PERSISTENT HYPERCALCIURIA AND ELEVATED 25-HYDROXYVITAMIN D-3 IN CHILDREN WITH INFANTILE HYPERCALCEMIA

Citation
E. Pronicka et al., PERSISTENT HYPERCALCIURIA AND ELEVATED 25-HYDROXYVITAMIN D-3 IN CHILDREN WITH INFANTILE HYPERCALCEMIA, Pediatric nephrology, 11(1), 1997, pp. 2-6
Citations number
14
Categorie Soggetti
Pediatrics,"Urology & Nephrology
Journal title
Pediatric nephrology
ISSN journal
0931041X → ACNP
Volume
11
Issue
1
Year of publication
1997
Pages
2 - 6
Database
ISI
SICI code
0931-041X(1997)11:1<2:PHAE2D>2.0.ZU;2-H
Abstract
The aim of the study was to characterize abnormalities of calcium-phos phate and vitamin D-3 metabolism in children with a past history of '' mild'' Lightwood-type idiopathic infantile hypercalcaemia. Seventeen s eemingly healthy children aged 2-12 years, with long-term idiopathic h ypercalcaemic syndrome since infancy were studied. Two reference group s were also included (vitamin D-3 intoxication/healthy and Williams gr oups). Despite a long-term milk-restricted diet and a restricted vitam in D-3 intake, urinary calcium excretion in the study group was 0.117 +/- 0.07 mmol/kg per 24 h. Compared with the reference groups (0.047 /- 0.029 and 0.067 +/- 0.06 mmol/kg per 24 h, P<0.05), there was signi ficant hypercalciuria in the children with idiopathic hypercalcaemia s ince infancy. Serum concentrations of 25-hydroxyvitamin D-3 in the stu dy group were also elevated compared with the reference groups (57.4 /- 15.5 vs. 34.6 +/- 9.3 and 22.7 +/- 10.5 ng/ml). 1,25-Dihydroxyvitam in D-3 levels were at the upper limit of normal (45.9 +/- 13.1 vs. 35. 0 +/- 8.1 and 30.0 +/- 13.7 pg/ml). Non-progressive, clinically silent nephrocalcinosis was visible on ultrasound examinations. The disturba nces of vitamin Dg and calcium-phosphate metabolism persistent in the normocalcaemic phase of idiopathic infantile hypercalcaemia may be a p rimary metabolic defect of the condition. The mechanisms leading to el evation of metabolites of 1,25-dihydroxy- and 25-hydroxyvitamin D-3 an d the relationship between this and persistent hypercalciuria and neph rocalcinosis need pathophysiological explanation.