RESUMEN
The objective was to evaluate the effect of dietary 25-hydroxycholecalciferol (25(OH)D3) or vitamin D3 (VitD3) and different total calcium (Ca) levels on the performance, carcass characteristics, blood, enzymatic, and bone biochemistry of broilers reared under heat stress between 1 and 42 days of age. A total of 504 male, Cobb 500, broiler chickens were distributed in a completely randomized design in a 2 × 4 factorial arrangement (VitD3 or 25(OH)D3 × four Ca levels (100, 90, 80 and 70% of the recommendations of Rostagno et al. (2011)), eight treatments, seven replicates and nine broilers per cage. Feed intake and feed conversion ratio did not (p>0.05) vary when levels of Ca were reduced and vitamin D3 sources were supplemented in the diets from 1 to 21 days for broilers chickens. 25 (OH)D3 increased weight gain results (p<0.05). From 1 to 42 d, no differences (p>0.05) were observed on performance, carcass yields and meat quality, bone deposition of Ca and P, and alkaline phosphatase concentration. Higher serum (p<0.05) concentrations of Ca and P were found in broilers fed with 25(OH)D3. The replacement of VitD3 with 25(OH)D3 and the Ca reduction of 30% in diets did not negatively affect performance, carcass characteristics, and Ca and P deposition in the tibia of broilers at 42 days of age, under heat stress.(AU)
Asunto(s)
Animales , Pollos/fisiología , Colecalciferol/efectos adversos , Hidroxicolecalciferoles/efectos adversos , Calcio de la Dieta/análisis , Respuesta al Choque Térmico/fisiologíaRESUMEN
La hipofosfatasia (HP) es una enfermedad congénita, causada por mutaciones con pérdida de función en el gen ALPL que codifica la isoenzima no específica de tejido de la fosfatasa alcalina (TNSALP). Su expresión clínica es muy variable, desde casos de muerte intraútero por alteración grave de la mineralización ósea, hasta casos solo con caída prematura de la dentición. Se presenta el caso clínico de un varón al que se le diagnosticó odontohipofosfatasia a los 30 meses por pérdida temprana de piezas dentarias y niveles anormalmente bajos de fosfatasa alcalina, sin signos de raquitismo ni deformidades óseas. Durante su seguimiento, hasta los 13 años, presentó síntomas compatibles con HP infantil leve, como cansancio al caminar, incoordinación en la marcha y dolor en miembros inferiores que aumentaban con la actividad física. Ante la aparición de edema bimaleolar y poca respuesta al tratamiento con calcitonina y antiinflamatorios, se descartaron patologías infecciosas o reumáticas o ambas y se diagnosticó, por biopsia de tibia y peroné, periostitis sin detección de cristales de pirofosfato. Los controles radiológicos durante su evolución mostraron ensanchamiento metafisario en muñeca, falta de remodelado de metacarpianos, hojaldrado perióstico en tibia y peroné e hipomineralización en metáfisis tibiales, con "lenguas radiolúcidas" características de HP. Como conclusión, la hipofosfatasia debe considerarse como una entidad clínica para descartar en niños que presentan pérdida temprana de dientes. La presencia de este cuadro clínico es en general suficiente para realizar el diagnóstico de HP de la niñez. (AU)
Hypophosphatasia (HP) is a congenital disease, caused by mutations with loss of function in the gene ALPL that encodes the non-specific tissue isoenzyme of alkaline phosphatase (TNSALP). Its clinical expression displays considerable variability, from cases of intrauterine death due to severe alteration of bone mineralization, to cases with only early loss of teeth. We report the case of a male, diagnosed as odontohypophosphatasia at 30 months of age due to early loss of teeth and abnormally low levels of alkaline phosphatase, without signs of rickets or bone deformities. During follow-up, up to 13 years of age, he presented symptoms consistent with mild infantile HP such as tiredness when walking, lack of gait coordination, and pain in lower limbs, especially after physical activity. Due to the appearance of bimalleolar edema and poor response to treatment with calcitonin and anti-inflammatory drugs, infectious and / or rheumatic pathologies were ruled out. Periostitis without pyrophosphate crystal detection was diagnosed by tibial and fibular biopsy. Radiological controls during follow up showed metaphyseal wrist enlargement, lack of remodeling of metacarpals, periosteal flaking in the tibia and fibula and hypomineralization in the tibial metaphysis, with "radiolucent tongues"; characteristic of HP. In conclusion, hypophosphatasia should be considered as a clinical entity in children who present early loss of teeth. The presentation of this clinical case is generally sufficient to make the diagnosis of childhood HP. (AU)
Asunto(s)
Humanos , Masculino , Preescolar , Niño , Adolescente , Fosfatasa Alcalina/genética , Hipofosfatasia/diagnóstico , Periostitis/diagnóstico , Trastorno por Déficit de Atención con Hiperactividad/diagnóstico , Trastorno por Déficit de Atención con Hiperactividad/terapia , Fluoruro de Sodio/administración & dosificación , Tibia/diagnóstico por imagen , Anomalías Dentarias/genética , Complejo Vitamínico B/uso terapéutico , Calcitonina/administración & dosificación , Carbamazepina/uso terapéutico , Fosfatasa Alcalina/sangre , Peroné/diagnóstico por imagen , Hidroxicolecalciferoles/efectos adversos , Hipofosfatasia/patología , Hipofosfatasia/sangre , Hipofosfatasia/terapia , Sulfato de Magnesio/uso terapéutico , Antiinflamatorios/uso terapéuticoRESUMEN
Combined treatment with oral phosphate and 1 alpha (OH)D3 was carried out in nine children with familial hypophosphatemic rickets. All nine had positive responses over a four- to six-year period as judged by healing of rickets, change in growth rate, decrease in alkaline phosphatase activity, and symptomatic improvement. In two patients therapy was stopped for a short time because of hypercalcemia. In one patient in whom therapy was effective there was a significant reduction in creatinine clearance which necessitated cessation of treatment. The results of this study suggest that combined treatment with 1 alpha(OH)D3 and oral phosphate is an effective form of therapy for this condition, but that the balancing of these two modalities of therapy in each patient is essential if hypercalcemia and hypercalciuria, on the one hand, and secondary hyperparathyroidism, on the other, are to be avoided. A simple means of balancing these therapeutic modalities is suggested.