Schwarz P, Madsen J C, Rasmussen A Q, Transbøl I, Brown E M
Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, Denmark.
Clin Endocrinol (Oxf). 1998 Jun;48(6):725-32. doi: 10.1046/j.1365-2265.1998.00414.x.
Despite the clear recognition that extracellular ionized calcium controls PTH secretion, there have been suggestions of hysteresis in the relationship between extracellular ionized calcium and PTH during recovery from induced hypo- and hypercalcaemia in vivo in humans. In this study, we examined the possibility that release of intracellular stored PTH during induced hypocalcaemia may explain hysteresis.
Eleven volunteers, five women and six men, were recruited to participate in the study.
A series of three protocols of repeated induction of hypocalcaemia or sequential induction of hypo- and hypercalcaemia.
We observed in a total of 13 trials that a drastic lowering of blood ionized calcium by 0.20 mmol/l within 30 min elicited an immediate large, transient peak release of PTH amounting to 6-16 times the baseline concentration. However, following a steady-state period of hypocalcaemia, a subsequent lowering of blood ionized calcium either following a brief return to normocalcaemia (protocol 1), from the initial hypocalcaemic level of blood ionized calcium (protocol 2) or after a brief period of induced hypercalcaemia (protocol 3) gave either no peak release of PTH or a markedly blunted peak. Thus, the PTH response during the initial induction of and the first recovery from hypocalcaemia in our protocol 3 showed significant hysteresis in the relationship between blood ionized calcium and PTH (P < 0.001), whereas, no hysteretic relationship could be shown during the second recovery from induced hypocalcaemia in four of five cases (NS). Moreover, no hysteretic relationship was observed during induction, recovery and re-induction of hypercalcaemia in protocol 3 (NS).
We believe that the release of what might be preformed, intracellular stored depot PTH can explain, at least in part, the observed hysteretic PTH-calcium relationship in normal humans.
尽管人们清楚地认识到细胞外游离钙控制甲状旁腺激素（PTH）的分泌，但有观点认为，在人体体内诱导性低钙血症和高钙血症恢复过程中，细胞外游离钙与PTH之间的关系存在滞后现象。在本研究中，我们探讨了诱导性低钙血症期间细胞内储存的PTH释放可能解释滞后现象的可能性。
招募了11名志愿者，其中5名女性和6名男性参与本研究。
一系列三个方案，重复诱导低钙血症或依次诱导低钙血症和高钙血症。
在总共13次试验中，我们观察到在30分钟内将血游离钙急剧降低0.20 mmol/L会引发PTH立即大幅、短暂的峰值释放，达到基线浓度的6 - 16倍。然而，在低钙血症的稳定期之后，随后血游离钙的降低，无论是在短暂恢复到正常钙血症之后（方案1）、从血游离钙的初始低钙血症水平开始（方案2）还是在短暂的诱导性高钙血症之后（方案3），要么没有PTH的峰值释放，要么峰值明显减弱。因此，在我们的方案3中，低钙血症初始诱导期间和首次恢复期间，血游离钙与PTH之间的关系显示出显著的滞后现象（P < 0.001），而在五分之四的病例中，第二次从诱导性低钙血症恢复期间未显示出滞后关系（无统计学意义）。此外，在方案3中，高钙血症的诱导、恢复和再次诱导期间均未观察到滞后关系（无统计学意义）。
我们认为，预先形成的、细胞内储存的储备PTH的释放至少可以部分解释在正常人体内观察到的PTH - 钙滞后关系。
