The limited usefulness of radioimmunoassays of parathyroid hormone in the differential diagnosis of hypercalcaemia invites the use of methods measuring effects of parathyroid hormone (PTH). Data from 4\p=n-\5-day metabolic studies in 107 hypercalcaemic patients (78 retrospective and 29 prospective cases) were combined in a hypercalcaemia discrimination index (HDI). HDI = (urine calcium (mg/24 h) x 100 x serum phosphate (mg/100 ml))/(serum total calcium (mg/100 ml) x 24-h clearance of creatinine (ml/min)) expresses in one figure the combined actions of PTH on the renal handling of calcium and on serum phosphate. A multivariate analysis confirmed that HDI offered optimal discrimination. An identical discrimination was observed in the prospective series. In the complete series HDI = 137 was the optimal discrimination point. Classification of the patients as having hyperparathyroidism (HPT) or pseudohyperparathyroidism (P-HPT) (< 137) or non-parathyroid hypercalcaemia (NON\x=req-\ PTH) ( #$x2267; 137) corresponded in 100 out of 107 patients (93.5%) with the final clinical diagnosis. The effects on HDI of sex, age, season, urine losses, high calcium intake and use of thiazides were also evaluated. HDI appears to be a valuable tool in the endocrine evaluation of hypercalcaemic patients. Used in combination with radioimmunoassays measuring genuine but not ectopic PTH HDI may serve to classify hypercalcaemic patients within the following 3 subgroups: HPT, P-HPT and NON-PTH.

Subcutaneous injection of 300 μmol magnesium raised the serum magnesium to 4.00 mmol/l after 30 min in 150 g male rats and reduced the serum calcium concentration by 0.17 mmol/l after 60 min. Magnesium also acutely diminished the serum concentration of 45Ca given three weeks previously. The administration of magnesium did not reduce the serum concentration of 45Ca and did not increase the rate of disappearance of 45Ca from the serum, when subcutaneous or intravenous labelling took place 180–210 min before the magnesium injection. The magnesium-induced hypocalcaemia therefore cannot be explained by an increased removal of calcium from the circulation. The results are compatible with the hypothesis that the magnesium-induced hypocalcaemia is caused by the release of calcitonin. Injections of 300 μmol magnesium chloride at 12 h intervals for 72 h trebled the 24 h renal excretion of both 40Ca and 45Ca given three weeks previously. The 24 h renal excretion of hydroxyproline was unaltered. Thus there was no indication that the intermittent magnesium injections produced any long-term inhibition of the turnover of bone matrix and bone mineral.