Lithium-Induced Goiter Medication

Updated: Apr 13, 2020
  • Author: Nicholas J Sarlis, MD, PhD, FACP; Chief Editor: George T Griffing, MD  more...
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Medication Summary

Levothyroxine (LT4) is the drug of choice for patients who develop lithium-induced hypothyroidism or goiter (when discontinuance of lithium therapy is not feasible). Slightly higher doses (enough to keep the thyrotropin level in the range of 0.4 mIU/L) may be necessary if the patient has rapidly growing or large nodules from goiter, especially in the presence of local compressive symptoms. LT4 is the most commonly used pharmacologic preparation of thyroid hormone for treating goiter and other hypothyroid states. The rationale for thyrotropin suppression therapy in persons with goiter is that a reduction in thyrotropin secretion may decrease the growth and function of abnormal thyroid tissue.


Thyroid hormone replacements

Class Summary

A normally functioning thyroid gland produces and secretes the major thyroid hormones (THs) levothyroxine (LT4) and L-triiodothyronine. Complex feedback mechanisms of the hypothalamic-pituitary-thyroid axis regulate the rate of production and secretion. [22, 23] The action of thyrotropin, which is produced in the anterior pituitary gland, stimulates the thyroid gland to secrete THs.

Thyrotropin secretion is mainly controlled by TRH produced in the hypothalamus and by circulating THs that act as feedback inhibitors of thyrotropin and TRH. When concentrations of T4 and T3 are decreased, secretion of thyrotropin and TRH is increased and vice versa. When the thyroid gland fails to function, hypothyroidism develops and therapy with TH is absolutely indicated. Additionally, exogenous administration of TH to euthyroid individuals results in the suppression of endogenous TH secretion.

Levothyroxine (Synthroid, Levoxyl)

In active form, influences growth and maturation of tissues. LT4 is involved in normal growth, metabolism, and development. LT4 preparations contain synthetic crystalline L-3,3',5,5'-tetraiodothyronine sodium salt. Synthetic LT4 is identical to that produced in the human thyroid gland.

The mechanism of action is complex and only partially understood. Following absorption from the GI tract, a large proportion of circulating T4 is converted into T3, and both are transported into cells. T3, the proposed active form (from cell cytoplasm), and T3 and T4 (generated in situ) diffuse into the nucleus and bind to specific thyroid receptor proteins, which appear to be attached primarily to DNA. Receptor binding leads to the activation or repression of DNA transcription, altering the amounts of mRNA and resultant proteins. Changes in the concentration of proteins in various tissues and organs are responsible for metabolic changes.

THs enhance oxygen consumption of most body tissues and increase the basal metabolic rate and metabolism of carbohydrates, lipids, and proteins, thus exerting a profound influence on every organ system.