Reports of hypovitaminosis D associated with anticonvulsant drugs in pediatric patients are conflicting. The effects of carbamazepine or sodium valproate on vitamin D status were evaluated prospectively in 51 ambulatory epileptic children who were followed during the first year of the study and in 25 and 6 children during the second and third year, respectively. Serum 25-hydroxyvitamin D, parathyroid hormone, calcium, and phosphorus levels were determined before and every 3 months during anticonvulsant therapy. Our subjects were grouped into four classes (0, 1, 2, and 3 consisted of the patients before and during the first, second, and third years of the treatment, respectively). The control group consisted of 80 healthy children. Comparisons between controls and patients of class 0 for the means for each season of all variables showed no significant differences. A decreasing trend in serum 25-hydroxyvitamin D ( P < .03) and an increasing trend in serum parathyroid hormone ( P < .04) levels were noticed in all seasons from class 0 to class 3. Twenty-five patients (49%) acquired hypovitaminosis D during the study period. The effects of seasonality on serum 25-hydroxyvitamin D, parathyroid hormone, and calcium were noticed in our patients grouped in classes 0, 2 and 3, as well as in controls. Evidence is provided that carbamazepine or sodium valproate can cause hypovitaminosis D in children. ( J Child Neurol 2006; 21:205—209; DOI 10.2310/7010.2006.00050)
Background: Henoch Schonlein purpura (HSP) is a common vasculitis of small vessels whereas endothelin-1 (ET-1) is usually reported elevated in vasculities and systematic inflammation. The aim of the present study was to investigate whether ET-1 levels are correlated with the clinical presentation and the outcome of HSP.
Idiopathic hypercalciuria has a familial or sporadic pattern. In the familial pattern an autosomal dominant inheritance is present. The type of the disease is identical in affected members of the same family. The absorptive subtype is more frequent.
We describe four patients (two pairs of children from two unrelated kindreds) from a Greek island, suffering from hereditary vitamin D-resistant rickets (HVDRR) with alopecia. There were two different homozygous mutations in the vitamin D receptor (VDR) gene of the affected members of the two kindreds that resulted in a truncated or missing receptor. The disorder began in early infancy with similar clinical, biochemical and radiological findings in all four patients, namely, alopecia (which provided the initial diagnostic evidence for HVDRR), rachitic deformities, hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and elevated serum levels of 1,25-dihydroxyvitamin D; however, the patients of kindred B had a more severe clinical expression. Treatment options include oral or intravenous calcium and active vitamin D metabolites. The response varies widely in different cases. Our patients were initially treated with high doses of 1alpha(OH)D3 and oral calcium supplementation. Kindred A patients had a satisfactory response to this regimen, while kindred B patients presented clinical and biochemical improvement when 1alpha(OH)D3 was changed to 1,25(OH)2D3. In the older patients of each kindred, treatment requirements gradually decreased during puberty, and therapy was finally discontinued before adulthood.
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