Published Online : 2025-08-10
Lithium carbonate is considered the gold standard to treat and prevent bipolar disorders, especially in developing countries. The treatment is prolonged, which may be associated with thyroid toxicities of a variable nature. The present minireview is written to explore the current status of knowledge regarding the impact of Lithium treatment on the structure and function of the thyroid gland which will help the clinicians in better management of patients on lithium therapy. PubMed databases and Google Scholar were searched for structural and functional effects of Lithium carbonate therapy on the thyroid gland. The pathophysiology of Lithium carbonate is intricate yet may incorporate increasing intrathyroidal iodine content, repressing the formation and release of thyroid hormones, modifying the hypothalamus-pituitary axis, and Wnt/β-catenin flagging. Goiter is commonly observed in 50% of patients and 25% of patients have hypothyroidism. Patients receiving lithium therapy have less incidence of hyperthyroidism than the general population. Lithium, given over a prolonged period, causes large and mini follicular goiter with hyperplastic epithelium and hyperchromatic nuclei, hyperplasia of stroma with expanded vascularity, sometimes hemorrhages, and finally may lead to thyroiditis, like the picture. Sometimes it may lead to eosinophilic infiltrates into the stroma of the thyroid gland, known as Hurthle cell infiltrate, which is the precursor of thyroid carcinoma. Thus, it is exhorted that those on lithium treatment ought to be periodically assessed for thyroid dysfunction.
Review Article
English
P. 57-62