背景及目的：Bisphosphonate 曾被報告能有效治療骨質疏鬆症。當患者使用此一藥物時，亦有引發低血鈣的可能性。然而，在副甲狀腺功能亢進合併骨質貧乏(Osteopenia) 的尿毒症患者，使用Bisphosphonate 是否會因低血鈣的發生，而加重次發性副甲狀腺功能亢進，目前仍未知曉。此一研究即在評估Bisphosphonate 對於合併次發性副甲狀腺功能亢進及骨質貧乏的尿毒症患者之血鈣及副甲狀腺功能之影響。方法：拾伍合併次發性副甲狀腺功能亢進(血清副甲狀腺濃度超過200 pg/ml) 及骨質貧乏(骨質密度T score < -1.0) 之尿毒症患者參與本研究。於血液透析最後壹小時，緩慢靜脈注射Bisphosphonate (Pamidronate 15mg)。給藥前及給藥後壹週，施行副甲狀腺功能動態試驗。本研究分別使用不同鈣離子濃度之血液透析液(分別為1meq/L 及4meq/L) 來進行血液透析，以誘導高血鈣及低血鈣的發生，藉以評估血漿鈣離子變化對副甲狀腺素分泌之動態功能狀況。結果：單一劑量Bisphosphonate 治療壹週後，可造成患者透析前基礎血漿鈣值顯著地從1.12 ± 0.03 下降到1.08 ± 0.05 mmol/L。而此一血鈣下降，不但使血中基礎副甲狀腺素值顯著地從362.3 ± 179.4 上升到630.1 ± 263.7 pg/ml；更可使副甲狀腺素-鈣曲線(PTH-Calcium curve) 之斜率(Slope) 顯著地增加(從-1872.6 ± 426.1 降到-2086.5 ± 571.1)。本研究也發現副甲狀腺素-鈣曲線中之副甲狀腺的鈣臨界點(calciumset point) 達到達統計學上之顯著增加情形。結論：短期使用Bisphosphonate 治療後，可使次發性副甲狀腺功能亢進之尿毒症患者，改變其經由血鈣的變動而調節副甲狀腺分泌之功能。Bisphosphonate 可經由血鈣的下降而加強刺激副甲狀腺素的分泌。同時，又可使副甲狀腺對血鈣的敏感度增加而更加劇次發性副甲狀腺功能亢進之嚴重度。

Background and Purpose: Bisphosphonates have been reported to be effective in thetreatment of patients with osteoporosis. Since patients on bisphosphonate may develophypocalcemia, it is very likely that such therapy may aggravate secondary hyperparathyroidism indialysis patientswith osteopenia. This study investigated the short-termeffects of bisphosphonateinfusion on plasma calcium, serumparathyroid hormone (PTH) levels, and the calcium set point ofthe parathyroid gland in hemodialysis patients with secondary hyperparathyroidism. Methods:Fifteen patientswith osteopenia on regular hemodialysis andwith serum intact-PTH (PTH) levelsof more than 200 pg/ml were included in this study. A second-generation bisphosphonate(pamidronate, Aredia®) 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- andhypercalcemia (induced with 1 and 4 meq/L of dialysate calcium, respectively) were evaluatedbefore and 1 week after bisphosphonate administration. Results: Bisphosphonate infusionresulted in a reduction of predialysis plasma ionized calcium (iCa) of from 1.12 ± 0.03 to 1.08 ± 0.05mmol/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 ofbisphosphonate (1.12 ± 0.03 vs. 1.15 ± 0.04 mmol/L, p < 0.05). The slope of the PTH-calcium curvewas slightly but significantly increased (-1872.6 ± 426.1 vs. – 2086.3 ± 571.1, p < 0.05) afterbisphosphonate administration. Conclusion: Regulation of PTH secretion by calcium is alteredafter bisphosphonate administration in hemodialysis patients with secondaryhyperparathyroidism. The reduction in plasma iCa not only induced a significant increase in PTHsecretion but also increased the sensitivity of the parathyroid glands to calcium, which suggeststhat secondary hyperparathyroidism might worsen after administration of bisphosphonate.