It has been demonstrated recently that human growth hormone (HGH) increases the tubular reabsorption of phosphate in man (1, 2). This effect is probably responsible for the fall in urinary excretion of phosphate and the rise in plasma level of phosphorus produced by growth hormone (GH) and may also explain the elevation of plasma phosphorus found in acromegaly.The action of GH on tubular transport of phosphate is not necessarily a direct one. Since parathormone decreases maximal tubular reabsorption of phosphate (Tmpo4), GH might affect phosphate reabsorption by inhibiting the secretion of parathormone or by preventing its peripheral action.Indeed the first of these two hypotheses receives some support from metabolic studies: the enhancement of gastrointestinal absorption of calcium, which may occur during treatment with HGH (3), might be expected to inhibit parathyroid secretion.The present study has been undertaken to determine whether the action of GH on tubular transport of phosphate could be explained by a decrease in parathyroid secretion or in parathormone activity. For MethodsFemale dogs fed constant diets were used for these experiments. Renal studies were performed 22 hours after the last feeding. The dogs were unanesthetized. The bladder was catheterized with a rubber catheter that remained in place throughout the experiment. Five hundred ml of water was given by stomach tube to increase urine volume. Blood was drawn from an indwelling arterial needle for control blood phosphorus and creatinine.A priming dose of creatinine and phosphate was administered intravenously (20 ml of a 10% creatinine solution, 20 ml of a solution containing Na2HPO4 12 H20, 10%, and KH2PO4, 0.75%o). A sustaining solution containing creatinine and phosphate was then infused at a rate such that a gradual increase of the plasma phosphorus value in the range of 9 to 14 mg per 100 ml was obtained, and serum creatinine value of about 50 to 70 mg per 100 ml was reached.Thirty minutes after the infusion was begun, urine was collected for consecutive periods varying in length from 10 to 15 minutes. Blood was drawn from the artery at the mid-point of each period. Each collection was ended by washing the bladder twice with distilled water and air.After five collection periods, 300 U of PTH 1 was injected intravenously.The infusion of creatinine and phosphorus was maintained, and eight further collections of urine were performed. Three days after such an experiment, intramuscular injections of bovine GH2 were given once a day (1.5 mg per kg per day) for 8 days; on day 8 of treatment, the renal study was repeated. The

The effect of 25-hydroxyvitamin D (25OHD), given orally during the reversal of hypomagnesaemia, was studied in five patients with hypomagnesaemic hypocalcaemia and low serum levels of 25OHD and 1,25-dihydroxyvitamin D (1,25(OH)2D). The results were compared to those obtained in five other patients with similar initial levels of magnesium, calcium, 25OHD and 1,25(OH)2D who did not receive 25OHD. Serum levels of 1,25(OH)2D in the ten hypomagnesaemic patients were lower than in ten control subjects with low serum levels of 25OHD. The reversal of hypomagnesaemia was similar in the two groups of patients and elicited a similar increase of circulating iPTH levels. The expected increase of circulating 25OHD was observed in patients supplemented with 25OHD; their circulating 1,25(OH)2D rose within 48 h to normal levels, contrasting with the delayed and poor increase of 1,25(OH)2D in patients receiving no 25OHD. The evolution of serum calcium was however identical in the two groups. Our results suggest that vitamin D deficiency was a significant factor leading to low circulating levels of 1,25(OH)2D in hypomagnesaemic hypocalcaemic patients. The biological consequences of low serum 1,25(OH)2D in these patients remain unclear, but clearly, normal levels of 1,25(OH)2D are not essential for the correction of hypomagnesaemic hypocalcaemia.

The effect of parenteral administration of magnesium was studied in five patients with hypomagnesaemic hypocalcaemia. The initial metabolic state was characterized by a normal level of serum immunoreactive parathyroid hormone (iPTH), and by low or undetectable serum 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D (1,25 (OH)2D). A parathyroid response was elicited by the acute intravenous injection of magnesium chloride. In contrast, 1,25(OH)2D did not change up to 24 h after the injection. Intramuscular magnesium sulphate restored serum magnesium and calcium to normal, whereas iPTH was transiently increased. 25OHD remained low and unchanged. 1,25(OH)2D rose very slowly, but the correction of hypocalcemia began before any change in 1,25(OH)2D levels could be demonstrated. Thus, the early correction of hypocalcemia mainly depended on the restoration of an adequate parathyroid function independently of the secretion of 1,25(OH)2D.