New treatments for rare bone diseases: hypophosphatemic rickets/osteomalacia.

Journal and index pages often block iframe embedding. This reader keeps the evidence details in Orthonotes and leaves the source page one click away.

Abstract

[Indexed for MEDLINE] Conflict of interest statement: Disclosure: Carolina Aguiar Moreira – honorarium for speaking: Amgen; investigator for Ultragenyx. Victoria Zeghbi Cochenski Borba – honorarium for speaking: Amgen. 16. Semin Musculoskelet Radiol. 2002 Sep;6(3):173-82. doi: 10.1055/s-2002-36714. Vitamin D metabolism, rickets, and osteomalacia. Berry JL(1), Davies M, Mee AP. Author information: (1)Vitamin D Research Group, University School of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, United Kingdom. Rickets in the growing child or adolescent and osteomalacia in the adult develop in a variety of clinical situations and have in common an absence or delay in the mineralization of growth cartilage and in newly formed bone collagen. Classically, deficiency of vitamin D, which is essential for the absorption of dietary calcium, has been the major cause. However, rickets is also seen as a result of hereditary defects in critical vitamin D signaling molecules. Disturbances of phosphate metabolism can also lead to signs of rickets and osteomalacia, notably X-linked hypophosphatemic rickets, and oncogenic osteomalacia. Extrarenal synthesis of 1,25-dihydroxyvitamin D, such as that associated with granulomatous disease, can also lead to disturbances in calcium metabolism, with associated skeletal and nonskeletal changes. DOI: 10.1055/s-2002-36714