Dibble J B, Penney M D
Acta Paediatr Scand. 1983 Mar;72(2):207-10. doi: 10.1111/j.1651-2227.1983.tb09698.x.
A fourteen-year-old boy developed severe symptomatic hypercalcaemia following prolonged supine bed rest for major trauma. Treatment consisted initially of intravenous saline and frusemide together with oral phosphate, followed by intramuscular salmon calcitonin. Only after mobilisation and weight bearing was a sustained fall of plasma calcium to normal achieved. Plasma immunoreactive parathormone levels using both N-terminal and mixed terminal specific antisera were always undetectable and urinary cyclic AMP levels were within the normal range throughout. However, before mobilisation, the tubular reabsorption of phosphate was reduced and that of calcium was increased thus indirectly suggesting increased parathormone activity. The hypercalcaemia was due to a combination of increased calcium release from bone and increased tubular reabsorption. We suggest that a factor other than parathormone is responsible for altered tubular handling of calcium and phosphate which develop following prolonged immobilisation in these patients.
一名14岁男孩因严重创伤后长期卧床休息而出现严重症状性高钙血症。治疗最初包括静脉输注生理盐水和呋塞米以及口服磷酸盐，随后肌肉注射鲑鱼降钙素。只有在活动和负重后，血浆钙才持续降至正常水平。使用N端和混合末端特异性抗血清检测的血浆免疫反应性甲状旁腺激素水平始终无法检测到，并且尿环磷酸腺苷水平始终在正常范围内。然而，在活动之前，磷酸盐的肾小管重吸收减少，而钙的肾小管重吸收增加，从而间接提示甲状旁腺激素活性增加。高钙血症是由于骨钙释放增加和肾小管重吸收增加共同作用所致。我们认为，在这些患者长期制动后，甲状旁腺激素以外的一种因素导致了钙和磷酸盐肾小管处理的改变。
