Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 1996
Lithium therapy and disorders of the parathyroid glands.
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McHenry C R, Lee K
Аннотация
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.
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.