Primary hyperparathyroidism is a rare but potentially life-threatening side effect of long-term lithium therapy. Lithium therapy is used for major depression and for affective bipolar disease. As much as 15% of lithium-treated patients become hypercalcemic.
The primary histopathological diagnosis is adenoma in 45 of patients, double adenomas in 3% and hyperplasia in 52%. At follow-up, the rate of persistent and recurrent HPT was 42% regardless of the histopathological diagnosis. The presence of pathologically active glands may manifest their function at different times during the disease course. Regardless of the actual rate of multiglandular disease, the data strongly suggest a significantly higher rate of multiglandular disease in patients exposed to lithium compared with those with sporadic primary hyperparathyroidism. This is probably because lithium, as it circulates systemically through the body, exerts its expected effect on all 4 parathyroid glands. At this time, on the basis of the available scientific evidence, no conclusive decision can be reached as to the best operative approach to LIH. Three main surgical approaches remain available to the surgeon: (a) unilateral/focused parathyroidectomy guided by preoperative localization and intraoperative PTH monitoring with bilateral exploration in those who do not meet curative criteria, (b) routine bilateral neck exploration with removal of only those visually abnormal glands with or without preoperative localization or intraoperative PTH monitoring, or (c) bilateral neck exploration with subtotal (3.5 gland) parathyroidectomy in all patients.
It is important routinely monitor serum calcium levels in patient who is been treated with lithium. When hyperparathyroidism develops than there are three main options: cessation of lithium and consideration of alternative psychiatric medication(s), monitoring of calcium levels while remaining on lithium, and parathyroid exploration and surgical excision of abnormal parathyroid tissue.
Consideration of surgical intervention is warranted in those patients with hypercalcemia greater than 1 mg/dL above upper limit of the reference range, end-organ damage (osteoporosis, nephrolithiasis), or worsening neurocognitive symptoms.
The results of conventional surgery for lithium-associated HPT are poor. The surgical approach should be adjusted for the multiglandular disease that is usually the cause of HPT in patients on chronic lithium therapy.
Rizwan MM, Perrier ND. Long-term lithium therapy leading to hyperparathyroidism: a case report. Perspect Psychiatr Care. 2009 Jan;45(1):62-5.
Br J Surg. 2010 Nov;97(11):1680-5. Järhult J, Ander S, Asking B, Jansson S, Meehan A, Kristoffersson A, Nordenström J. Long-term results of surgery for lithium-associated hyperparathyroidism.
Lithium use and primary hyperparathyroidism. Broome JT, Solorzano CC. Endocr Pract. 2011 Mar-Apr;17 Suppl 1:31-5