背景與目的：次發性副甲狀腺功能亢奮，骨骼一般會表現出高置換率的情行，且會改變血中骨置換因子之濃度或活性。檢測血中骨置換因子以評估副甲狀腺功能亢奮之血液透析患者其骨生成及骨吸收，為一較不具侵犯性且較便宜的方法。本實驗目的即在釐清長期血液透析患，其次發性副甲狀腺功能亢奮對骨生成因子(造骨細胞專一性之鹼性磷酸) 及骨吸收因子(蝕骨細胞特異性之酸性磷酸) 的影響。方法：我們篩選94 位長期血液透析患者(多數為次發性副甲狀腺功能亢奮患者)， 採血檢驗其血清完整副甲狀腺素(PTH)、造骨細胞專一性之鹼性磷酸及蝕骨細胞特異性之酸性磷酸 (5 乙型抗酒石酸酸性磷酸) 以分析副甲狀腺素對其之影響。我們將患者依血中完整副甲狀腺素的高低，區分為高副甲狀腺素(> 200 pg/ml，69 人)及低副甲狀腺素(< 200 pg/ml，25 人)兩組。結果：高副甲狀腺素組比低副甲狀腺素組有較高的血清完整副甲狀腺素、造骨細胞專一性之鹼性磷酸及蝕骨細胞特異性之5 乙型抗酒石酸酸性磷酸。在高副甲狀腺素這一組患者，我們發現副甲狀腺素與造骨細胞專一性之鹼性磷酸 (r = 0.78, p < 0.001)及與5 乙型抗酒石酸酸性磷酸 (r = 0.77, p < 0.001) 均呈現有意義的相關。且造骨細胞專一性之鹼性磷酸及5 乙型抗酒石酸酸性磷酸彼此又呈現有意義的相關(r = 0.92, p <0.001)。而在低副甲狀腺素這一組患者，我們發現副甲狀腺素與造骨細胞專一性之鹼性磷酸 (r = 0.30, p = 0.152) 及與5 乙型抗酒石酸酸性磷酸 (r = 0.03, p = 0.889) 均呈現無意義的相關。但造骨細胞專一性之鹼性磷酸及蝕骨細胞特異性之5 乙型抗酒石酸酸性磷酸彼此卻又呈現有意義的相關(r = 0.67, p < 0.001)。結論：長期血液透析患者，其次發性副甲狀腺功能亢奮，會增加血清造骨細胞專一性之鹼性磷酸及蝕骨細胞特異性之5乙型抗酒石酸酸性磷酸。而此兩種骨置換因子的增加量與血清副甲狀腺素增加情形呈現有意義的相關。而血清副甲狀腺素較低的患者，此兩種骨置換因子與血清副甲狀腺素呈現無意義的相關。但造骨細胞專一性之鹼性磷酸及5 乙型抗酒石酸酸性磷酸彼此卻又呈現有意義的相關。此一結果反應出，當次發性副甲狀腺功能亢奮時，血清副甲狀腺素決定這兩種骨置換因子的調節。而當血清副甲狀腺素較低時，這兩種骨置換因子的調節可能以局部因素為主。

Background and Purpose: Secondary hyperparathyroidism is characterized by highturnoverbone disease and altered serumbone remodeling markers. The aimof the present studywasto clarify the effect of parathyroid hormone (PTH) on the tartrate-resistant (type 5b) acidphosphatase (TRACP5b) serum bone resorption markers and bone-specific alkaline phosphatase(BAP) and bone formation marker in maintenance hemodialysis patients. Methods: We screenedserum iPTH, BAP, and TRACP5b in a dialysis population of 94 patients. By arbitrarily taking a cutoffpoint of 200 pg/ml for serumiPTH, patients were divided into 2 groups. There were 69 patients in thehigh iPTH (serum iPTH > 200 pg/ml) group and 25 patients in the low iPTH (serum iPTH < 200 pg/ml) group. Results: The high iPTH group showed significantly higher levels of iPTH (753.8 ± 424.6vs. 55.56 ± 38.85 pg/ml, p < 0.001), total calcium(9.24 ± 1.3 vs. 8.87 ± 1.1mg/dl, p < 0.05),TRACP5b (4.75± 3.66 vs.2.49 ± 0.61U/L, p < 0.05), and BAP (81.03 ± 67.56 vs. 58.05 ± 22.55 IU/L, p < 0.05) than the lowiPTH group. Among the high iPTH population, significant correlations were found between serumlevels of iPTH and BAP (r = 0.78, p < 0.001), iPTH and TRACP5b (r = 0.77, p < 0.001), and TRACP5bandBAP(r= 0.92,p<0.001). In the lowiPTHpopulation, therewas no significant correlation betweeniPTH and BAP (r = 0.30, p = 0.152), or between iPTH and TRACP5b (r = 0.03, p = 0.889 ). However,there was a significant correlation between TRACP5b and BAP (r = 0.67, p < 0.001). Conclusion:Both serum BAP and TRACP5b levels were strongly correlated with each other and were elevated inmaintenance hemodialysis patients with hyperparathyroidism. In patients with high iPTH, theincreased BAP and TRACP5b were significantly correlatedwith iPTH. This highlights the importantrole of systemic iPTH in regulating bone remodeling, whereas in patients with lower serum iPTHlevels, bone resorption and formation are probably 'coupled' locally by mechanisms other than PTH.