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家族性孤立性甲状旁腺功能减退伴甲状旁腺激素残留分泌中的GCMB突变

GCMB mutation in familial isolated hypoparathyroidism with residual secretion of parathyroid hormone.

作者信息

Thomée Caroline, Schubert Steffen W, Parma Jasmine, Lê Phu Quoc, Hashemolhosseini Said, Wegner Michael, Abramowicz Marc J

机构信息

Department of Internal Medicine,Children's Unit, Centre Hospitalier Etterbeek-Ixelles, Brussels.

出版信息

J Clin Endocrinol Metab. 2005 May;90(5):2487-92. doi: 10.1210/jc.2004-2450. Epub 2005 Feb 22.

Abstract

Isolated hypoparathyroidism is an uncommon metabolic disorder characterized by hypocalcemia and hyperphosphatemia, with absent or low levels of PTH. It may present as an apparently sporadic disorder or may be transmitted in families as a genetic trait. Mutations of the calcium-sensing receptor gene and of the preproPTH gene have been reported in occasional cases, and a mutation of the parathyroid-specific transcription factor GCMB gene has been reported in one familial case. We report a second family with isolated hypoparathyroidism and a GCMB mutation. The patients were two siblings from asymptomatic, first-cousin parents, indicating autosomal recessive inheritance. The mutation consisted of the substitution of a glycine residue with a serine at position 63 (G63S) in the DNA-binding GCM domain of GCMB. Functional studies in transfected cells showed that the mutation caused loss of GCMB function, as it abolished transactivation capacity, despite normal subcellular localization, protein stability, and DNA-binding specificity. Contrary to the previously reported family, our patients displayed low but clearly detectable levels of PTH in plasma. This residual hormone secretion probably results from a very small residual activity of the G63S mutant GCMB.

摘要

孤立性甲状旁腺功能减退症是一种罕见的代谢紊乱疾病,其特征为低钙血症和高磷血症,甲状旁腺激素(PTH)水平缺失或降低。它可能表现为一种明显的散发性疾病,也可能作为一种遗传性状在家族中遗传。偶尔有病例报道钙敏感受体基因和前甲状旁腺激素原基因发生突变,在一个家族性病例中报道了甲状旁腺特异性转录因子GCMB基因发生突变。我们报告了第二个患有孤立性甲状旁腺功能减退症且存在GCMB突变的家族。患者是来自无症状的近亲父母的两个兄弟姐妹,提示为常染色体隐性遗传。该突变是指GCMB的DNA结合GCM结构域中第63位的甘氨酸残基被丝氨酸取代(G63S)。在转染细胞中的功能研究表明,该突变导致GCMB功能丧失,因为尽管亚细胞定位正常、蛋白质稳定性正常且DNA结合特异性正常,但它消除了反式激活能力。与之前报道的家族不同,我们的患者血浆中PTH水平较低但明显可检测到。这种残余的激素分泌可能是由G63S突变型GCMB非常小的残余活性导致的。

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