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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
Worldwide, nutritional rickets continues to be an evolving problem with several causes. This paper provides an updated literature review characterising the prevalence, aetiology, pathophysiology and t...
We describe a case of vitamin-D-deficiency rickets in a young child to highlight its existence in Malaysia where sunlight is abundant throughout the year. The child presented with deformity of both le...
Hereditary vitamin D-resistant rickets (HVDRR) is an autosomal recessive disorder characterized by the early onset of rickets and is caused by mutations in the vitamin D receptor (VDR) gene. Some HVDR...
Ectopic ossification of the spinal ligaments is not uncommon in patients with Vitamin D-resistant rickets (VDRR), but the long-term consequences of this condition have not been reported.
In recent years it has been shown that vitamin D deficiency is associated with an increased incidence as well as the progression of a broad range of diseases including osteoporosis, rickets, cardiovas...
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...
Determine differences in serum vitamin D metabolism by genetic ancestry.
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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