SAT-781 - When Lithium Raises More than Mood: Lithium-Induced Hyperparathyroidism

Introduction: The prevalence of hyperparathyroidism (HPT) in patients with bipolar disorder is found to be 8.6%, 86 times higher than the prevalence of primary hyperparathyroidism (PHPT) in the general population (1, 2). The culprit is often lithium therapy, as the absolute risk for hypercalcemia and HPT in patients prescribed lithium is 10%. The risk is time-dependent: there is a threefold higher risk of parathyroid (PT) mass in patients on lithium therapy for 3 years compared to those with less than 6 months of lithium use (1). Lithium is thought to increase the calcium-sensing receptor set point, resulting in multi-gland parathyroid hyperplasia.

Case Presentation: A 59-year-old female with a history of hypothyroidism, bipolar II disorder (on lithium treatment since 1994), and longstanding hypercalcemia presented for endocrine evaluation for HPT. Since 2014, the patient has had a history of hypercalcemia (calcium range 10.4-11.1 mg/dL detected on routine labs) despite remaining asymptomatic. Parathyroid hormone (PTH) was inappropriately elevated within the range of 88-115 pg/mL. She denied nephrolithiasis, malabsorption, granulomatous disease, and relevant family history. The patient’s 24-hour urinary calcium levels were normal on two occasions, and dual-energy X-ray absorptiometry demonstrated osteopenia of both femoral necks. The patient sustained a wrist fracture after a fall as well as a metatarsal fracture. Parathyroid scintigraphy revealed multi-gland hyperplasia, consistent with lithium-associated hyperparathyroidism. Therapy was continued given the long-standing benefit of lithium for mood stabilization. Although parathyroidectomy was recommended, the patient opted for medical management and was initiated on bisphosphonate therapy.

Conclusion: The treatment of lithium-induced hypercalcemia and HPT is uniquely challenging as discontinuation of the offending medication is often not an option due to the potential for destabilizing the patient’s mental health, resulting in manic episodes. Additionally, the discontinuation of lithium after long-term use, even if tolerated from a psychiatric standpoint, may not reverse HPT once hyperplasia of the PT glands occurs (1). Gold standard treatment remains localized or subtotal parathyroidectomy, but medical management in non-surgical candidates remains ill-defined. Similar to management of PHPT, asymptomatic patients may be monitored while continuing lithium therapy, while patients who develop osteoporosis would likely benefit from treatment with cinacalcet or bisphosphonates.
1. Shapiro HI, Davis KA. Hypercalcemia and “primary” hyperparathyroidism during lithium therapy. Am J Psychiatry 2015;172:12-5
2. Zahrani, Ali Al et al. Primary hyperparathyroidism. The Lancet, Volume 349, Issue 9060, 1233 - 1238

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