及MRS显示脑内肌酸缺乏。两名患者的尿肌酸/肌酐比值均升高,成纤维细胞中的肌酸摄取受损。对SLC6A8/肌酸转运蛋白基因进行DNA序列分析时,在每名患者中均发现了一个半合子突变:一个突变是新发现的,由外显子5中两个核苷酸c.878 - 879delTC缺失组成,导致移码突变(p.Lys293fsX3),另一名患者是外显子8中已知的三个核苷酸1222 - 1224delTTC缺失,导致p.Phe408del。两名患者接受为期一年的肌酸治疗均未能改善神经症状,且均伴有体重显著增加(分别增加13千克和16千克)。

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