The Possible Molecular Effect of Lithium Carbonate on the Thyroid Gland Functions

Abstract

For over a century, lithium carbonate has been an effective mental medicine. It is now a standard treatment for manic-depressive episodes, both bipolar and unipolar, as well as a preventative measure against these conditions. In rare cases, lithium salts can induce hyperthyroidism, hypothyroidism, or goitre. Little is known about how lithium carbonate affects the thyroid gland at the moment. Articles published up until February 2020 that discussed the effects of lithium treatment on thyroid gland function were sought after using the Pubmed and Google Scholar databases. Studies that concentrated on lithium effects on the thyroid gland and investigated its molecular mechanism of action, including pharmacokinetics, were included. The intricate mechanism of action of lithium as a mood stabiliser is quite remarkable. Despite a concentration gradient, the thyroid gland accumulates three to four times as much lithium as the plasma does due to the active transit of Na+/I-ions. It has the potential to alter thyroglobulin structure, weaken tyrosine iodination, and disrupt their coupling, as well as limit colloid formation in thyrocytes. Moreover, it decreases the elimination of free thyroxine from the blood, which in turn decreases the activity of 5-deiodinase type 1 and 2 and the deiodination of these hormones in the liver. This review suggests ways to follow up patients' thyroid glands when they're receving lithium for an extended period of time. It is recommended to do a thyroid ultrasound and evaluate the levels of thyroid hormones (fT3 and fT4), TSH, antithyroid peroxidase, and antithyroglobulin antibodies before starting lithium therapy. It is recommended to measure the TSH level and conduct thyroid ultrasounds every 6 to 12 months for patients with normal thyroid function. These tests should be continued over the long term