Department of Pharmacology, Poznan University of Medical Sciences, Poznan, Poland.
Chair and Department of Endocrinology, Metabolism and Internal Medicine, Poznan University of Medical Sciences, Poznan, Poland.
J Physiol Pharmacol. 2020 Apr;71(2). doi: 10.26402/jpp.2020.2.03. Epub 2020 Jul 2.
Lithium carbonate, a drug known for more than 100 years, has been successfully used as a psychiatric medication. Currently, it is a commonly used drug to treat patients with unipolar and bipolar depression, and for the prophylaxis of bipolar disorders and acute mania. Lithium salts may cause the development of goiter, hypothyroidism, or rarely hyperthyroidism. The present review examined the current state of knowledge on the effect of lithium carbonate on the thyroid gland. The Pubmed database and Google Scholar were searched for articles related to the effects of lithium therapy on the thyroid gland function published up to February 2020. Studies that examined the mechanism of action of lithium at the molecular level, including pharmacokinetics, and focused on its effects on the thyroid gland were included. Lithium as a mood-stabilizing drug has a complex mechanism of action. Because of the active transport of Na/I ions, lithium, despite its concentration gradient, is accumulated in the thyroid gland at a concentration 3 - 4 times higher than that in the plasma. It can inhibit the formation of colloid in thyrocytes, change the structure of thyroglobulin, weaken the iodination of tyrosines, and disrupt their coupling. In addition, it reduces the clearance of free thyroxine in the serum, thereby indirectly reducing the activity of 5-deiodinase type 1 and 2 and reducing the deiodination of these hormones in the liver. Taken together, this review provides recommendations for monitoring the thyroid gland in patients who require long-term lithium therapy. Prior to the initiation of lithium therapy, thyroid ultrasound should be performed, and the levels of thyroid hormones (fT3 and fT4), TSH, and antithyroid peroxidase and antithyroglobulin antibodies should be measured. If the patient shows normal thyroid function, TSH level measurement and thyroid ultrasound should be performed at 6- to 12-month intervals for long term.
碳酸锂，一种已有 100 多年历史的药物，已成功用作精神科药物。目前，它是一种常用药物，用于治疗单相和双相抑郁症患者，以及预防双相障碍和急性躁狂。锂盐可能导致甲状腺肿、甲状腺功能减退症，或很少导致甲状腺功能亢进症。本综述检查了碳酸锂对甲状腺影响的现有知识状况。在 2020 年 2 月之前，在 Pubmed 数据库和 Google Scholar 上搜索了有关锂治疗对甲状腺功能影响的文章。包括研究锂在分子水平上的作用机制的研究，包括药代动力学，并专注于其对甲状腺的影响。作为一种情绪稳定药物的锂具有复杂的作用机制。由于 Na / I 离子的主动转运，尽管存在浓度梯度，锂仍在甲状腺中积累，浓度比血浆中高 3-4 倍。它可以抑制甲状腺细胞胶体的形成，改变甲状腺球蛋白的结构，削弱酪氨酸的碘化作用，并破坏它们的偶联。此外，它降低了血清中游离甲状腺素的清除率，从而间接降低了 5-脱碘酶 1 型和 2 型的活性，并降低了这些激素在肝脏中的脱碘作用。总之，本综述为需要长期锂治疗的患者提供了监测甲状腺的建议。在开始锂治疗之前，应进行甲状腺超声检查，并测量甲状腺激素（fT3 和 fT4）、TSH 以及抗甲状腺过氧化物酶和抗甲状腺球蛋白抗体的水平。如果患者表现出正常的甲状腺功能，应在 6-12 个月的间隔内进行 TSH 水平测量和甲状腺超声检查。
