24-25-dihydroxyvitamin-d-3 and Syndrome

Evidence has emerged over the last several years indicating that aluminum accumulation in patients with chronic renal failure can cause certain forms of renal osteodystrophy, in particular osteomalacia and an aplastic lesion. The lines of evidence include epidemiological associations, chemical measurement and histological staining of bone aluminum, animal models of aluminum loading, and a favorable response to the removal of aluminum by chelation therapy. The primary sources of aluminum are dialysate solutions prepared from water with a high aluminum content and the oral ingestion of aluminum-containing phosphate binders. Desferrioxamine, a chelating agent with a high affinity for aluminum, can be used to remove aluminum during dialysis by increasing ultrafilterable plasma aluminum; preliminary results show that symptomatic patients markedly improve, both clinically and in their bone histology, after long-term chelation therapy with desferrioxamine. Treating water to ensure that aluminum levels are appropriately reduced in dialysate and the development of non-aluminum-containing phosphate binders are necessary to prevent aluminum-related osteodystrophy.

Topics: 24,25-Dihydroxyvitamin D 3; Aluminum; Animals; Bone and Bones; Calcitriol; Caseins; Chronic Kidney Disease-Mineral and Bone Disorder; Deferoxamine; Diet; Dihydroxycholecalciferols; Dogs; Drug Therapy, Combination; Humans; Osteomalacia; Parathyroid Hormone; Parenteral Nutrition, Total; Protein Hydrolysates; Rats; Renal Dialysis; Syndrome; Water Supply

Metabolites of vitamin D were measured in plasma from 83 patients with idiopathic infantile hypercalcaemia syndrome who were mentally handicapped but had normal calcium values at the time of the study. No significant difference was detected in the mean plasma concentrations of 25-hydroxyvitamin D2, 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D3, or 25,26-dihydroxyvitamin D3 between patients and age matched controls. The mean plasma concentration of 25-hydroxyvitamin D3 was significantly lower in patients than controls but this may be a secondary phenomenon related to less sunlight exposure. In addition, two hypercalcaemic patients with this syndrome were studied during the first year of life, and were found to have normal concentrations of vitamin D metabolites. These findings do not support a role for abnormal vitamin D metabolism in the pathogenesis of this syndrome.

Topics: 24,25-Dihydroxyvitamin D 3; 25-Hydroxyvitamin D 2; Adolescent; Calcitriol; Calcium; Child; Dihydroxycholecalciferols; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Infant; Intellectual Disability; Male; Syndrome; Vitamin D