Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure.
Abnormal regulation of parathyroid hormone release by calcium in secondary hyperparathyroidism due to chronic renal failure.
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慢性肾功能衰竭引起的继发性甲状旁腺功能亢进症中钙对甲状旁腺激素释放的异常调节。
DOI：
10.1210/jcem-54-1-172
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
S. Marynick
中科院分区：
文献类型：
--
作者：
E. Brown;R. Wilson;R. Eastman;J. Pallotta;S. Marynick
本文应用游离甲状旁腺细胞研究了慢性肾功能不全继发性甲状旁腺功能亢进患者钙调节的甲状旁腺激素（PTH）释放。细胞制剂从6例因甲状旁腺骨病和/或高钙血症接受甲状旁腺次全切除术的患者的16个甲状旁腺中获得。环境钙浓度的增加对免疫反应性甲状旁腺素释放在体外的影响进行了评估，并与从7腺瘤和6正常甲状旁腺制备的细胞中观察到的结果进行了比较。3种组织的最大PTH释放无差异（平均值± SEM，8.48 ± 1.9、8.1 ± 3和10.1 ± 0.78 ng/10（5）个细胞）。h分别）。在16个增生腺体中的14个、7个腺瘤中的6个和所有正常腺体中，PTH释放被2-3 mM钙抑制超过50%（可抑制腺体）。在正常腺体中，6例中有5例在低于1.03 mM钙时发生PTH释放（设定点）的最大抑制的一半。另一方面，在14个可抑制增生腺体中的12个和所有6个可抑制腺瘤中，设定点为1.03 mM或更高（分别为P小于0.01和P小于0.002）。因此，在由于慢性肾功能不全引起的严重继发性甲状旁腺增生中，钙的设定点经常增加，而每个细胞的最大分泌速率没有变化。因此，在细胞水平上钙调节的PTH释放异常不仅限于甲状旁腺瘤形成（即腺瘤或原发性增生），也可能发生在继发性增生中。
Dispersed parathyroid cells were employed to study calcium-regulated parathyroid hormone (PTH) release in severe secondary hyperparathyroidism due to chronic renal insufficiency. Cell preparations were obtained from 16 parathyroid glands of 6 patients undergoing subtotal parathyroidectomy for parathyroid bone disease and/or hypercalcemia. The effects of increasing ambient calcium concentration on immunoreactive PTH release in vitro were assessed and compared with results observed in cells prepared from 7 adenomas and 6 normal parathyroid glands. There was no difference in maximal PTH release for the 3 types of tissue (mean +/- SEM, 8.48 +/- 1.9 , 8.1 +/- 3, and 10.1 +/- 0.78 ng/10(5) cells. h respectively). In 14 of 16 hyperplastic glands, 6 of 7 adenomas, and all of the normal glands, PTH release was inhibited more than 50% by 2-3 mM calcium (suppressible glands). Of the normal glands, half of the maximal inhibition of PTH release (the set-point) occurred at less than 1.03 mM calcium in 5 of 6 cases. In 12 of 14 suppressible hyperplastic glands and all of the 6 suppressible adenomas, on the other hand, the set-point was 1.03 mM or higher (p less than 0.01 and P less than 0.002, respectively). Thus, in severe secondary parathyroid hyperplasia due to chronic renal insufficiency, there is frequently an increase in the set-point for calcium without a change in the maximal secretory rate per cell. Abnormal calcium-regulated PTH release at the cellular level, therefore, is not limited to parathyroid neoplasia (i.e. adenoma or primary hyperplasia), but may occur in secondary hyperplasia as well.