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1.
Actas Dermosifiliogr ; 107(9): 758-764, 2016 Nov.
Artículo en Inglés, Español | MEDLINE | ID: mdl-27418183

RESUMEN

INTRODUCTION AND OBJECTIVES: Patients with melanoma appear to take extreme sun-protection measures, which could influence 25-hydroxyvitamin D [25(OH)D] levels. The aim of this study was to measure 25(OH)D levels in patients with cutaneous melanoma and identify factors associated with inadequate levels. MATERIAL AND METHODS: Over a period of 1 year, we prospectively measured serum 25(OH)D in patients with cutaneous melanoma and used logistic regression analysis to identify environmental, phenotypic, and genotypic factors that were associated with insufficient and deficient levels. RESULTS: Of 215 patients analyzed, 8.8% had deficient 25(OH)D levels (<10ng/mL) and just 24.7% had normal levels. Insufficient levels (<30ng/mL) were associated with obesity (odds ratio [OR], 4.2; 95% confidence interval [CI], 1.3-13.3) and blood sampling in autumn/winter (OR, 2.1; 95% CI, 1.1-4). Deficient levels (<10ng/mL) were associated with obesity (OR, 7.1; 95% CI, 1.1-46.9), blood sampling in autumn/winter (OR, 9.0; 95% CI, 1.7-47.0), absence of freckles (OR, 5.4; 95% CI, 1.2-23.4), and, with marginal significance, the presence of fewer than 2 nonsynonymous melanocortin-1 receptor (MC1R) polymorphisms (OR, 5.0; 95% CI, 0.9-28.9). LIMITATIONS: Some factors related to 25(OH)D levels, such as food, were not included in the analyses. CONCLUSIONS: 25(OH)D levels should be monitored in patients with melanoma and the need for oral supplements should be contemplated where appropriate.


Asunto(s)
Melanoma/sangre , Neoplasias Cutáneas/sangre , Deficiencia de Vitamina D/sangre , Vitamina D/análogos & derivados , Adulto , Anciano , Anciano de 80 o más Años , Estudios de Casos y Controles , Comorbilidad , Femenino , Humanos , Masculino , Melanoma/epidemiología , Melanosis/epidemiología , Persona de Mediana Edad , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/fisiología , Obesidad/sangre , Obesidad/epidemiología , Polimorfismo de Nucleótido Simple , Receptor de Melanocortina Tipo 1/genética , Receptor de Melanocortina Tipo 1/fisiología , Estudios Retrospectivos , Estaciones del Año , Neoplasias Cutáneas/epidemiología , Pigmentación de la Piel , Luz Solar , Vitamina D/sangre , Vitamina D/fisiología , Vitamina D/uso terapéutico , Deficiencia de Vitamina D/tratamiento farmacológico , Deficiencia de Vitamina D/epidemiología , Melanoma Cutáneo Maligno
2.
Rev. diagn. biol ; 50(1): 28-32, ene. 2001. tab
Artículo en Es | IBECS | ID: ibc-7963

RESUMEN

Fundamento: analizar la hipercalcemia de origen tumoral detectada en un hospital oncológico de 130 camas. En el análisis se han tenido en cuenta los siguientes datos: localización topog´rafica tumoral, perfil bioquímico y supervivencia de los pacientes.Pacientes y métodos: se han recogido los valores de calcio corregido en 10.283 pacientes con el diagnóstico de cáncer. Se consideró hipercalcemia un valor mayor de 11 mg/dl (2,75 mmol/l).Resultados: hemos encontrado una incidencia global de hipercalcemia de 1,3 por ciento. Por localización tumoral, la tasa más elevada se detectó en el cáncer de mama y en los tumores hematológicos. La supervivencia media global es de 312 días.Conclusiones: aún siendo una complicación muy frecuente, no encontramos una incidencia alta (1,3 por ciento). Su hallazgo sugiere un mal pronóstico en la mayoría de las neoplasias consideradas. Los pacientes más jóvenes presentan las tasas más altas de hipercalcemia y los niveles mayores de fosfatasas alcalinas y lactato deshidrogenasa (AU)


Asunto(s)
Femenino , Masculino , Persona de Mediana Edad , Humanos , Hipercalcemia/etiología , Neoplasias de la Mama/complicaciones , Neoplasias Pulmonares/complicaciones , Neoplasias Urológicas/complicaciones , Hipercalcemia/diagnóstico , Calcio , Calcio/sangre , Pronóstico , Fosfatasa Alcalina , Incidencia , Supervivencia sin Enfermedad , Instituciones Oncológicas/estadística & datos numéricos , Fósforo/sangre , L-Lactato Deshidrogenasa , Neoplasias Hematológicas/complicaciones
3.
J Clin Invest ; 61(3): 573-81, 1978 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-641138

RESUMEN

The effects of phosphate depletion on magnesium (Mg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell significantly (P < 0.01) from 10.1+/-0.27 (SE) to 5.0+/-0.54 mg/100 ml within 1 day and continued to fall gradually to a level of 1.2+/-0.21 mg/100 ml by the end of the 8th wk. A significant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46+/-2.7 to 126+/-24 mueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300+/-24 mueq/24 h by the 3rd day and remained high ranging between 150-300 mueq/24 h, thereafter. The magnitude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2+/-0.02 to 0.79+/-0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which became evident by the 3rd wk of phosphate depletion. Mg content of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral content because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 mueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or weight of the animals. Our results indicate that phosphate depletion is associated with (a) magnesuria due to a decrease in the net renal tubular reabsorption of Mg with the main source of the urinary losses being bone Mg; (b) hypomagnesemia secondary to the renal leak of Mg; (c) negative Mg balance; and (d) increase in the intestinal fractional absorption of Mg. The latter was not adequate to compensate for the urinary losses of Mg.


Asunto(s)
Homeostasis , Magnesio/metabolismo , Fosfatos/deficiencia , Animales , Peso Corporal/efectos de los fármacos , Calcio/metabolismo , Dieta , Homeostasis/efectos de los fármacos , Magnesio/sangre , Magnesio/orina , Masculino , Fosfatos/farmacología , Fósforo/sangre , Ratas , Distribución Tisular
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