C R McHenry1, K Lee. 1. Department of Surgery, Case Western Reserve University School of Medicine, and MetroHealth Medical Center, Cleveland, Ohio 44109-1998, USA.
Abstract
OBJECTIVE: To review the effects of lithium (Li+) on the parathyroid glands. METHODS: We describe the incidence and clinical features of Li(+)-associated hyperparathyroidism and summarize the current state of knowledge of the in vitro and in vivo effects of Li+ on the parathyroid cell. RESULTS: Li+ treatment is known to increase the calcium set-point in the parathyroid glands for inhibition of parathyroid hormone secretion. Evidence suggests that this change in calcium set-point occurs as a result of Li+ interference with transmembrane signal transduction in the parathyroid cell. Li+ therapy may accentuate the set-point error in patients with primary hyperparathyroidism and unmask preexisting hyperplastic or adenomatous changes in the parathyroid glands. Li+ may also cause de novo hypercalcemia and hyperparathyroidism that are usually mild, clinically insignificant, and reversible with discontinuation of Li+ therapy. In some patients receiving long-term Li+ therapy, however, persistent hyperparathyroidism develops despite discontinuation of Li+ therapy, and it may be symptomatic and associated with serious organ system sequelae. Li(+)-associated hypercalcemia can be a challenging clinical dilemma in patients with bipolar affective disorder because of the lack of effective therapeutic alternatives, as well as the potential for Li(+)-induced hypercalcemia to exacerbate psychopathologic symptoms. CONCLUSION: Because severe hypercalcemia may occur as a result of toxic Li+ levels, Li+ and calcium levels should be monitored in patients on long-term Li+ therapy.
OBJECTIVE: To review the effects of lithium (Li+) on the parathyroid glands. METHODS: We describe the incidence and clinical features of Li(+)-associated hyperparathyroidism and summarize the current state of knowledge of the in vitro and in vivo effects of Li+ on the parathyroid cell. RESULTS: Li+ treatment is known to increase the calcium set-point in the parathyroid glands for inhibition of parathyroid hormone secretion. Evidence suggests that this change in calcium set-point occurs as a result of Li+ interference with transmembrane signal transduction in the parathyroid cell. Li+ therapy may accentuate the set-point error in patients with primary hyperparathyroidism and unmask preexisting hyperplastic or adenomatous changes in the parathyroid glands. Li+ may also cause de novo hypercalcemia and hyperparathyroidism that are usually mild, clinically insignificant, and reversible with discontinuation of Li+ therapy. In some patients receiving long-term Li+ therapy, however, persistent hyperparathyroidism develops despite discontinuation of Li+ therapy, and it may be symptomatic and associated with serious organ system sequelae. Li(+)-associated hypercalcemia can be a challenging clinical dilemma in patients with bipolar affective disorder because of the lack of effective therapeutic alternatives, as well as the potential for Li(+)-induced hypercalcemia to exacerbate psychopathologic symptoms. CONCLUSION: Because severe hypercalcemia may occur as a result of toxic Li+ levels, Li+ and calcium levels should be monitored in patients on long-term Li+ therapy.
Authors: C Marcocci; M L Brandi; A Scillitani; S Corbetta; A Faggiano; L Gianotti; S Migliaccio; S Minisola Journal: J Endocrinol Invest Date: 2015-03-28 Impact factor: 4.256