Lambert P W, Heath H, Sizemore G W
J Clin Invest. 1979 Apr;63(4):602-8. doi: 10.1172/JCI109342.
The importance of calcitonin in the homeostatic response to the chronic hypercalcemia of primary hyperparathyroidism is uncertain. To clarify this issue, we have used a new, sensitive radioimmunoassay for human calcitonin to measure basal plasma calcitonin concentrations in 50 patients with primary hyperparathyroidism (32 female, 18 male). We assayed calcium-stimulated calcitonin concentrations preoperatively in 22 of the patients (16 female, 6 male) and postoperatively in 6. Finally, we assayed pentagastrin-stimulated calcitonin concentrations preoperatively in eight of the patients (three female, five male). Plasma calcitonin values after an overnight fast were indistinguishable from those in normal subjects (mean+/-SE, males, 48+/-3 normal and 46+/-5 pg/ml hyperparathyroid, females, 31+/-2 normal and 37+/-3 pg/ml hyperparathyroid.) Among hyperparathyroid patients of both sexes, increases of calcitonin during Ca infusion (15 mg Ca/kg in 4 h) were within normal limits. However, the mean maximal increase of calcitonin was significantly lower in hyperparathyroid than in normal subjects (P < 0.05). In six patients normocalcemic 5-15 mo after parathyroid surgery, fasting plasma calcitonin values were not significantly different, but responses to Ca infusion were greater than preoperatively (Delta calcitonin +/-SE: 13+/-4 preoperatively and 53+/-35 pg/ml postoperatively). The mean maximal increase of calcitonin after pentagastrin (0.5 mug/kg i.v.) was slightly lower than normal in the patients (mean+/-SE, males, 45+/-8 normal and 38+/-10 pg/ml hyperparathyroid, females, 6+/-2 normal and 0 pg/ml hyperparathyroid). Thus, primary hyperparathyroidism is accompanied by normal steady-state concentrations of circulating calcitonin, and normal-to-blunted C-cell responses to pentagastrin or induced hypercalcemia, the response to calcium generally increasing after successful parathyroid surgery. These results clearly show that primary hyperparathyroidism is not characterized by hypercalcitoninemia. The seemingly paradoxical absence of elevated steady-state calcitonin concentrations may be accounted for partly by decreased secretory reserve. However, primary hyperparathyroidism may also be accompanied by an increase in the threshold of sensitivity for calcium stimulation of calcitonin secretion.
降钙素在原发性甲状旁腺功能亢进症慢性高钙血症稳态反应中的重要性尚不确定。为阐明这一问题，我们采用了一种新的、灵敏的人降钙素放射免疫分析法，测定了50例原发性甲状旁腺功能亢进症患者（32例女性，18例男性）的基础血浆降钙素浓度。我们对22例患者（16例女性，6例男性）术前及6例患者术后测定了钙刺激后的降钙素浓度。最后，我们对8例患者（3例女性，5例男性）术前测定了五肽胃泌素刺激后的降钙素浓度。禁食过夜后的血浆降钙素值与正常受试者无差异（均值±标准误，男性，正常组48±3 pg/ml，甲状旁腺功能亢进组46±5 pg/ml；女性，正常组31±2 pg/ml，甲状旁腺功能亢进组37±3 pg/ml）。在男女甲状旁腺功能亢进患者中，静脉输注钙（4小时内输注15 mg Ca/kg）期间降钙素的升高在正常范围内。然而，甲状旁腺功能亢进患者降钙素的平均最大升高显著低于正常受试者（P<0.05）。在甲状旁腺手术后5 - 15个月血钙正常的6例患者中，空腹血浆降钙素值无显著差异，但对钙输注的反应比术前更大（降钙素变化量±标准误：术前13±4 pg/ml，术后53±35 pg/ml）。五肽胃泌素（0.5 μg/kg静脉注射）后降钙素的平均最大升高在患者中略低于正常（均值±标准误，男性，正常组45±8 pg/ml，甲状旁腺功能亢进组38±10 pg/ml；女性，正常组6±2 pg/ml，甲状旁腺功能亢进组0 pg/ml）。因此，原发性甲状旁腺功能亢进症伴有循环降钙素的正常稳态浓度，以及C细胞对五肽胃泌素或诱导性高钙血症的正常至迟钝反应，甲状旁腺手术成功后对钙的反应通常会增加。这些结果清楚地表明，原发性甲状旁腺功能亢进症并非以高降钙素血症为特征。稳态降钙素浓度未升高这一看似矛盾的现象可能部分归因于分泌储备的降低。然而，原发性甲状旁腺功能亢进症也可能伴有降钙素分泌钙刺激敏感性阈值的增加。
