Takuwa Y, Yamamoto M, Matsumoto T, Hata K, Ogata E
Miner Electrolyte Metab. 1986;12(2):119-24.
The change in phosphate metabolism after surgical correction of Cushing's syndrome was examined in 3 consecutive patients. During replacement therapy with hydrocortisone after successful operation, when serum cortisol levels were undetectable in the early morning, serum inorganic phosphate (PI) levels increased gradually with reduction of the replacement dose of hydrocortisone. Hyperphosphatemia developed 3-7 weeks after surgery when the patients was given 20-25 mg/day of hydrocortisone, and 2 patients demonstrated clinical manifestation of glucocorticoid deficiency. During these periods, there was a significant inverse relationship between serum Pi and the replacement dose of hydrocortisone in each patient. Thereafter, serum Pi started to decrease despite administration of the same amount of hydrocortisone and became normal by 26 weeks after surgery. Daily urinary Pi excretion was decreased compared to that before surgery, and the maximal tubular reabsorptive capacity for Pi (TmP/GFR) changed in parallel with serum Pi in all patients. Serum immunoreactive parathyroid hormone and urinary 3',5'-cyclic adenosine monophosphate excretion remained unchanged during the postoperative course. The serum concentrations of 1,25-dihydroxyvitamin D decreased from preoperatively normal values to subnormal levels after surgery with development of hyperphosphatemia and returned to normal with the fall of serum Pi. In summary, the present study demonstrates that surgical correction of hypercortisolism is accompanied by a transient hyperphosphatemia during the postoperative periods, probably due to increased renal Pi reabsorption, and that parameters of parathyroid function do not change during these periods. These results suggest that glucocorticoid has a direct action on Pi metabolism and that during the replacement therapy after surgical treatment of hypercortisolism hyperphosphatemia may develop due to relative glucocorticoid deficiency.
对连续3例库欣综合征手术矫正后的磷酸盐代谢变化进行了研究。在成功手术后用氢化可的松替代治疗期间，当清晨血清皮质醇水平检测不到时，血清无机磷（PI）水平随着氢化可的松替代剂量的减少而逐渐升高。术后3 - 7周，当患者接受20 - 25毫克/天的氢化可的松治疗时出现高磷血症，2例患者表现出糖皮质激素缺乏的临床表现。在这些时期，每位患者的血清磷与氢化可的松替代剂量之间存在显著的负相关关系。此后，尽管给予相同剂量的氢化可的松，血清磷仍开始下降，并在术后26周恢复正常。与术前相比，每日尿磷排泄减少，所有患者的肾小管对磷的最大重吸收能力（TmP/GFR）与血清磷平行变化。术后过程中血清免疫反应性甲状旁腺激素和尿3',5'-环磷酸腺苷排泄保持不变。随着高磷血症的出现，血清1,25 - 二羟维生素D浓度从术前正常水平降至低于正常水平，并随着血清磷的下降恢复正常。总之，本研究表明，高皮质醇血症的手术矫正术后会伴随短暂的高磷血症，可能是由于肾脏对磷的重吸收增加，并且在此期间甲状旁腺功能参数没有变化。这些结果表明，糖皮质激素对磷代谢有直接作用，并且在高皮质醇血症手术治疗后的替代治疗期间，由于相对糖皮质激素缺乏可能会发生高磷血症。
