首页> 外文期刊>Open Journal of Endocrine and Metabolic Diseases >Inhibited 131I Uptake but Normal Release of Thyroid Hormone by Thyroid Gland in Response to TSH Administration in Subclinical Hypothyroidism
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Inhibited 131I Uptake but Normal Release of Thyroid Hormone by Thyroid Gland in Response to TSH Administration in Subclinical Hypothyroidism

机译:在亚临床甲状腺功能减退症中响应TSH给药,甲状腺抑制131I摄取但正常释放甲状腺激素

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Background: Subclinical hypothyroidism is characterized by normal circulating thyroid hormone levels with super-normal TSH concentrations in absence of clinical manifestations. In majority of subjects, an etiologic factor is often identified. Moreover, therapy with levothyroxine normalizes serum TSH concentration while maintaining normal thyroid hormone concentrations. However, the exact pathophysiology of these thyroid hormone alterations is not well defined. Objective: Major steps in synthesis i.e. iodine uptake and the release of thyroid hormones in response to SC TSH administration were assessed in subjects with subclinical hypothyroidism. Methods: 10 men and 5 women with subclinical hypothyroidism, ages 42 - 76 years and 10 euthyroid men (39 - 70 years) participated. 24 hr 131Iodine thyroid uptake and serum T3, T4 and TSH concentrations were determined prior to and after SC administration of recombinant human TSH, 0.9 mg for two consecutive days. Comparisons were conducted for 24 hour uptake values as well as serum T3, T4 and TSH levels obtained prior to and after TSH administration. Results: In subjects with subclinical hypothyroidism 24 hour 131I thyroidal uptakes were normal (10% - 30%). However, the mean value was significantly lower, (p 3 and T4 concentrations in subjects with subclinical hypothyroidism were not significantly different in comparison to normal subjects. Serum TSH concentrations were supernormal and therefore were significantly higher in subjects with subclinical hypothyroidism in comparison to normal subjects and rose markedly in both groups following TSH administration with no significant difference among groups. Serum T4 and T3 rose significantly from PreTSH levels in both groups (p 131I Thyroid uptake is inhibited prior to as well as following SC TSH administration in comparison to normal subjects with maintenance of normal hormone release.
机译:背景:亚临床甲状腺功能减退症的特征是正常的循环甲状腺激素水平,TSH浓度超正常,而无临床表现。在大多数受试者中,通常会识别出病因。此外,用左甲状腺素治疗可使血清TSH浓度正常化,同时维持正常的甲状腺激素浓度。然而,这些甲状腺激素改变的确切病理生理学尚未明确。目的:评估亚临床甲状腺功能减退症患者的合成主要步骤,即摄取碘和响应SC TSH给药释放甲状腺激素。方法:参加了亚临床甲状腺功能减退症的10例男性和5例女性,年龄42-76岁,甲状腺功能正常的10例男性(39-70岁)参加了研究。连续两天SC施用0.9 mg重组人TSH之前和之后,测定24小时131碘甲状腺摄取量和血清T3,T4和TSH浓度。比较了24小时摄取值以及在施用TSH之前和之后获得的血清T3,T4和TSH水平。结果:在亚临床甲状腺功能减退症患者中,24小时131I甲状腺摄取正常(10%-30%)。但是,平均值显着较低(亚临床甲减的受试者的p 3和T4浓度与正常受试者相比无显着差异。亚临床甲减的受试者的血清TSH浓度超常,因此与正常受试者相比显着更高两组的血清T4和T3均较PreTSH水平显着上升(p 131I与正常TSH组相比,SC TSH给药前和给药后甲状腺摄取受到抑制)。维持正常的激素释放。

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