Rujirabanjerd Sinitdhorn, Tongsippunyoo Kobkul, Sripo Thanya, Limprasert Pornprot
Department of Pathology, Faculty of Medicine, Prince of Songkla University, Hat Yai, Songkhla, 90110, Thailand.
Eur J Med Genet. 2007 Sep-Oct;50(5):346-54. doi: 10.1016/j.ejmg.2007.05.003. Epub 2007 May 27.
Mutations in the Aristaless-related homeobox gene, ARX, have been a cause of X-linked mental retardation (XLMR) and are responsible for a vast phenotypic spectrum including syndromic and non-syndromic forms of mental retardation. Since the gene was initially identified, it has been generally screened in several patients with XLMR. This study is the first report of ARX mutational screening in Thai pediatric patients with delayed development. Two hundred and fifty-one patients participated in this study. Two hundred and three of the 251 patients were initially referred for molecular diagnosis of the Fragile XA syndrome and had negative test results. The remaining 48 patients were specifically recruited for the ARX mutational analysis and had previously reported phenotypes of the ARX mutations. Screening for the c.428_451 dup mutation was performed in all samples. Screening for other point mutations in all coding exons was performed in all 48 patients recruited for the ARX mutational analysis and in 29 patients initially referred for diagnosis of the Fragile XA syndrome who had two or more affected males in the family suggesting an X-linked inheritance pattern. Two patients were found to have the c.428_451 dup mutation. Considering genotype-phenotype correlation, we suggest screening of the most common mutation, the c.428_451 dup mutation by PCR, in patients with infantile spasm syndrome, Partington syndrome and non-syndromic X-linked mental retardation. Screening in patients who have negative Fragile XA test results should be considered when no other known causes of mental retardation are identified especially in families with suggestive X-linked inheritance pattern.
无翅相关同源框基因(ARX)的突变一直是X连锁智力迟钝(XLMR)的病因,并且导致了包括综合征型和非综合征型智力迟钝在内的广泛表型谱。自该基因最初被鉴定以来,已对数名XLMR患者进行了普遍筛查。本研究是泰国发育迟缓儿科患者中ARX突变筛查的首次报告。251名患者参与了本研究。251名患者中有203名最初被转诊进行脆性X A综合征的分子诊断,检测结果为阴性。其余48名患者是专门招募来进行ARX突变分析的,他们之前已报告过ARX突变的表型。对所有样本进行了c.428_451dup突变的筛查。对所有48名招募来进行ARX突变分析的患者以及29名最初被转诊进行脆性X A综合征诊断且家族中有两名或更多受影响男性提示X连锁遗传模式的患者,进行了所有编码外显子中其他点突变的筛查。发现两名患者有c.428_451dup突变。考虑到基因型-表型相关性,我们建议对患有婴儿痉挛综合征、帕廷顿综合征和非综合征型X连锁智力迟钝的患者,通过聚合酶链反应(PCR)筛查最常见的突变,即c.428_451dup突变。当未发现其他已知的智力迟钝病因时,尤其是在具有提示性X连锁遗传模式的家族中,应考虑对脆性X A检测结果为阴性的患者进行筛查。