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Four patients with familial hypophosphataemic rickets developed significant hypercalcaemia which persisted after discontinuation of vitamin D therapy. They had increased PTH levels and were operated for hyperparathyroidism at the ages of 18, 20, 24 and 45 years, respectively. Three of the patients had previously received phosphate treatment and one patient developed hyperparathyroidism 7 years after treatment with calcitriol. Histological evaluation revealed different degrees of parathyroid hyperplasia in all patients, with persistently increased PTH and/or calcium levels after surgery. The possibility of autonomous hyperparathyroidism should be evaluated in the follow-up of patients with X-linked hypophosphataemic rickets.

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Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids were studied in fasted rabbits by infusing epinephrine, norepinephrine, isoproterenol, phentolamine (an adrenergic alpha-receptor blocking drug) and propranolol (an adrenergic beta-receptor blocking drug). The adrenergic effects on the plasma levels of insulin, glucose and free fatty acids were similar to those found in other species. The plasma levels of insulin were increased by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) and decreased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine). The plasma levels of glucose were increased by both alpha- and beta-receptor stimulation, and the epinephrine-induced hyperglycaemia was only blocked by combined infusions with phentolamine and propranolol. The plasma levels of free fatty acids were increased by saline and further increased by beta-receptor stimulation (isoproterenol), while epinephrine and norepinephrine gave variable results. Alpha-receptor stimulation (propranolol + epinephrine) slightly decreased the plasma levels of free fatty acids. The plasma levels of glucagon, however, were mainly increased by alpha-receptor stimulation (epinephrine, norepinephrine, propranolol + epinephrine) and increased only to a minor extent by beta-receptor stimulation (isoproterenol, phentolamine + epinephrine) in rabbits. This is in contrast to results reported for humans, where beta-receptor stimulation seems to be most important in stimulating glucagon release.