Rickets
Mostrando 13-24 de 92 artigos, teses e dissertações.
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13. Investigação molecular do gene do receptor de vitamina D em pacientes com raquitismo e alopecia / Molecular investigation of the vitamin D receptor inpatients with rickets and alopecia
A 1,25-dihidroxivitamina D é de fundamental importância na homeostase do cálcio. A vitamina D exerce suas ações através da interação com o seu receptor. O receptor da vitamina D (VDR) é membro da superfamília de receptores nucleares. O raquitismo é uma doença causada por mineralização deficiente na matriz óssea ou osteóide, afetando o desenvo
Publicado em: 2006
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14. 25-Hydroxycholecalciferol. A COMPARATIVE STUDY IN DEFICIENCY RICKETS AND DIFFERENT TYPES OF RESISTANT RICKETS
The effects of 25-hydroxycholecalciferol were studied in 4 children with deficiency rickets and 22 children with D-resistant rickets, including patients with hereditary hypophosphatemic D-resistant rickets, “pseudo-deficiency” rickets, and rickets secondary to cystinosis or to tyrosinosis. Three protocols were used. (a) 8 days after a single oral dose of
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15. Hypocalcaemic fit in an adolescent boy with undiagnosed rickets
Rickets in early childhood has been well documented in the literature. We present a case report on a teenage Somalian boy who had a generalised tonic clonic fit (an unusual presentation of rickets in late childhood) and was diagnosed with vitamin D deficient rickets.
BMJ Group.
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16. Metabolism of Vitamin D3-3H in Vitamin D-Resistant Rickets and Familial Hypophosphatemia*
The fate of an intravenous dose of tritiated vitamin D3 was studied in seven normal subjects, four children with vitamin D-resistant rickets, and four adults with a familial history of vitamin D-resistant rickets and persistent hypophosphatemia. An abnormal metabolism of vitamin D in vitamin D-resistant rickets was defined and characterized by a decrease in
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17. Vitamin D-responsive rickets in neonatal lambs
An unusual clinical presentation of rickets in nursing lambs is described. Two sets of twin nursing lambs were presented for enlarged joints and mild angular deformity. Rickets was suspected, based on radiographic evidence. Vitamin D deficiency was determined to be the cause, based on serum concentration and response to therapy.
Canadian Veterinary Medical Association.
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18. Neurological involvement in X-linked hypophosphataemic rickets.
X-linked hypophosphataemic rickets is a familial form of Vitamin D resistant rickets in which gross bony and ligamentous changes may occur. Two patients showing severe spinal disease with evidence of spinal cord compression requiring neurosurgical intervention are reported. The management of such lesions may be problematic as cord compression may be found at
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19. Hypophosphatemic Rickets with Hypercalciuria due to Mutation in SLC34A3/Type IIc Sodium-Phosphate Cotransporter: Presentation as Hypercalciuria and Nephrolithiasis
Context: Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a metabolic disorder due to homozygous loss-of-function mutations in the SLC34A3 gene encoding the renal type IIc sodium-phosphate cotransporter (NaPi-IIc). The typical presentation is severe rickets and hypophosphatemia, and hypercalciuria is often discovered later or overlooked.
The Endocrine Society.
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20. The Effect of Vitamin D2 and Vitamin D3 on Intestinal Calcium Absorption in Nigerian Children with Rickets
Context: Children with calcium-deficiency rickets have high 1,25-dihydroxyvitamin D values.
The Endocrine Society.
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21. Meals and Dephytinization Affect Calcium and Zinc Absorption in Nigerian Children with Rickets12
Nutritional rickets resulting from calcium insufficiency is common in Nigeria and high dietary phytate is thought to inhibit calcium and zinc absorption. We compared the effects of a high-phytate meal and enzymatic dephytinization on calcium and zinc absorption in Nigerian children with and without rickets. Nineteen children with rickets and 15 age-matched c
American Society for Nutrition.
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22. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes
Rickets is seen in association with vitamin D deficiency and in several genetic disorders associated with abnormal mineral ion homeostasis. Studies in vitamin D receptor (VDR)-null mice have demonstrated that expansion of the late hypertrophic chondrocyte layer, characteristic of rickets, is secondary to impaired apoptosis of these cells. The observation tha
National Academy of Sciences.
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23. Rickets: An Overview and Future Directions, with Special Reference to Bangladesh: A Summary of the Rickets Convergence Group Meeting, Dhaka, 26–27 January 2006
Rickets has emerged as a public-health problem in Bangladesh during the past two decades, with up to 8% of children clinically affected in some areas. Insufficiency of dietary calcium is thought to be the underlying cause, and treatment with calcium (350–1,000 mg elemental calcium daily) is curative. Despite this apparently simple treatment, little is know
International Centre for Diarrhoeal Disease Research.
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24. Bridging markers defining the map position of X linked hypophosphataemic rickets.
Hypophosphataemic rickets is commonly an X linked dominant hereditary disorder associated with a renal tubular defect in phosphate transport and bone deformities. The gene causing this disorder has been mapped to Xp22.31----p21.3 by using cloned human X chromosome sequences identifying restriction fragment length polymorphisms (RFLPs) in linkage studies of a