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The biologic effects of a purified long-acting porcine calcitonin (pTCT) were investigated in 45 children without any known renal, skeletal, endocrine, or metabolic disorder. pTCT was given as a single im injection at dose levels varying from 1 to 150 MRC u/1.73 m2. Administration of the highest dose was followed by a decrease in serum calcium and phosphorus concentrations and in tubular reabsorption of phosphorus, serum calcium and phosphorus concentrations and in tubular reabsorption of phosphorus. Mean maximal variation of serum calcium was -- 13.8 +/- 2.1 mg/l in children less than 3 years old, versus -- 8.2 +/- 0.9 mg/l (p less than 0.01) in older ones. Such an age-related differences was not observed for the hypophosphatemic action of pTCT. In 40 subjects aged 3 to 14 years the threshold for pTCT hypocalcemic activity was between 1 and 5 MRC u/1.73 m2. No significant differences in the effects on serum calcium of either 10, 25, 75 or 150 MRC u/1.73(2) m could be found. The threshold for pTCT hypophosphatemic activity was between 10 and 25 MRC u/1.73 m2 with, similary, no dose-response relationship for doses varying from 25 to 150 MRC u/1.73 m2. The present data demonstrate the high sensitivity of children, especially those younger than 3 years, to pTCT; furthermore, the lack of a dose-response relationship indicates that the pharmacological use of pTCT in pediatrics at doses higher than 10 to 25 MRC u/1.73 m2 is unnecessary.

The iliac crest biopsy of an uremic child, suffering from nephronophtisis, and hemodialyzed since the age of 11 1/2 years, was examined by histomorphometry, electron-probe X-ray microanalysis and ion microscopy. The results have been compared with those obtained with the same techniques in the bone tissue of 11 hemodialyzed aluminum-intoxicated adults. In this child, radiology of the skeleton and plasma biochemistry suggested secondary hyperparathyroidism; by contrast, histology showed impaired mineralization, little bone resorption, and aluminum deposits at the limit between osteoid and calcified tissue similar to those observed in the bone tissue of the adults. This observation, and the fact that the child had a high plasma aluminum level, and that dialysis was performed with softened aluminum-rich water, strongly suggests that the severe osteomalacia of this child was due to aluminum toxicity.

This study of the three main vitamin D metabolites namely 25-(OH) D, 24, 25-(OH) 2D and 1, 25-(OH) 2D includes (1) a summary of the usual assay techniques, (2) a discussion about the concentrations and the role of these metabolites during the neonatal and childhood periods, (3) a report of the results obtained during the past seven years in our laboratory with comments on the interest and limits of these assays for the diagnosis of different types of rickets.

This report concerns a 13 year old girl with the clinical and radiological features of mild idiopathic juvenile osteoporosis. In this patient, no alteration was detected in serum calcium (total + ionized) and phosphorus concentration, serum alkaline phosphatase activity, nor in urinary calcium and phosphorus excretions. Plasma concentrations of cortisol were normal during daytime and sleep. Circulating immunoreactive parathyroid hormone was normal or low. The serum 25-(OH)D and 24,25-(OH)2D concentrations were below the normal range, and the 1,25-(OH)2D concentrations were above the normal range (720 pmol/l) at the beginning of the investigation. All vitamin D metabolites concentrations returned to normal values at the time of radiological recovery and after calcium and 25-(OH)D3 supplementation. A possible relationship between alterations of bone and of circulating vitamin D metabolites is discussed.

Circulating vitamin D metabolite concentrations, i.e. 25-(OH)D, 24,25-(OH)2D, 1,25-(OH)2D have been assayed in 14 hypercalcemic children. Results are as follows: a) Children with vitamin D intoxication (n = 2) had elevated serum 25-(OH)D and 24,25-(OH)2D concentrations but their 1,25-(OH)2D concentrations were similar to those found in normocalcemic children (10-110 pg/ml); b) Children with familial idiopathic hypercalcemia and hypocalciuria (n = 5), children with hypercalcemia and either Bartter's syndrome (n = 1), hemangiomatosis (n = 1), osteopetrosis after medullary graft (n = 1), also had 1,25-(OH)2D concentrations in the normal range; c) In contrast, 1,25-(OH)2D were elevated (160-470 pg/ml) in the four children with severe idiopathic hypercalcemia and elfin facies.

Three siblings, respectively 20, 16 and 12 years old, presented with hypocalcemic vitamin D resistant rickets (Prader's type). Their clinical history included several periods of spontaneous cessation of therapy, with severe relapses. Since 1973, treatment was strictly observed, allowing to test the therapeutic effects of 25 OH D3, 1-25 (OH) 2 D3 and 1-alpha (OH) D3. The clinical effects are reported as well as biochemical data. Among them, an inactive form of hyperparathyroidism is emphasized, which may resemble some cases of pseudohypoparathyroidism. Simultaneous resistance to exogenous PTE was also demonstraded.