Rickets
Author:
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology, Diabetes and Metabolism
Link
http://link.springer.com/content/pdf/10.1007/s11914-011-0081-0.pdf
Reference61 articles.
1. Kronenberg HM. Developmental regulation of the growth plate. Nature. 2003;423:332–6.
2. Sabbagh Y, Carpenter TO, Demay MB. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Proc Natl Acad Sci USA. 2005;102:9637–42.
3. •• Tiosano D & Hochberg Z Hypophosphatemia: the common denominator of all rickets. J Bone Miner Metab. 2009;27(4):392–401. This paper proposes a new classification for the differential diagnosis of rickets, which is based on the mechanisms leading to hypophosphatemia-high PTH activity, high FGF23 activity, or renal phosphaturia.
4. Casella SJ, Reiner BJ, Chen TC, Holick MF. A possible defect in 25-hydroxylation as a cause of rickets. J Pediatr. 1994;124:929–32.
5. Cheng JB, Levine MA, Bell NH, Mangelsdorf DJ, Russell DW. Genetic evidence that the human CYP2R1 enzyme is a key vitamin D 25-hydroxylase. Proc Natl Acad Sci USA. 2004;101:7711–5.
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1. Refractory rickets: A case of X-linked hypophosphatemic rickets (PHEX gene variation);Journal of Pediatric Endocrinology and Diabetes;2024-05-27
2. Vitamin D and pediatric bone health: Important information and considerations for the pediatric orthopaedic surgeon;Journal of the Pediatric Orthopaedic Society of North America;2024-05
3. Family analysis and literature study of hereditary hypophosphatemic rickets with hypercalciuria;BMC Pediatrics;2024-02-14
4. Rickets Types and Treatment with Vitamin D and Analogues;Nutrients;2024-01-31
5. Mineral Metabolism in Children: Interrelation between Vitamin D and FGF23;International Journal of Molecular Sciences;2023-04-03
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