Pituitary secretion of free alpha and beta subunit of human thyrotropin in patients with thyroid disorders.
Pituitary secretion of free alpha and beta subunit of human thyrotropin in patients with thyroid disorders.
复制标题
甲状腺疾病患者垂体分泌人促甲状腺素的游离α和β亚基。
DOI：
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发表时间：
1975
影响因子：
5.8
通讯作者：
Farahe Maloof
中科院分区：
文献类型：
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作者：
I. Kourides;B. Weintraub;E. Ridgway;Farahe Maloof
利用敏感和特异的放射免疫测定法，在正常个体、原发性甲状腺功能减退症患者和其他甲状腺功能障碍患者静脉注射促甲状腺素释放激素（TRH）之前和之后测量了人促甲状腺素（hTSH）、糖蛋白激素免疫学上常见的α亚基和hTSH的特定β亚基（hTSH-β）的血清浓度。在 29 名正常个体中，TRH 前后血清中未检测到 hTSH-β（小于 0.5 ng/ml）；男性和绝经前女性的α小于0.5-2.0 ng/ml，绝经后女性的α小于1.0-5.0 ng/ml，且TRH后不增加。在 20 名原发性甲状腺功能减退症患者中，平均血清 hTSH-β 为 1.3 ng/ml，TRH 后增加至峰值 3.7 ng/ml； TRH 后平均 α 值为 4.3 ng/ml，增加至 6.3 ng/ml。患有格雷夫斯病、甲状腺结节功能亢进或促甲状腺功能减退症的患者在 TRH 前后均未检测到血清 hTSH-β 浓度或 α 浓度高于正常值。在 3 名原发性甲状腺功能减退症患者静脉推注标记 hTSH 后，至少 3 小时内未检测到 hTSH 解离为亚基，这表明 TRH 后血清 α 和 hTSH-β 的增加代表垂体分泌游离亚基。此外，对 2 名甲状腺功能减退患者施用 L-甲状腺素 (L-T4) 降低了 TRH 前后的 α 和 hTSH-β 血清浓度。每天 100-300 杯 L-T4 可以完全抑制血清 hTSH-β，但存在残留的血清 α 成分，不能用甲状腺激素抑制，可能代表促性腺激素分泌垂体细胞产生的 α 亚单位。除了 hTSH 之外，正常垂体还含有相对于 hTSH-β 而言占优势的游离 α 亚基。甲状腺功能减退症中游离亚基的分泌可能仅与正常状态存在数量差异，并且 hTSH 亚基似乎对与完整 hTSH 相同的控制机制做出反应。
Utilizing sensitive and specific radioimmunoassays, serum concentrations of human thyrotropin (hTSH), the immunologically common alpha subunit of the glycoprotein hormones, and the specific beta subunit of hTSH ( hTSH-beta) have been measured in normal individuals, in patients with primary hypothyroidism, and in patients with other disorders of thyroid function before and after intravenous administration of thyrotropin releasing hormone (TRH). In 29 normal individuals hTSH-beta was not detectable in serum (smaller than 0.5 ng/ml) before or after TRH; alpha was smaller than 0.5-2.0 ng/ml in men and premenopausal women and 1.0-5.0 ng/ml in postmenopausal women and did not increase after TRH. In 20 patients with primary hypothyroidism mean serum hTSH-beta was 1.3 ng/ml and increased to a peak value of 3.7 ng/ml after TRH; mean alpha was 4.3 ng/ml and increased to 6.3 ng/ml after TRH. None of the patients with Graves' disease, a hyperfunctioning thyroid nodule, or hypothyrotropic hypothyroidism had detectable serum hTSH-beta concentrations or alpha concentrations higher than the normals before or after TRH. In 3 patients with primary hypothyroidism given an intravenous bolus of labeled hTSH, no dissociation of hTSH into subunits was detectable for at least 3 h, indicating that the increment in serum alpha and hTSH-beta after TRH represented secretion of free subunits from the pituitary. In addition, L-thyroxine (L-T4) administered to 2 hypothyroid patients decreased the serum concentrations of alpha and hTSH-beta before and after TRH. Serum hTSH-beta was fully suppressed with 100-300 mug L-T4 daily, but there was a residual serum alpha component, which could not be suppressed with thyroid hormone and probably represented alpha subunits arising from gonadotropin-secreting pituitary cells. Normal pituitary glands also contained a predominance of free alpha subunit relative to hTSH-beta, in addition to hTSH. The secretion of free subunits in hypothyroidism may represent only a quantitative difference from the normal state, and subunits of hTSH appear to respond to the same control mechanisms as complete hTSH.