Department of Paediatrics, The First Affiliated Hospital, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, PR China.
Nephrol Dial Transplant. 2010 May;25(5):1697-702. doi: 10.1093/ndt/gfq071. Epub 2010 Feb 22.
Schimke immuno-osseous dysplasia (SIOD) is a rare autosomal recessive pleiotropic disease caused by mutations in the SMARCAL1 gene. To date there have been no data from the Chinese population. Here, we report the first SIOD case in the Chinese population. No case with gross carpal bone age retardation has been reported previously.
The index patient was diagnosed by clinical and laboratory investigations. Mutations analysis of the SMARCAL1 gene and haplotype analysis were performed in the family. Structural predictions of the wild-type and mutant proteins were conducted.
Severe SIOD was diagnosed in an 8-year-old boy, who exhibited growth failure, recurrent infection, neutropaenia, spondyloepiphyseal dysplasia, focal segmental glomerulosclerosis, T cell immunodeficiency and facial dysmorphism. Marked carpal bone age retardation was also observed. Sequence analysis of the SMARCAL1 gene revealed two novel mutations: c.3G>A (p.Met1?) and c.1682G>A (p.Arg561His) in the boy. Haplotype analysis and mutation detection showed that the father is the carrier of c.3G>A (p.Met1?) and the mother is the carrier of c.1682G>A (p.Arg561His). The paternal mutation, c.3G>A (p.Met1?), is predicted to introduce a new open reading frame, resulting in truncation of 103 amino acids at the N-terminus. The maternal mutation occurred in the SNF2-related domain involved in ATP hydrolyzation and DNA binding and is predicted to alter the local spatial structure of the protein.
We report the first SIOD patient from China, who exhibited gross carpal bone age retardation and carried two novel mutations, c.3G>A (p.Met1?) and c.1682G>A (p.Arg561His), in the SMARCAL1 gene.
Schimke 免疫骨发育不良(SIOD)是一种罕见的常染色体隐性多系统疾病,由 SMARCAL1 基因突变引起。迄今为止,尚未有来自中国人群的数据。在此,我们报告首例中国人群中的 SIOD 病例。此前没有报道过伴有严重腕骨发育迟缓的病例。
通过临床和实验室检查对先证者进行诊断。对 SMARCAL1 基因进行突变分析,并对家系进行单倍型分析。对野生型和突变型蛋白进行结构预测。
诊断为 8 岁男孩患有严重的 SIOD,表现为生长发育迟缓、反复感染、中性粒细胞减少、脊椎骨骺发育不良、局灶节段性肾小球硬化、T 细胞免疫缺陷和面部畸形。还观察到明显的腕骨发育迟缓。SMARCAL1 基因序列分析发现两个新突变:c.3G>A(p.Met1?)和 c.1682G>A(p.Arg561His)。单倍型分析和突变检测显示,父亲是 c.3G>A(p.Met1?)的携带者,母亲是 c.1682G>A(p.Arg561His)的携带者。父源性突变 c.3G>A(p.Met1?)预计会引入一个新的开放阅读框,导致 N 端 103 个氨基酸缺失。母源性突变发生在涉及 ATP 水解和 DNA 结合的 SNF2 相关结构域,预计会改变蛋白的局部空间结构。
我们报告了首例来自中国的 SIOD 患者,该患者表现为严重的腕骨发育迟缓,并携带 SMARCAL1 基因中的两个新突变 c.3G>A(p.Met1?)和 c.1682G>A(p.Arg561His)。