Comparison of treatments for mild secondary hyperparathyroidism in hemodialysis patients
Comparison of treatments for mild secondary hyperparathyroidism in hemodialysis patients
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DOI：
10.1046/j.1523-1755.2000.00819.x
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发表时间：
2000-01-01
影响因子：
19.6
通讯作者：
Quarles, LD
中科院分区：
文献类型：
--
作者：
Indridason, OS;Quarles, LD
背景 在轻度继发性甲状旁腺功能亢进症患者的治疗中，尚不清楚单独补钙是否足以纠正骨和矿物质代谢异常，或者是否需要生理口服或静脉注射药物剂量的骨化三醇。方法。这是一项为期 40 周的前瞻性非掩蔽试验，纳入了 52 名患者 [甲状旁腺激素 (PTH) 150 至 600 pg/mL]，这些患者被随机分配接受递增剂量的单独碳酸钙 (CaCO3)（钙组，N = 11）、每日口服骨化三醇（口服组，N = 20）或间歇性静脉注射骨化三醇（IV 组，N = 21）。比较各组血清完整 PTH、血清骨特异性碱性磷酸酶 (BAP) 的变化、高钙血症 (>10.5 mg/dL) 和高磷血症 (>6.5 mg/dL) 的发生率。结果。所有组中的 PTH 水平均下降（P < 0.01，配对 t 检验）。在钙剂组中，PTH（平均值+/-SEM）从325+/-46.2下降至160+/-44.5pg/mL。在口服组中，它从 265 +/- 26.4 下降到 125 +/- 23.7 pg/mL，在 IV 组中，它从 240 +/- 27.7 下降到 65 +/- 10.0 pg/mL。通过协方差分析，控制初始 PTH 水平，我们发现各组之间的 PTH 反应没有差异 (P > 0.10)。相比之下，钙剂组的BAP浓度从20.7+/-7.6增加到27.5+/-7.0μg/L（P=0.17），口服组从20.6+/-3.9减少到17.8+/-4.5μg/L（P=0.26），从19.1+/-2.6减少到10.6+/-10.6+/-10.6μg/L。 IV组为1.1μg/L（P = 0.007）。所有组的血清钙均显着增加，钙剂组、口服组和静脉注射组分别从 8.4 +/- 0.25 至 9.0 +/- 0.28、8.5 +/- 0.16 至 9.2 +/- 0.27、8.7 +/- 0.16 至 9.4 +/- 0.18 mg/dL（P = 组间 NS 差异）。在整个研究过程中，钙组的血清磷显着降低（P = 0.02）。钙剂组、口服组和静脉注射组的高钙血症发作次数分别为 2.0 +/-: 0.8、3.0 +/- 0.6 和 3.4 +/- 0.6 (P > 0.10)，高磷血症发作次数分别为 0.9 +/- 0.56、4.2 +/- 0.79 和 4.9 +/- 0.84 (P < 0.01).结论。对于轻度继发性甲状旁腺功能亢进症，这三种策略均有效。单独使用高剂量 CaCO3 可能足以控制 PTH，且具有良好的副作用，但骨化三醇似乎对骨骼具有额外的抑制作用，这种抑制作用在静脉给药途径后更大，并可能增加动力性骨病的风险。
Background In the management of patients with mild secondary hyperparathyroidism, it is not known whether calcium supplementation alone is sufficient to correct abnormalities in bone and mineral metabolism or if calcitriol is needed in either physiologic oral or intravenous pharmacologic doses.Methods. This was a 40-week prospective nonmasked trial of 52 patients [parathyroid hormone (PTH) 150 to 600 pg/mL] who were randomized to receive escalating doses of either calcium carbonate (CaCO3) alone (calcium group, N = 11), daily oral calcitriol (oral group, N = 20),or intermittent intravenous calcitriol (IV group, N = 21). The groups were compared with regard to changes in serum intact PTH, serum bone-specific alkaline phosphatase (BAP), incidence of hypercalcemia (>10.5 mg/dL), and hyperphosphatemia (>6.5 mg/dL).Results. PTH levels decreased in all groups (P < 0.01, paired t-test). In the calcium group, PTH (mean +/- SEM) decreased from 325 +/- 46.2 to 160 +/- 44.5 pg/mL. In the oral group, it decreased from 265 +/- 26.4 to 125 +/- 23.7 pg/mL, and in the IV group, it decreased from 240 +/- 27.7 to 65 +/- 10.0 pg/mL. Upon analysis of covariance, controlling for the initial PTH level, we found no differences in the PTH response between the groups (P > 0.10). In contrast, the BAP concentration increased from 20.7 +/- 7.6 to 27.5 +/- 7.0 mu g/L in the calcium group (P = 0.17), decreased from 20.6 +/- 3.9 to 17.8 +/- 4.5 mu g/L in the oral group (P = 0.26), and from 19.1 +/- 2.6 to 10.6 +/- 1.1 mu g/L in the IV group (P = 0.007). Serum calcium increased significantly in all groups from 8.4 +/- 0.25 to 9.0 +/- 0.28, 8.5 +/- 0.16 to 9.2 +/- 0.27, and 8.7 +/- 0.16 to 9.4 +/- 0.18 mg/dL in the calcium, oral, and IV groups, respectively (P = NS difference between groups). Serum phosphorus was significantly lower in the calcium group throughout the study (P = 0.02). Hypercalcemic episodes were 2.0 +/-: 0.8, 3.0 +/- 0.6, and 3.4 +/- 0.6 per patient-year (P > 0.10), and hyperphosphatemic episodes were 0.9 +/- 0.56, 4.2 +/- 0.79 and 4.9 +/- 0.84 in the calcium, oral, and IV groups, respectively (P < 0.01).Conclusion. In mild secondary hyperparathyroidism, all three strategies are effective. High-dose CaCO3 alone may be sufficient to control PTH with a favorable side-effect profile, but calcitriol appears to have additional suppressive effects on bone that are greater following the intravenous route of administration and may increase the risk of adynamic bone disease.