Grady Lauren O, Zoltick Emilie S, Zouk Hana, He Wei, Perez Emma, Clarke Lorne, Gold Jessica, Strong Alanna, Sahai Inderneel, Yeo Julie, Green Robert C, Karaa Amel, Gold Nina B
Division of Medical Genetics and Metabolism, Massachusetts General Hospital for Children, Boston, Massachusetts, USA.
Department of Population Medicine, Harvard Pilgrim Health Care Institute, Boston, Massachusetts, USA.
Am J Med Genet A. 2025 Apr;197(4):e63940. doi: 10.1002/ajmg.a.63940. Epub 2024 Nov 19.
Mucopolysaccharidosis type I (MPS I), a lysosomal disorder caused by variants in IDUA, was added to the Recommended Uniform Screening Panel for newborn screening in 2016. Positive screening results for MPS I are commonly due to variants known as "pseudodeficiency alleles," which decrease in vitro alpha-L-iduronidase enzyme activity but are thought to provide sufficient in vivo activity. Despite the historic assumption that these variants are biologically benign, the possibility that they could give rise to complex, multigenic, or attenuated phenotypes has not been systemically evaluated in adults. We completed a retrospective matched cohort study using a hospital-based biorepository with data from 65,309 participants, we identified 1803 individuals harboring homozygous IDUA pseudodeficiency alleles. Using electronic medical records (EMR), we compared the prevalence of features of MPS I in participants with homozygous pseudodeficiency alleles to a cohort of matched control participants. We found no clinically relevant significant differences between cases and controls nor genotype-phenotype associations across four alleles. These findings provide empiric support that adults with homozygous IDUA pseudodeficiency alleles are unlikely to develop mild symptoms of disease compared with controls. This study provides a proof-of-concept model for other nonclassical disease variants related to other inherited metabolic disorders, which is necessary as newborn screening expands.
I型黏多糖贮积症(MPS I)是一种由IDUA基因变异引起的溶酶体疾病,于2016年被添加到新生儿筛查推荐统一筛查 panel 中。MPS I的筛查阳性结果通常归因于被称为“假缺陷等位基因”的变异,这些变异会降低体外α-L-艾杜糖醛酸酶的活性,但被认为在体内能提供足够的活性。尽管历史上一直认为这些变异在生物学上是良性的,但它们是否会导致复杂、多基因或减弱的表型,在成年人中尚未得到系统评估。我们利用一个基于医院的生物样本库,对65309名参与者的数据进行了回顾性匹配队列研究,确定了1803名携带纯合IDUA假缺陷等位基因的个体。我们使用电子病历(EMR),将携带纯合假缺陷等位基因的参与者中MPS I特征的患病率与一组匹配的对照参与者进行了比较。我们发现病例组和对照组之间在临床上没有显著差异,并且在四个等位基因中也没有发现基因型-表型关联。这些发现提供了实证支持,即与对照组相比,携带纯合IDUA假缺陷等位基因的成年人不太可能出现疾病的轻微症状。这项研究为与其他遗传性代谢疾病相关的其他非经典疾病变异提供了一个概念验证模型,随着新生儿筛查的扩大,这是必要的。