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Rickets and osteomalacia are increasing in prevalence in people because of cultural practices, breast-feeding, decreased sun exposure, and increased sunscreen usage. Several hereditary forms of rickets owing to either renal phosphate wasting or defects in vitamin D metabolism are also reported in people. Rickets is well recognized in domestic animals, but published reports are not always supported by microscopic findings, and diagnoses based on clinical signs and radiology are unreliable. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported in pigs, sheep, cats, and dogs. There is variation between species in susceptibility to dietary vitamin D and phosphorus deficiency and in the ability to manufacture vitamin D in their skin. A number of mouse models have been discovered or created to study human skeletal diseases and skeletal homeostasis. With the discovery that vitamin D is involved in not only calcium and phosphorus homeostasis but also in the immune system and cancer, there is great potential for new and existing animal models to generate valuable information about vitamin D and its many functions. This review presents an overview of vitamin D metabolism and rickets in domestic and laboratory animals and makes comparisons where appropriate with the disease in humans.
This article was published in the following journal.
Name: Veterinary pathology
Abstract Background: Rickets and vitamin D deficiency appeared to increase in Alaskan children starting in the 1990s. We evaluated the epidemiology of rickets and vitamin D deficiency in Alaska native...
Slipped capital femoral epiphysis (SCFE) is a common disorder of the growing hip; however, its etiology remains unknown. Vitamin D (25-OH) is a major regulator of bone homeostasis and calcium metaboli...
Vitamin D deficiency is common in the general population and even more frequent in patients with chronic diseases. The prevention of rickets with native vitamin D supplementation is one of the oldest ...
Although the role of vitamin D in the prevention of rickets has long been well established, controversies still exist on the ideal dose of vitamin D supplementation in infants.
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The purpose of this study is: 1. To compare the response of rickets to calcium with and without vitamin D. 2. To assess whether vitamin D increases calcium absorption in calcium defi...
Some experts recommend that all breastfed babies receive supplemental vitamin D. The purpose of this study is to determine the rate of vitamin D use in breastfed babies, the recommendatio...
We aimed to determine the effect of vitamin D replacement therapy on serum FGF-23 concentrations in vitamin D deficient women and to compare the FGF-23 concentrations of vitamin D deficien...
Vitamin D is a fat soluble vitamin that has important effects on calcium (including absorption of calcium from the diet) and bone metabolism. Vitamin D is known to be stored in fat tissue...
The Williams syndrome is a disease in which supravalvular aortic stenosis, an elfin facies, mental retardation and other congenital defects are sometimes associated with abnormal vitamin D...
A vitamin that includes both CHOLECALCIFEROLS and ERGOCALCIFEROLS, which have the common effect of preventing or curing RICKETS in animals. It can also be viewed as a hormone since it can be formed in SKIN by action of ULTRAVIOLET RAYS upon the precursors, 7-dehydrocholesterol and ERGOSTEROL, and acts on VITAMIN D RECEPTORS to regulate CALCIUM in opposition to PARATHYROID HORMONE.
An X-linked disorder characterized by HYPOPHOSPHATEMIA; RICKETS; OSTEOMALACIA; renal defects in phosphate reabsorption and vitamin D metabolism; and growth retardation. This disorder is caused by mutations in PHEX PHOSPHATE REGULATING NEUTRAL ENDOPEPTIDASE.
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
9,10-Secoergosta-5,7,10(19),22-tetraene-3,25-diol. Biologically active metabolite of vitamin D2 which is more active in curing rickets than its parent. The compound is believed to attach to the same receptor as vitamin D2 and 25-hydroxyvitamin D3.
The major circulating metabolite of VITAMIN D3. It is produced in the LIVER and is the best indicator of the body's vitamin D stores. It is effective in the treatment of RICKETS and OSTEOMALACIA, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties.
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