CALCIUM-REGULATED PARATHYROID-HORMONE RELEASE IN PRIMARY HYPER-PARATHYROIDISM - STUDIES INVITRO WITH DISPERSED PARATHYROID CELLS
CALCIUM-REGULATED PARATHYROID-HORMONE RELEASE IN PRIMARY HYPER-PARATHYROIDISM - STUDIES INVITRO WITH DISPERSED PARATHYROID CELLS
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DOI：
10.1016/0002-9343(79)90446-7
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发表时间：
1979-01-01
影响因子：
5.9
通讯作者：
AURBACH, GD
中科院分区：
文献类型：
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作者：
BROWN, EM;GARDNER, DG;AURBACH, GD
从3个正常人甲状旁腺和30例原发性甲状旁腺功能亢进患者病理组织（腺瘤17例，原发性增生12例，癌1例）制备分散的甲状旁腺细胞。正常腺体细胞释放的免疫反应性甲状旁腺激素（PTH）的设定点（Ca浓度半最大抑制PTH释放）为1.0 mM，与正常牛和犬甲状旁腺细胞相似。来自I型多发性内分泌瘤（MEN I）和未分类家族性甲状旁腺功能亢进症患者的1例甲状旁腺组织细胞和来自散发性增生患者的12例腺体中的8例的设定点为1.0-1.1 mM。相比之下，来自腺瘤的17例细胞制剂中只有2例的设定点< 1.2 mM。12个散发性增生性腺体中的4个和1例多发性内分泌瘤II型（MEN II）患者的1个腺体的设定点为1.2-1.5 mM。其余7个腺瘤的分散细胞释放PTH。1例散发性增生性腺体和转移性甲状旁腺癌患者对3.0 mM Ca的抑制作用相对较差（12-43%）。本实验室对另外20例原发性甲状旁腺功能亢进症患者的研究结果和之前的数据表明，这种疾病对Ca的反应存在异质性。在某些情况下（大多数原发性增生和偶尔的腺瘤），钙调节的甲状旁腺激素释放是相对正常的。在其他情况下（大多数腺瘤和一些散发性原发性增生），最大分泌抑制是正常的，但设定点升高。在其余腺瘤中，在罕见的原发性增生和本系列的单个癌中，观察到相对自主性。讨论了这些不同的分泌模式与原发性甲状旁腺功能亢进的病理生理关系。
Dispersed parathyroid cells were prepared from 3 normal human parathyroid glands as well as from pathologic parathyroid tissue of 30 patients with primary hyperparathyroidism (17 with adenoma, 12 with primary hyperplasia and 1 with carcinoma). Immunoreactive parathyroid hormone (PTH) release from cells of normal glands showed a set point (the Ca concentration half-maximally inhibiting PTH release) of 1.0 mM, similar to that of normal bovine and canine parathyroid cells. Cells from parathyroid tissue of 1 patient each with multiple endocrine neoplasia type I(MEN I) and unclassified familial hyperparathyroidism and from 8 of 12 glands from patients with sporadic hyperplasia had set-points of 1.0-1.1 mM. By contrast, only 2 of 17 cell preparations from adenomas had set-points of < 1.2 mM. Hormone secretion from cells of 8 of 17 adenomas, 4 of 12 sporadic hyperplastic glands and a gland from a single patient with multiple endocrine neoplasia type II (MEN II) had set-points of 1.2-1.5 mM. PTH release from dispersed cells from the remaining 7 adenomas, 1 sporadic hyperplastic gland and metastic parathyroid carcinoma in a single patient showed relatively poor suppressibility (12-43%) by 3.0 mM Ca. The present results and previous data from this laboratory in 20 additional patients with primary hyperparathyroidism suggest heterogeneous responsiveness to Ca in this disorder. In some cases (most primary hyperplasia and occasional adenomas), Ca-regulated PTH release is relatively normal. In others (most adenomas and some sporadic primary hyperplasia), maximal suppressibility of secretion is normal but with an elevated set-point. In the remaining adenomas, in rare primary hyperplasia and in the single carcinoma in this series, relative autonomy was observed. The relationship of these various secretory patterns to the pathophysiology of primary hyperparathyroidism is discussed.