Brown E M, Wilson R E, Eastman R C, Pallotta J, Marynick S P
J Clin Endocrinol Metab. 1982 Jan;54(1):172-9. doi: 10.1210/jcem-54-1-172.
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.
采用分散的甲状旁腺细胞研究慢性肾功能不全所致严重继发性甲状旁腺功能亢进时钙调节的甲状旁腺激素(PTH)释放。细胞制剂取自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患者的16个甲状旁腺。评估了环境钙浓度升高对体外免疫反应性PTH释放的影响,并与从7个腺瘤和6个正常甲状旁腺制备的细胞中观察到的结果进行比较。3种组织的最大PTH释放量无差异(平均值±标准误,分别为8.48±1.9、8.1±3和10.1±0.78 ng/10⁵细胞·小时)。在16个增生性腺中的14个、7个腺瘤中的6个以及所有正常腺体中,2 - 3 mM钙可使PTH释放抑制超过50%(可抑制腺体)。在正常腺体中,6例中有5例在钙浓度低于1.03 mM时发生PTH释放最大抑制的一半(设定点)。另一方面,在14个可抑制增生性腺中的12个以及所有6个可抑制腺瘤中,设定点为1.03 mM或更高(分别为p < 0.01和P < 0.002)。因此,在慢性肾功能不全所致严重继发性甲状旁腺增生中,钙的设定点经常升高,而每个细胞的最大分泌率无变化。因此,细胞水平上异常的钙调节PTH释放不仅限于甲状旁腺肿瘤(即腺瘤或原发性增生),也可能发生在继发性增生中。