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  • Title: Hyperphosphatemia after surgical correction of hypercortisolism in patients with Cushing's syndrome.
    Author: Takuwa Y, Yamamoto M, Matsumoto T, Hata K, Ogata E.
    Journal: Miner Electrolyte Metab; 1986; 12(2):119-24. PubMed ID: 3960015.
    Abstract:
    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.
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