Pohlenz J, Wildhardt G, Zabel B, Willgerodt H
Children's Hospital of the Johannes-Gutenberg-University, Mainz, Germany.
Thyroid. 1997 Feb;7(1):39-41. doi: 10.1089/thy.1997.7.39.
Resistance to thyroid hormone (RTH) is an inherited defect manifesting as variable tissue hyporesponsiveness to thyroid hormone, usually caused by mutations in the thyroid hormone receptor beta (TR beta) gene. Up to now 78 mutations in this gene have been identified, mostly clustered in two regions located in exon 9 and 10. We describe a new point mutation replacing the normal thymidine-1274 with a cytosine that results in the substitution of the normal leucine-330 with a serine (L330S) in the receptor protein. This mutation was identified in an 11-year-old boy who presented with symptoms and signs suggestive of both hyperthyroidism and hypothyroidism. Interestingly a mutation in the same codon (L330F) has been previously described in a patient who presented with stigmata suggestive of thyrotoxicosis.
甲状腺激素抵抗(RTH)是一种遗传性缺陷,表现为组织对甲状腺激素的反应性降低,通常由甲状腺激素受体β(TRβ)基因突变引起。到目前为止,该基因已鉴定出78种突变,大多集中在外显子9和10的两个区域。我们描述了一种新的点突变,正常的胸腺嘧啶-1274被胞嘧啶取代,导致受体蛋白中正常的亮氨酸-330被丝氨酸取代(L330S)。该突变在一名11岁男孩中被发现,他表现出提示甲亢和甲减的症状和体征。有趣的是,先前在一名表现出甲状腺毒症特征的患者中描述了同一密码子的突变(L330F)。