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BACKGROUND: Vitamin D is a secosteroid hormone with important roles in the control of bone and mineral metabolism of vertebrates and in the maintenance of systemic homeostasis. This study aimed (i) to evaluate the serum concentrations of 25-hydroxy-vitamin D levels [25(OH)D], parathyroid hormone (PTH) and ionized calcium (iCa) of wild Callithrix penicillata (black-tufted marmosets) and (ii) to propose reference ranges for those analytes for free-living marmosets. METHODS: Blood samples were collected from 15 wild animals and analyzed for 25(OH)D, PTH and iCa. Reference values were calculated following standard analytical criteria. RESULTS: The observed mean serum levels (±standard deviation) were 25(OH)D, 61.7 (±20.8) ng/ml; PTH, 275.2 (±34.1) pg/ml; iCai 4.0 (±0.6) mg/dl. CONCLUSIONS: For free-living marmosets, the proposed physiological range for 25(OH)D is 20.1-103.3 ng/ml and for PTH is 207.0-343.3 pg/dl, with a confidence interval of 95%.

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BACKGROUND: Animals in captivity should receive adequate sunlight exposure for sufficient generation of vitamin D [25(OH)D]. In the present study, 25(OH)D serum levels of 84 Callithrix penicillata primates were evaluated. OBJECTIVES: To determine 25(OH)D levels of those animals; to evaluate the influence of gender and period of sunlight exposure on their 25(OH)D levels. METHODS: Three groups were evaluated: group 1 (n = 29) on free sunlight exposure; group 2 (n = 34) on partial sunlight exposure; group 3 (n = 21) without sunlight exposure. RESULTS: The obtained 25(OH)D values were: group 1, 121.2 +/- 33.3 ng/ml; group 2, 115.2 +/- 32.2 ng/ml; group 3, 53.3 +/- 10.4 ng/ml. Significant statistical differences were obtained between groups 1 and 3 (p < 0.001) and groups 2 and 3 (p < 0.001); no statistical difference was found between genders. CONCLUSION: Direct sunlight exposure is essential for 25(OH)D sufficiency and it is proposed that the 25(OH)D normal range for captive Callithrix penicillata would be from 104.8 to 137.1 ng/ml (CI = 95%).

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The hypophosphatemic conditions that interfere in bone mineralization comprise many hereditary or acquired diseases, all of them sharing the same pathophysiologic mechanism: reduction in the phosphate reabsorption by the renal tubuli. This process leads to chronic hyperphosphaturia and hypophosphatemia, associated with inappropriately normal or low levels of calcitriol, causing osteomalacia or rickets in children and osteomalacia in adults. X-linked hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and tumor-induced osteomalacia are the main syndromes involved in the hypophosphatemic rickets. Although these conditions exhibit different etiologies, there is a common link among them: increased activity of a phosphaturic factor, being the fibroblast growth factor 23 (FGF-23) the most studied one and to which is attributed a central role in the pathophysiology of the hyperphosphaturic disturbances. Activating mutations of FGF-23 and inactivating mutations in the PHEX gene (a gene on the X chromosome that codes for a Zn-metaloendopeptidase proteolytic enzyme which regulates the phosphate) involved in the regulation of FGF-23 have been identified and have been implicated in the pathogenesis of these disturbances. Genetic studies tend to show that the phosphorus homeostasis depends on a complex osteo-renal metabolic axis, whose mechanisms of interaction have been poorly understood so far. This paper reviews the current knowledge status concerning the pathophysiology of phosphate metabolism regulation and the pathophysiologic basis of hypophosphatemic rickets. It also analyzes the clinical picture and the therapeutic aspects of these conditions as well.

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RESUMO

The hypophosphatemic conditions that interfere in bone mineralization comprise many hereditary or acquired diseases, all of them sharing the same pathophysiologic mechanism: reduction in the phosphate reabsorption by the renal tubuli. This process leads to chronic hyperphosphaturia and hypophosphatemia, associated with inappropriately normal or low levels of calcitriol, causing osteomalacia or rickets in children and osteomalacia in adults. X-linked hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and tumor-induced osteomalacia are the main syndromes involved in the hypophosphatemic rickets. Although these conditions exhibit different etiologies, there is a common link among them: increased activity of a phosphaturic factor, being the fibroblast growth factor 23 (FGF-23) the most studied one and to which is attributed a central role in the pathophysiology of the hyperphosphaturic disturbances. Activating mutations of FGF-23 and inactivating mutations in the PHEX gene (a gene on the X chromosome that codes for a Zn-metaloendopeptidase proteolytic enzyme which regulates the phosphate) involved in the regulation of FGF-23 have been identified and have been implicated in the pathogenesis of these disturbances. Genetic studies tend to show that the phosphorus homeostasis depends on a complex osteo-renal metabolic axis, whose mechanisms of interaction have been poorly understood so far. This paper reviews the current knowledge status concerning the pathophysiology of phosphate metabolism regulation and the pathophysiologic basis of hypophosphatemic rickets. It also analyzes the clinical picture and the therapeutic aspects of these conditions as well.

Os distúrbios hipofosfatêmicos que comprometem a mineralização óssea englobam várias doenças, hereditárias e adquiridas, as quais compartilham um mesmo mecanismo fisiopatológico: a diminuição da reabsorção de fosfato nos túbulos renais. Este processo promove hiperfosfatúria e hipofosfatemia crônicas, associadas a níveis inapropriadamente normais ou baixos de 1,25 (OH)2D3, com conseqüente desordem do metabolismo ósteo-mineral, resultando em raquitismo e osteomalácia na faixa etária pediátrica e em osteomalácia nos adultos. O raquitismo hipofosfatêmico ligado ao X, o raquitismo hipofosfatêmico autossômico dominante e a osteomalácia induzida por tumor são as principais síndromes que constituem os raquitismos hipofosfatêmicos. Apesar de estas doenças apresentarem etiopatogenias distintas, as evidências bioquímico-moleculares indicam uma base fisiopatológica em comum: maior atividade de um agente fosfatúrico, sendo o fator de crescimento do fibroblasto 23 (FGF-23) o mais estudado e ao qual é atribuído um papel central na fisiopatologia destes distúrbios. Várias mutações ativadoras do gene do FGF-23 e mutações inativadoras do gene localizado no cromossomo X que codifica uma enzima proteolítica Zn-metaloendopeptidase reguladora do fosfato (PHEX), implicada na regulação do FGF-23, já foram identificadas, e sua participação reconhecida na gênese destes distúrbios. Os dados dos estudos genéticos nesta área convergem para a hipótese de que a homeostase do fósforo estaria vinculada a um complexo eixo metabólico ósteo-renal, cujos mecanismos de interação entre seus vários componentes têm sido aos poucos elucidados. Este artigo revisa o atual estado de conhecimento dos mecanismos fisiológicos envolvidos na regulação do metabolismo do fosfato, das bases fisiopatológicas dos raquitismos hipofosfatêmicos e analisa aspectos clínicos e de tratamento disponíveis para estas condições.

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