Vitamin D and RicketsZ. Hochberg Karger, 2003 - 291 páginas A comprehensive update on vitamin D deficiency Centuries ago, during the industrial revolution, rickets, also called 'the English disease', spread rapidly among city-dwelling poor children and became endemic due to vitamin D deficiency and insufficient access to sunlight. Nowadays it appears to be endemic again as the increase of vitamin D deficiency is paralleling the primacy of breast-feeding in Western societies. Breastfeeding, nutritional status and dark skin are the main risk factors for rickets or 'rachitis' as is the correct medical term. Rickets is a childhood disorder and the basis for understanding the disease is rooted in the concept of mineral metabolism and its control mechanisms in the growing fetus, infant and child. As it is now understood that rickets is not only caused by vitamin D deficiency, it has to be kept in mind that vitamin D and calcium deficiency is prevalent in developing countries as well as in affluent societies, where children and their mothers are not exposed to as much sunlight as they need. The rapid growth in molecular biology has been exemplified in the application of subcellular technologies to study vitamin D in human and animal models. In this volume the latest research on vitamin D and rickets is presented from different perspectives such as the interesting historical overview to bone metabolism, molecular genetics of vitamin D and conclusions for disease prevention. It will be of special interest to pediatricians, endocrinologists and health care specialists who work with children at risk for the disease. |
Contenido
Parathyroid Physiology and Pathophysiology | 15 |
Calcium Homeostasis | 24 |
Maternal Fetal and Neonatal Vitamin D and Calcium | 34 |
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1,25-dihydroxyvitamin 25-hydroxyvitamin abnormalities activity alkaline phosphatase amino acid binding biochemical Biol bone disease Bone Miner Res breast milk breast-fed infants calcitriol calcium absorption calcium intake calcium-deficiency rickets cause cDNA cells chondrocyte Clin Endocrinol Metab clinical cloning concentrations decreased defect deficiency rickets developing countries diet disorders doses Drezner MK enzyme exon factors Fanconi's syndrome gene genetic Glorieux FH growth plate Hochberg homeostasis human HVDRR hypercalciuria hyperparathyroidism hypocalcemia hypophosphatemic rickets increased intestinal kidney la-hydroxylase deficiency lactation levels ligand ligand-binding maternal molecular mutations Natl Acad Sci normal nutritional rickets osteoblasts osteoid osteomalacia parathyroid hormone patients Pediatr phenotype PHEX phosphate phosphorus pregnancy Proc Natl Acad protein radiographic regulation renal phosphate risk skeletal skin sunlight exposure syndrome therapy tissue tumor VDR null mice vitamin D deficiency vitamin D metabolism vitamin D receptor vitamin D status vitamin D supplementation vitamin D3