Clinical and Chemical Pathology Department, Faculty of Medicine, Cairo University, Cairo University Children's Hospital, Monira, 11628, Cairo, Egypt.
Central laboratories, Cairo University Hospitals, Cairo University, Cairo, Egypt.
Sci Rep. 2024 Nov 18;14(1):28391. doi: 10.1038/s41598-024-78105-y.
Maple Syrup Urine Disease (MSUD, OMIM# 248600) is an autosomal recessive inborn error of metabolism characterized by elevated branched chain amino acids (BCAA) leucine/isoleucine and valine in blood of affected children. The phenotypic and genotypic spectrum of MSUD is largely unreported in Egypt. We recruited ten patients (4 males/6 females, 2weeks-12years) from nine unrelated families with clinical and biochemical evidence of MSUD. We performed Sanger sequencing for the three most-commonly responsible genes: BCKDHA, BCKDHB and DBT and conducted exome sequencing for unresolved cases. Through Sanger sequencing, we detected eight homozygous pathogenic/likely pathogenic variants (four in BCKDHB, three in BCKDHA and one in DBT gene) in eight different families. The proband of family VI, who had no significant genetic findings by Sanger, had a peculiar phenotype and atypical radiological findings. His exome sequencing revealed a previously reported homozygous likely pathogenic variant in the RARS2 gene (NM_020320.5:c.1026G > A;p.(Met342Ile)) causing the mitochondrial-encephalopathy disorder pontocerebellar hypoplasia, type 6 (OMIM# 611523). Furthermore, the copy-number-variant analysis of the exome data revealed a biallelic duplication affecting exons 2-6 of the BCKDHB gene (GRCh38: Chr.6-g.80127496:80171441dup) evaluated as variant of uncertain significance but expected to cause a breakpoint and may disrupt gene function, which can explain the markedly elevated BCAA levels in the patient's blood. In conclusion, we expanded the genotypic and phenotypic spectrum of the disease and showed that aggressive intervention with specific treatment in the first few days of life resulted in normal development even in a developing country setting. Inclusion of MSUD in the national newborn screening program in Egypt is highly recommended.
枫糖尿症(MSUD,OMIM#248600)是一种常染色体隐性遗传的代谢性疾病,其特征是受影响儿童血液中的支链氨基酸(BCAA)亮氨酸/异亮氨酸和缬氨酸升高。MSUD 的表型和基因型谱在埃及尚未得到广泛报道。我们从 9 个无关的家庭中招募了 10 名患者(4 名男性/6 名女性,年龄 2 周至 12 岁),这些患者具有 MSUD 的临床和生化证据。我们对三个最常见的致病基因:BCKDHA、BCKDHB 和 DBT 进行了 Sanger 测序,并对未解决的病例进行了外显子组测序。通过 Sanger 测序,我们在 8 个不同的家庭中检测到 8 个纯合的致病性/可能致病性变异(BCKDHB 基因中有 4 个,BCKDHA 基因中有 3 个,DBT 基因中有 1 个)。第 VI 个家庭的先证者,通过 Sanger 未发现明显的遗传发现,具有特殊的表型和非典型的放射学发现。他的外显子组测序显示了一个先前报道的 RARS2 基因(NM_020320.5:c.1026G>A;p.(Met342Ile))纯合的可能致病性变异,导致线粒体脑病-小脑桥脑发育不良,6 型(OMIM#611523)。此外,外显子组数据的拷贝数变异分析显示了影响 BCKDHB 基因外显子 2-6 的双等位基因重复(GRCh38:Chr.6-g.80127496:80171441dup),评估为意义不确定的变异,但预计会导致断裂点并可能破坏基因功能,这可以解释患者血液中明显升高的 BCAA 水平。总之,我们扩展了疾病的基因型和表型谱,并表明在生命的最初几天内进行积极的特殊治疗干预可以导致正常发育,即使在发展中国家也是如此。强烈建议在埃及的国家新生儿筛查计划中纳入 MSUD。