Three Patients with Lithium-Associated Hyperparathyroidism: Literature Review Regarding Medical and Surgical Management

Abstract

Lithium (Li) carbonate has been established as a mood stabilizer and an efficacious treatment for bipolar disorder since its discovery by Dr. John Cade in 1948. Li interacts significantly with organ systems and endocrine pathways. One of the most challenging side effects of Li to manage is its effect on the parathyroid glands. Dysregulation of parathyroid signaling due to Li results in hypercalcemia due to increased vitamin D3 generation, increased calcium absorption from the gut, and bone resorption, occasionally resulting in concomitant hypercalciuria. However, hypercalciuria is not a definitive feature for hyperparathyroidism, and normal calcium excretion might be seen in these patients. Hypercalcemia may also result from volume contraction and decreased renal clearance, which are commonly seen in these patients. Anatomically the parathyroid abnormalities can present as single or multiglandular disease. We report 3 cases where the patients developed multiple side effects of Li therapy as well as hypercalcemia due to hyperparathyroidism. The literature is reviewed with regard to medical and surgical management of Li-associated hyperparathyroidism in the context of these 3 presented cases.

Dose Dependent Effects Of Lithium Carbonate On Rat Thyroid Hormones, Parathormon and Calcium Levels With Thyroid Tissue

“…Livingstone C et al [22] also revealed that PTH levels change through a similar mechanism. [39] Kidney related side effects occur in approximately 20% of patients after long-term treatment with lithium. [40] Hestbech et al [41] in a study conducted in patients with lithium intoxication, they revealed the development of chronic tubulointerstitial nephritis.…”

“…[43] The risk of chronic kidney damage occurring in the later stages of chronic lithium administration may contribute to the formation of hyperparathyroidism. [39] It has been reported that the cause of hypercalcemia that occurs may also be the result of hyperparathyroidism. [44] In this study, where subacute lithium was administration, we observed increased PTH and Ca levels similar to previous studies.…”

Hypercalcemia syndrome: differential diagnostic search and treatment tactics

“…Однако важно понимать, что литий токсически действует на все ОЩЖ, следовательно, риск рецидива после хирургического лечения крайне высок. C другой стороны, в связи с тем, что литий токсически действует на все ОЩЖ, терапия кальцимиметиками оправдана только при кратковременном приеме данных препаратов [16,35]. Bernstein J, et al было высказано предположение, что пациентам с бессимптомной гиперкальциемией или легкой гиперкальциемией целесообразно назначение цинакальцета, а пациентам с тяжелой гиперкальциемией -проведение паратиреоидэктомии [36].…”

Is there a consensus between clinical practice guidelines for conventional and molecular nuclear medicine studies in parathyroid pathology?

“…There are other less frequent indications with an evidence level 4 grade C for: finding of causal lesions in lithiuminduced hyperparathyroidism [20], functional parathyroid cyst [21] and with an evidence level 2b grade B the followup pharmacological management with Cinacalcet [22].…”