Severe hypophosphatemia is associated in man with low intracellular stores of ATP and a set of specific cellular dysfunctions. To investigate whether hypophosphatemia affects myocardial performance, we measured cardiac output by thermodilution and calculated stroke work in seven patients with severe hypophosphatemia before, during and after repletion with an intravenous potassium phosphate solution. Mean left ventricular stroke work for these patients increased from 49.57 to 71.71 g-m per beat (P less than 0.01) at the same or higher afterload whereas pulmonary-artery wedge pressure fell from a mean value of 10.1 to 6.7 torr (P less than 0.02). Return of serum phosphate to normal, therefore, improved myocardial stroke work independently of the Starling effect. The mechanism of this improvement in contractile force is unknown but may be related to intracellular availability of ATP.
A B S T R A C T Urinary cyclic AMP (UcAMP) appropriate for the serum calcium concentration was determined in normal subjects during the base-line state and during alteration in their serum calcium concentrations by saline and calcitum infusions. This was compared to the UcAMP in 76 patients with hypercalcemia and 5 patients with hypocalcemia. In 54 of 56 patients with primary hyperparathyroidism, the UcAMP was inappropriately high for their serum calcium concentration, the 2 exceptions having renal failure. In four patients with vitamin D intoxication, sarcoidosis, milkalkali syndrome, and thiazide-induced hypercalcemia and in five patients with hypocalcemia due to hypoparathyroidism, the UcAMP was appropriately low for their serum calcium concentration. In 16 patients with nonparathyroid neoplasms, 10 had UcAMP levels that were inappropriately high suggesting ectopic parathyroid hormone (PTH)-mediated hypercalcemia and 6 had UcAMP levels that were appropriately low suggesting that their hypercalcemia was due to osteolytic factors other than PTH. Correlations between UcAMP, senrm calcium concentration, and carboxyl-terminal immtunoreactive PTH suggest that random UcAMP is a sensitive accurate reflection of circulating biologically active PTH.If there is adequate renal function (serum creatinine concentration less than 2.0 mg/dl), a random UcAMP expressed as ,umol/g creatinine and analyzed as a function of the serum calcium concentration completely separates patients with PTH and non-PTHmediated hypercalcemia.
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