轻度或重度继发性甲状旁腺功能亢进患者中钙调节的甲状旁腺激素释放

Goodman W G, Belin T, Gales B, Juppner H, Segre G V, Salusky I B

Department of Radiological Sciences, UCLA School of Medicine, USA.

Kidney Int. 1995 Nov;48(5):1553-8. doi: 10.1038/ki.1995.446.

Differences in the regulation of parathyroid hormone (PTH) release by calcium are thought to account for excess PTH secretion in patients with secondary hyperparathyroidism (2 degrees HPTH). To determine whether calcium-regulated PTH release varies with the severity of 2 degrees HPTH in patients with end-stage renal disease, dynamic tests of parathyroid gland function were done using the four-parameter model in 26 patients with 2 degrees HPTH documented by bone biopsy. Estimates of the set point did not differ among patients categorized as mild (basal serum PTH < 400 pg/ml), moderate (basal PTH 400 to 600 pg/ml) or severe (basal PTH > 600 pg/ml) 2 degrees HPTH; values were 1.23 +/- 0.06 mmol/liter, 1.24 +/- 0.06 mmol/liter and 1.23 +/- 0.05 mmol/liter, respectively, and none of these set point estimates differed from results obtained in normal volunteers, 1.21 +/- 0.02 mmol/liter (NS). The slope of the sigmoidal ionized calcium-PTH curve also did not differ among groups. Set point values did not correspond to basal serum PTH levels, to the maximum serum PTH level observed during hypocalcemia or to the minimum serum PTH level seen during hypercalcemia in patients with 2 degrees HPTH. In contrast, basal serum PTH values were positively correlated with both the maximum serum PTH level observed during hypocalcemia (r = 0.76, P < 0.01), and the minimum serum PTH level attained during calcium infusions (r = 0.78, P < 0.01). Calcium-regulated PTH release does not differ with the degree of 2 degrees HPTH, and set point abnormalities do not account for excess PTH secretion in patients with chronic renal failure as judged by in vivo dynamic tests of parathyroid gland function. The results suggest that variations in parathyroid gland size are the major contributor to excessive PTH secretion in patients with chronic renal failure.

钙对甲状旁腺激素（PTH）释放调节的差异被认为是继发性甲状旁腺功能亢进（2度HPTH）患者PTH分泌过多的原因。为了确定终末期肾病患者中钙调节的PTH释放是否随2度HPTH的严重程度而变化，对26例经骨活检证实为2度HPTH的患者采用四参数模型进行了甲状旁腺功能的动态测试。在分类为轻度（基础血清PTH<400 pg/ml）、中度（基础PTH 400至600 pg/ml）或重度（基础PTH>600 pg/ml）的2度HPTH患者中，设定点估计值没有差异；数值分别为1.23±0.06 mmol/升、1.24±0.06 mmol/升和1.23±0.05 mmol/升，这些设定点估计值均与正常志愿者的结果（1.21±0.02 mmol/升）无差异（无显著性差异）。S形离子钙-PTH曲线的斜率在各组之间也没有差异。在2度HPTH患者中，设定点值与基础血清PTH水平、低钙血症期间观察到的最大血清PTH水平或高钙血症期间看到的最小血清PTH水平均不对应。相比之下，基础血清PTH值与低钙血症期间观察到的最大血清PTH水平（r = 0.76，P<0.01）以及钙输注期间达到的最小血清PTH水平（r = 0.78，P<0.01）均呈正相关。钙调节的PTH释放与2度HPTH的程度无关，根据甲状旁腺功能的体内动态测试判断，设定点异常不能解释慢性肾衰竭患者PTH分泌过多的原因。结果表明，甲状旁腺大小的变化是慢性肾衰竭患者PTH分泌过多的主要原因。