Fuhrer D, Warner J, Sequeira M, Paschke R, Gregory J, Ludgate M
Department of Medicine, UWCM, Cardiff, Wales, UK.
Thyroid. 2000 Dec;10(12):1035-41. doi: 10.1089/thy.2000.10.1035.
Hereditary nonautoimmune hyperthyroidism is caused by activating germline mutations in the thyrotropin (TSH) receptor (TSHR) gene. We describe an extended Welsh kindred with toxic thyroid hyperplasia affecting 8 family members in three generations and a history consistent with thyrotoxicosis in a further three generations now deceased. A novel heterozygous germline mutation (ATG --> GTG; Met463Val) was identified in the second membrane spanning TSHR region in 6 relatives with thyrotoxicosis and goiter and absence of TSHR antibodies. Screening of 5 additional family members led to the identification of 2 siblings with the mutation, who were asymptomatic at the time, although subsequent thyroid function tests in these children showed suppressed serum TSH and increased serum free triiodothyronine (FT3) and free thyroxine (FT4) concentrations. Functional studies of the novel TSHR germline mutation demonstrated a constitutive activation of the cAMP pathway, which in the thyroid controls both thyroid hormone production and stimulation of thyroid growth. The molecular diagnosis in this family has clinical implications: genetic counseling is required, and primary thyroid ablation should be advocated as the preferred treatment in the patients with the constitutively activating TSHR germline mutation.
遗传性非自身免疫性甲状腺功能亢进症是由促甲状腺激素(TSH)受体(TSHR)基因的种系激活突变引起的。我们描述了一个威尔士大家族,三代中有8名家族成员患有毒性甲状腺增生,另有三代现已去世的家族成员有甲状腺毒症病史。在6名患有甲状腺毒症、甲状腺肿大且无TSHR抗体的亲属中,在TSHR第二个跨膜区域发现了一种新的杂合种系突变(ATG --> GTG;Met463Val)。对另外5名家族成员进行筛查后,发现2名携带该突变的兄弟姐妹,他们当时无症状,不过这些儿童随后的甲状腺功能测试显示血清TSH受到抑制,血清游离三碘甲状腺原氨酸(FT3)和游离甲状腺素(FT4)浓度升高。对新的TSHR种系突变进行的功能研究表明,cAMP途径存在组成性激活,而在甲状腺中,cAMP途径控制甲状腺激素的产生和甲状腺生长的刺激。该家族的分子诊断具有临床意义:需要进行遗传咨询,对于携带组成性激活TSHR种系突变的患者,应提倡将原发性甲状腺消融作为首选治疗方法。