Burman K D, Dimond R C, Earll J M, Wright F D, Wartofsky L
J Clin Endocrinol Metab. 1976 Sep;43(3):606-13. doi: 10.1210/jcem-43-3-606.
Seven patients judged to be euthyroid following treatment of diffuse toxic goiter were studied to determine if they were susceptible to lithium induced hypothyroidism. Lithium carbonate was administered for 4-7 weeks in a dosage (900 mg/day) which maintained serum lithium levels between 0.5-1.0 mEq/l. Blood was obtained weekly for the determination of serum 3,5,3'-triiodothyronine (T3), thyroxine (T4), 3,3',5'-TRIIODO-L-thyronine (reverse T3, rT3) and thyrotropin (TSH). Values observed during lithium therapy were compared to those obtained prior to, and approximately one week after discontinuing lithium. During the pretreatment preiod, mean (+/- SE) serum T3, T4, and rT3 concentrations were 130 +/- 21 ng/100 ml, 7.6 +/- 0.4 mug/100 ml and 48 +/- 8 ng/100 ml, respectively, and decreased during lithium administration with the lowest T3, T4 and reverse T3 concentrations of the lowest T3, T4 and reverse T3 concentrations of 92 +/- 8 ng/100 ml, 4.9 +/- 0.6mug/100 ml, and 33 +/- 6 ng/100, ml, respectively, being reached between the fourth and sixth weeks of study. Thereafter, and in spite of continued treatment with lithium, values for serum concentrations of T3, T4, and rT3 plateaued, or actually increased in 4, 6, and 5 subjects, respectively. Serum TSH concentrations remained 3.0 muU/ml or less throughout the study in 6 patients; 2 of these subjects had no TSH response to thyrotropin-releasing hormone (TRH), even though they had been euthyroid for 3 and 10 months. These data suggest that patients euthyroid following treatment of diffuse toxic goiter display sensitivity to the antithyroid effects of lithium. Furthermore, these observations support the thesis that the inhibitory effects of lithium and iodine upon thyroid hormone synthesis or secretion may involve a similar mechanism of action since increased thyroidal iodine content may be a consequence of therapy with either agent.
对7名弥漫性毒性甲状腺肿治疗后判定为甲状腺功能正常的患者进行了研究,以确定他们是否易患锂诱导的甲状腺功能减退症。给予碳酸锂4 - 7周,剂量为900毫克/天,使血清锂水平维持在0.5 - 1.0毫当量/升之间。每周采血以测定血清3,5,3'-三碘甲状腺原氨酸(T3)、甲状腺素(T4)、3,3',5'-三碘-L-甲状腺原氨酸(反T3,rT3)和促甲状腺激素(TSH)。将锂治疗期间观察到的值与治疗前及停用锂后约一周获得的值进行比较。在治疗前阶段,血清T3、T4和rT3的平均(±标准误)浓度分别为130±21纳克/100毫升、7.6±0.4微克/100毫升和48±8纳克/100毫升,在锂给药期间降低,在研究的第四至六周达到最低T3、T4和反T3浓度,分别为92±8纳克/100毫升、4.9±0.6微克/100毫升和33±6纳克/100毫升。此后,尽管继续用锂治疗,但T3、T4和rT3的血清浓度值分别在4名、6名和5名受试者中趋于平稳或实际上升高。在6名患者中,整个研究期间血清TSH浓度保持在3.0微单位/毫升或更低;其中2名受试者对促甲状腺激素释放激素(TRH)无TSH反应,尽管他们甲状腺功能正常已达3个月和10个月。这些数据表明,弥漫性毒性甲状腺肿治疗后甲状腺功能正常的患者对锂的抗甲状腺作用表现出敏感性。此外,这些观察结果支持这样的论点,即锂和碘对甲状腺激素合成或分泌的抑制作用可能涉及类似的作用机制,因为甲状腺碘含量增加可能是这两种药物治疗的结果。