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Bisphosphonate Aggravates Secondary Hyperparathyroidism in Hemodialysis Patients

Bisphosphonate可加劇尿毒症患者次發性副甲狀腺功能之亢進

摘要


Background and Purpose: Bisphosphonates have been reported to be effective in the treatment of patients with osteoporosis. Since patients on bisphosphonate may develop hypocalcemia, it is very likely that such therapy may aggravate secondary hyperparathyroidism in dialysis patients with osteopenia. This study investigated the short-term effects of bisphosphonate infusion on plasma calcium, serum parathyroid hormone (PTH) levels, and the calcium set point of the parathyroid gland in hemodialysis patients with secondary hyperparathyroidism. Methods: Fifteen patients with osteopenia on regular hemodialysis and with serum intact-PTH (PTH) levels of more than 200 pg/ml were included in this study. A second-generation bisphosphonate (pamidronate, Aredia(superscript ®) was administered intravenously as a single 15-mg dose in 150 ml of a 5% glucose solution for 1 h during the last hour of hemodialysis. The PTH responses to hypo- and hypercalcemia (induced with 1 and 4 meq/L of dialysate calcium, respectively) were evaluated before and 1 week after bisphosphonate administration. Results: Bisphosphonate infusion resulted in a reduction of predialysis plasma ionized calcium (iCa) of from 1.12±0.03 to 1.08±0.05 mmol/L (p<0.05), and an increase in the baseline PTH of from 362.3±179.4 to 630.1±263.7 pg/ml (p<0.001). The calcium set point for PTH showed an increasing trend after administration of bisphosphonate (1.12±0.03 vs. 1.15±0.04 mmol/L, p<0.05). The slope of the PTH calcium curve was slightly but significantly increased (-1872.6±426.1 vs. -2086.3±571.1, p<0.05) after bisphosphonate administration. Conclusion: Regulation of PTH secretion by calcium is altered after bisphosphonate administration in hemodialysis patients with secondary hyperparathyroidism. The reduction in plasma iCa not only induced a significant increase in PTH secretion but also increased the sensitivity of the parathyroid glands to calcium, which suggests that secondary hyperparathyroidism might worsen after administration of bisphosphonate.

並列摘要


Background and Purpose: Bisphosphonates have been reported to be effective in the treatment of patients with osteoporosis. Since patients on bisphosphonate may develop hypocalcemia, it is very likely that such therapy may aggravate secondary hyperparathyroidism in dialysis patients with osteopenia. This study investigated the short-term effects of bisphosphonate infusion on plasma calcium, serum parathyroid hormone (PTH) levels, and the calcium set point of the parathyroid gland in hemodialysis patients with secondary hyperparathyroidism. Methods: Fifteen patients with osteopenia on regular hemodialysis and with serum intact-PTH (PTH) levels of more than 200 pg/ml were included in this study. A second-generation bisphosphonate (pamidronate, Aredia(superscript ®) was administered intravenously as a single 15-mg dose in 150 ml of a 5% glucose solution for 1 h during the last hour of hemodialysis. The PTH responses to hypo- and hypercalcemia (induced with 1 and 4 meq/L of dialysate calcium, respectively) were evaluated before and 1 week after bisphosphonate administration. Results: Bisphosphonate infusion resulted in a reduction of predialysis plasma ionized calcium (iCa) of from 1.12±0.03 to 1.08±0.05 mmol/L (p<0.05), and an increase in the baseline PTH of from 362.3±179.4 to 630.1±263.7 pg/ml (p<0.001). The calcium set point for PTH showed an increasing trend after administration of bisphosphonate (1.12±0.03 vs. 1.15±0.04 mmol/L, p<0.05). The slope of the PTH calcium curve was slightly but significantly increased (-1872.6±426.1 vs. -2086.3±571.1, p<0.05) after bisphosphonate administration. Conclusion: Regulation of PTH secretion by calcium is altered after bisphosphonate administration in hemodialysis patients with secondary hyperparathyroidism. The reduction in plasma iCa not only induced a significant increase in PTH secretion but also increased the sensitivity of the parathyroid glands to calcium, which suggests that secondary hyperparathyroidism might worsen after administration of bisphosphonate.

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