IDUA假缺失等位基因个体的长期健康结果可为I型黏多醣症的新生儿筛查实践提供参考。

IF 1.7 4区 生物学 Q3 GENETICS & HEREDITY
Lauren O Grady, Emilie S Zoltick, Hana Zouk, Wei He, Emma Perez, Lorne Clarke, Jessica Gold, Alanna Strong, Inderneel Sahai, Julie Yeo, Robert C Green, Amel Karaa, Nina B Gold
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引用次数: 0

摘要

I 型粘多糖病(MPS I)是一种由 IDUA 变异引起的溶酶体疾病,于 2016 年被添加到新生儿筛查的推荐统一筛查面板中。MPS I 的阳性筛查结果通常是由被称为 "假性缺陷等位基因 "的变异引起的,这些变异会降低体外α-L-阿糖醛酸酶的活性,但被认为可提供足够的体内活性。尽管人们历来认为这些变异体在生物学上是良性的,但在成人中,这些变异体可能会导致复杂、多基因或衰减的表型,而这种可能性尚未得到系统的评估。我们完成了一项回顾性匹配队列研究,该研究使用了医院生物库中 65,309 名参与者的数据,发现了 1803 名携带同源 IDUA 伪缺等位基因的个体。利用电子病历(EMR),我们比较了同型假性缺失等位基因参与者与匹配对照参与者的 MPS I 特征患病率。我们发现病例与对照之间没有临床相关的显著差异,四个等位基因之间也没有基因型与表型之间的关联。这些发现提供了经验支持,即与对照组相比,具有同源 IDUA 假缺失等位基因的成年人不太可能出现轻微的疾病症状。这项研究为与其他遗传性代谢紊乱有关的其他非经典疾病变异提供了概念验证模型,随着新生儿筛查范围的扩大,这一点很有必要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long-Term Health Outcomes of Individuals With Pseudodeficiency Alleles in IDUA May Inform Newborn Screening Practices for Mucopolysaccharidosis Type I.

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.

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来源期刊
CiteScore
3.50
自引率
5.00%
发文量
432
审稿时长
2-4 weeks
期刊介绍: The American Journal of Medical Genetics - Part A (AJMG) gives you continuous coverage of all biological and medical aspects of genetic disorders and birth defects, as well as in-depth documentation of phenotype analysis within the current context of genotype/phenotype correlations. In addition to Part A , AJMG also publishes two other parts: Part B: Neuropsychiatric Genetics , covering experimental and clinical investigations of the genetic mechanisms underlying neurologic and psychiatric disorders. Part C: Seminars in Medical Genetics , guest-edited collections of thematic reviews of topical interest to the readership of AJMG .
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