Ramirez J A, Goodman W G, Gornbein J, Menezes C, Moulton L, Segre G V, Salusky I B
Department of Pediatrics, University of California School of Medicine, Los Angeles 90024.
J Clin Endocrinol Metab. 1993 Jun;76(6):1489-94. doi: 10.1210/jcem.76.6.8501155.
The regulation of PTH secretion by calcium is altered in patients with primary hyperparathyroidism. A similar disturbance may occur in secondary hyperparathyroidism, but direct in vivo comparisons of PTH secretion in normal subjects and those with secondary hyperparathyroidism have not been made. Thus, 13 patients with end-stage renal failure and secondary hyperparathyroidism and 20 healthy volunteers underwent dynamic tests of PTH secretion. Changes in ionized calcium were induced by 2-h iv infusions of calcium gluconate or sodium citrate on consecutive days, and the sigmoidal relationship between serum ionized calcium and PTH levels was examined. During sodium citrate infusions, serum ionized calcium levels decreased by 0.21 +/- 0.04 and 0.20 +/- 0.05 mmol/L, respectively (mean +/- SD), in normal volunteers and dialyzed patients (P = NS). Serum PTH levels rose from 27 +/- 7 to 107 +/- 33 pg/mL in controls and from 480 +/- 238 to 859 +/- 412 pg/mL in dialyzed subjects; thus, maximum PTH levels were 396% of preinfusion values in normal subjects, but only 79% greater than baseline values in dialyzed patients (P < 0.001). During the first 30 min of calcium infusions, the increase in serum ionized calcium did not differ between groups, but PTH levels fell more rapidly in normal volunteers; values were 24% of preinfusion levels in controls, but only 56% of the baseline in dialyzed patients (P < 0.01) after 30 min. Minimum PTH levels were attained after 50 min of calcium infusion in normal volunteers and after 70 min in dialyzed patients. The derived values for set-point were 1.21 +/- 0.04 and 1.24 +/- 0.06 mmol/L, respectively, in control and dialyzed subjects (P = NS). These results do not support the contention that the set-point for calcium-regulated PTH secretion is greater than normal in patients with secondary hyperparathyroidism due to end-stage renal disease.
原发性甲状旁腺功能亢进患者体内钙对甲状旁腺激素(PTH)分泌的调节发生了改变。继发性甲状旁腺功能亢进可能出现类似紊乱,但尚未对正常受试者和继发性甲状旁腺功能亢进患者的PTH分泌进行直接的体内比较。因此,对13例终末期肾衰竭合并继发性甲状旁腺功能亢进患者和20名健康志愿者进行了PTH分泌动态试验。连续数天通过静脉输注葡萄糖酸钙或柠檬酸钠2小时诱导游离钙变化,并检测血清游离钙与PTH水平之间的S形关系。在输注柠檬酸钠期间,正常志愿者和透析患者的血清游离钙水平分别下降了0.21±0.04和0.20±0.05 mmol/L(均值±标准差)(P=无显著性差异)。对照组血清PTH水平从27±7 pg/mL升至107±33 pg/mL,透析受试者从480±238 pg/mL升至859±412 pg/mL;因此,正常受试者的最大PTH水平是输注前值的396%,而透析患者仅比基线值高79%(P<0.001)。在输注钙的前30分钟内,两组血清游离钙的升高无差异,但正常志愿者的PTH水平下降更快;30分钟后,对照组的值为输注前水平的24%,而透析患者仅为基线的56%(P<0.01)。正常志愿者在输注钙50分钟后达到最低PTH水平,透析患者在70分钟后达到。对照组和透析受试者的设定点推导值分别为1.21±0.04和1.24±0.06 mmol/L(P=无显著性差异)。这些结果不支持以下观点:终末期肾病所致继发性甲状旁腺功能亢进患者中,钙调节PTH分泌的设定点高于正常。