Endocrine Abstracts

JOINT2353

Background: Lithium remains one of the most effective treatments for bipolar disorder and has been associated with the development of hyperparathyroidism. Even experienced physicians can be perplexed when caring for such patients since there is a paucity of data regarding the management of lithium-induced hyperparathyroidism.

Case presentation: A 33-year-old female with bipolar disorder who is on long-term Lithium treatment presented to the hospital with a three-day history of tremors, nausea, vomiting, and constipation. She denied any fever, vision changes, hematuria, abdominal or flank pain. Vital signs were normal. Physical examination was only remarkable for fine tremors. Laboratory tests showed a serum Creatinine of 1.7mg/dL (baseline 0.5mg/dL), corrected Calcium 12.6 mg/dL (ref 8.5-10mg/dL), PTH 153 pg/mL (ref 15-65pg/mL), Phosphate 0.8 mmol/l (ref 0.8-1. 45mmol.L), 1,25 dihydroxy Vitamin D 83pg/mL (ref 18-78 pg/mL), 24-hour urinary calcium 410 mg/day (ref 100-300mg/d), Lithium level 3.1mmol/l (ref 0.5-1.2mmol/l), EKG showed a normal QTc. The endocrinology team was consulted, and the patient was started on fluids, calcitonin, cinacalcet, and pamidronate, which lowered her calcium level. Lithium was discontinued, and Valproic acid was started as an alternative. However, she had a relapse of mania during hospitalization. Psychiatry suggested restarting Lithium while continuing medical treatment for hypercalcemia. Parathyroid technetium 99m Sestamibi-CT scan showed findings of parathyroid hyperplasia and the patient deferred surgery. She was later discharged with strict outpatient Endocrinology and Psychiatry follow-up.

Discussion: Lithium alters the set point of calcium-sensing receptors in the parathyroid cells, causing increased PTH release and elevation of the calcium threshold required to suppress PTH. It affects the Wnt/B catenin pathway, causing parathyroid growth. A trial of Lithium dose reduction, discontinuation, or switching to other mood stabilizers can be attempted; however, it is associated with relapse of the mood disorder in patients on chronic lithium. Cinacalcet, which sensitizes calcium-sensing receptors, can be used while on Lithium with close monitoring of calcium levels. Parathyroidectomy can be considered for non-responders and the treatment of choice for patients who develop parathyroid adenoma.

Conclusion: Lithium-induced hyperparathyroidism is a rare complication of long-term lithium therapy. Individualized patient education regarding the risks and benefits of Lithium continuation, medical and surgical options, and the importance of a multidisciplinary follow-up with regular calcium and PTH monitoring at least every 6 months.

Reference: Pattan V, Singh B, Abdelmoneim SS, Gopinath C, Sundaresh V. Lithium-Induced Hyperparathyroidism: An Ill-defined Territory. Psychopharmacol Bull. 2021 Jun 1;51(3):65-71. PMID: 34421145; PMCID: PMC8374931.