| Literature DB >> 32088313 |
Rui-Jia Zhang1, Feng Sun1, Feng Chen2, Ya Fang1, Chen-Yan Yan1, Chang-Run Zhang1, Ying-Xia Ying1, Zheng Wang1, Cao-Xu Zhang1, Feng-Yao Wu1, Bing Han1, Jun Liang3, Shuang-Xia Zhao1, Huai-Dong Song4.
Abstract
Inborn defects in thyroid hormone biosynthesis contribute to nearly half of congenital hypothyroidism (CH) cases in China. The thyroid peroxidase (TPO) mutation is one of the most frequent mutations that results in thyroid dyshormonogenesis. In this study, 35 non-synonymous mutations in 15 TPO sites, including 6 novel mutations, were identified in 230 Chinese patients with CH. The enzyme activity of the mutations in TPO was investigated in vitro, and patients with less than 15% residual enzyme activity showed severe CH, such as markedly increased thyroid-stimulating hormone (TSH) at diagnosis (>100 μIU/mL) and pronounced goiter, and required a higher dose of L-thyroxine to maintain the euthyroid. However, CH patients with greater than 16% TPO activity showed mild CH, a typical childhood socially without L-thyroxine treatment before 3 years of age, and the appearance of a macroscopic goiter at childhood. The findings indicated that the residual enzymatic activity of TPO was correlated with clinical phenotypes of CH patients with TPO biallelic mutations.Entities:
Keywords: Congenital hypothyroidism; Genotype-phenotype analysis; Next-generation sequencing; Thyroid peroxidase
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Year: 2020 PMID: 32088313 DOI: 10.1016/j.mce.2020.110761
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN: 0303-7207 Impact factor: 4.102