Rude R K, Oldham S B, Sharp C F, Singer F R
J Clin Endocrinol Metab. 1978 Oct;47(4):800-6. doi: 10.1210/jcem-47-4-800.
The effect of an acute elevation of the serum magnesium concentration on the concentrations of serum immunoreactive parathyroid hormone (IPTH) were studied in hypocalcemic hypomagnesemic patients, hyperparathyroid patients, and normal individuals. Basal serum IPTH concentrations in the hypomagnesemic patients ranged from undetectable to 3 times the upper limit of normal. All hypomagnesemic patients were observed to have an immediate rise in the serum IPTH concentration after magnesium administration regardless of the basal IPTH concentration. In contrast, normal individuals and patients with primary and secondary hyperparathyroidism responded to magnesium administration with either a decrease or little change in the serum IPTH concentration. These date indicate that an acute stimulation of PTH secretion induced by magnesium is characteristic of the magnesium-deficient state. The consistency of this response suggests that impaired PTH secretion is a significant factor contributing to the hypocalcemia of magnesium deficiency.
在低钙血症性低镁血症患者、甲状旁腺功能亢进患者和正常个体中,研究了血清镁浓度急性升高对血清免疫反应性甲状旁腺激素(IPTH)浓度的影响。低镁血症患者的基础血清IPTH浓度范围从检测不到到正常上限的3倍。观察到所有低镁血症患者在给予镁后血清IPTH浓度立即升高,无论基础IPTH浓度如何。相比之下,正常个体以及原发性和继发性甲状旁腺功能亢进患者在给予镁后血清IPTH浓度降低或变化不大。这些数据表明,镁诱导的甲状旁腺激素分泌急性刺激是镁缺乏状态的特征。这种反应的一致性表明,甲状旁腺激素分泌受损是导致镁缺乏性低钙血症的一个重要因素。