Levothyroxine dose requirements for thyrotropin suppression in the treatment of differentiated thyroid cancer.
Levothyroxine dose requirements for thyrotropin suppression in the treatment of differentiated thyroid cancer.
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DOI：
10.1210/jcem.75.2.1639933
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发表时间：
1992-08
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影响因子：
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通讯作者：
L. Burmeister;M. Goumaz;C. Mariash;J. Oppenheimer
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作者：
L. Burmeister;M. Goumaz;C. Mariash;J. Oppenheimer
我们比较了两个临床组中将血清 TSH 抑制至给定水平所需的左旋甲状腺素 (L-T4) 剂量：1) 44 名甲状腺癌患者，其甲状腺已通过手术甲状腺切除术和 131I 治疗被切除；2) 113 名因自发性原发性甲状腺功能减退症（31 名患者）或因 Graves 甲状腺功能亢进症接受 131I 治疗后（82 名患者）而导致甲状腺功能衰竭的患者。甲状腺癌患者中达到甲状腺功能正常范围内的血清 TSH 水平 (0.5-6.2 microU/mL) 所需的 L-T4 剂量 (2.11 微克/公斤·天) 显着高于原发性甲状腺功能减退症患者 (1.63 微克/公斤·天) (P 小于 0.01)。同样，甲状腺癌患者需要更高剂量的 L-T4 才能将血清 TSH 抑制至特定的低于正常水平。这些发现表明，未接受近乎完全甲状腺消融的患者残余甲状腺组织分泌的激素对血清 T4 和 T3 的循环水平有很大贡献。因此，我们推断良性原因导致的甲状腺功能减退症患者的残余甲状腺分泌相对独立于TSH刺激。对良性甲状腺功能减退症患者的进一步细分显示，在 131I 治疗后出现甲状腺功能减退症的 Graves 患者的平均剂量需求低于自发性甲状腺功能减退症患者。这提出了一种可能性，即此类患者持续分泌甲状腺刺激性免疫球蛋白可能是甲状腺功能减退联合组中剂量需求较低的原因。我们的研究还使我们能够对 4 名血清甲状腺球蛋白水平升高的甲状腺癌患者进行连续观察。在这个有限的系列中，L-T4 剂量产生了对血清甲状腺球蛋白的最大抑制，将循环 TSH 降低至 0.4 mU/L。
We have compared the dose of levothyroxine (L-T4) required to suppress serum TSH to given levels in two clinical groups: 1) 44 patients with thyroid cancer whose thyroid glands had been ablated by surgical thyroidectomy and 131I treatment, and 2) 113 patients with thyroidal failure due either to spontaneous primary hypothyroidism (31 patients) or after 131I treatment for Graves' hyperthyroidism (82 patients). The dose of L-T4 needed to attain serum TSH levels in the euthyroid range (0.5-6.2 microU/mL) was significantly greater (P less than 0.01) in patients with thyroid cancer (2.11 micrograms/kg.day) than in the patients with primary hypothyroidism associated with nonmalignant disease (1.63 micrograms/kg.day). Similarly, patients with thyroid cancer required a higher dose of L-T4 to suppress serum TSH to a given subnormal level. These findings suggest that the secretion of hormone from residual thyroid tissue in patients who have not been subjected to near-total thyroid ablation contributes substantially to the circulating levels of serum T4 and T3. We, therefore, infer that residual thyroidal secretion in the patients with hypothyroidism due to benign causes is relatively independent of TSH stimulation. Further subdivision of patients with benign hypothyroidism revealed that patients with Graves' who developed hypothyroidism after 131I treatment showed a lower mean dose requirement than patients with spontaneous hypothyroidism. This raises the possibility that continued secretion of thyroid-stimulating immunoglobulin in such patients might account for the lower dose requirement in the combined group with hypothyroidism. Our studies also have allowed us to make serial observations in 4 patients with thyroid cancer who exhibited elevated levels of serum thyroglobulin. In this limited series, maximal suppression of serum thyroglobulin was produced by doses of L-T4, which reduced circulating TSH to 0.4 mU/L.