Vía clínica de terapia metabólica con 131I en cáncer diferenciado de tiroides / Clinical pathway of metabolic therapy with 131I in differentiated thyroid cancer

Las vías clínicas son planes asistenciales que se aplican a procesos clínicos de curso predecible con la intención de protocolizarlos y disminuir la variabilidad en su manejo. Nuestro objetivo ha sido desarrollar una vía clínica para la terapia metabólica con 131I, proceso asistencial aplicado a los pacientes con carcinoma diferenciado de tiroides. Se organizó un equipo de trabajo formado por médicos (endocrinología y medicina nuclear), personal de enfermería (unidad de hospitalización y medicina nuclear), de radiofísica y del servicio de apoyo a la gestión clínica y continuidad asistencial. Para el diseño de la vía clínica se realizaron varias reuniones del equipo, en las que se pusieron en común las revisiones bibliográficas y se abordó el diseño y el desarrollo de la vía, respetando las guías clínicas vigentes. Este equipo ha logrado mediante consenso la elaboración del plan asistencial, estableciendo sus puntos clave y redactando los distintos documentos que componen la vía clínica: matriz temporal, documento de registro de variaciones de la vía clínica, documentos de información al paciente, encuesta de satisfacción del paciente, folleto de pictogramas, indicadores de evaluación de calidad. Por último, la vía clínica se ha presentado a todos los servicios clínicos involucrados y a la dirección médica del hospital, procediendo a su implementación en la práctica clínica (AU)

Clinical pathways are care plans that are applied to clinical processes with a predictable course, with the intention of protocolizing them, and reducing the variability in their management. Our objective was to develop a clinical pathway for 131I metabolic therapy, in its application to differentiated thyroid cancer. A work team was organised consisting of doctors (Endocrinology and Nuclear Medicine), nursing staff (Hospitalisation Unit and Nuclear Medicine), Radiophysics and the Clinical Management and Continuity of Care Support Service. For the design of the clinical pathway, several team meetings were held, in which the literature reviews were pooled and the design and development of the clinical pathway was undertook, in accordance with current clinical guidelines. This team has achieved consensus on the development of the care plan, establishing its key points and drafting the different documents that make up the clinical pathway: timeframe-based schedule, clinical pathway variation record document, patient information documents, patient satisfaction survey, pictogram brochure, quality assessment indicators. Finally, the clinical pathway was presented to all clinical departments involved and to the medical director of the hospital, and it is now being implemented in clinical practice (AU)

Clinical pathway of metabolic therapy with 131I in differentiated thyroid cancer.

Clinical Pathways are care plans that are applied to clinical processes with a predictable course, with the intention of protocolizing these processes and reducing the variability in their management. Our objective was to develop a clinical pathway for 131I metabolic therapy in its application to differentiated thyroid cancer. A work team was organized consisting of doctors (Endocrinology and Nuclear Medicine), nursing staff (Hospitalization Unit and Nuclear Medicine), Radiophysics and the Clinical Management and Continuity of Care Support Service. For the design of the clinical pathway, several team meetings were held, in which the literature reviews were pooled and the design and development of the clinical pathway was undertaken in accordance with current clinical guidelines. This team achieved consensus on the development of the care plan, establishing its key points and drafting the different documents that make up the Clinical Pathway: Timeframe-based schedule, Clinical Pathway Variation Record Document, Patient Information Documents, Patient Satisfaction Survey, Pictogram Brochure, Quality Assessment Indicators. Finally, the clinical pathway was presented to all the clinical departments involved and to the Medical Director of the Hospital and is now being implemented in clinical practice.

Correction to: X-linked hypophosphatemia and growth.

The authors of the article would like to note an error in the acknowledgements section of this paper.

X-linked hypophosphatemia and growth.

X-Linked hypophosphatemia (XLH) is the most common form of hereditary rickets caused by loss-of function mutations in the PHEX gene. XLH is characterized by hypophosphatemia secondary to renal phosphate wasting, inappropriately low concentrations of 1,25 dihydroxyvitamin D and high circulating levels of fibroblast growth factor 23 (FGF23). Short stature and rachitic osseous lesions are characteristic phenotypic findings of XLH although the severity of these manifestations is highly variable among patients. The degree of growth impairment is not dependent on the magnitude of hypophosphatemia or the extent of legs´ bowing and height is not normalized by chronic administration of phosphate supplements and 1α hydroxyvitamin D derivatives. Treatment with growth hormone accelerates longitudinal growth rate but there is still controversy regarding the potential risk of increasing bone deformities and body disproportion. Treatments aimed at blocking FGF23 action are promising, but information is lacking on the consequences of counteracting FGF23 during the growing period. This review summarizes current knowledge on phosphorus metabolism in XLH, presents updated information on XLH and growth, including the effects of FGF23 on epiphyseal growth plate of the Hyp mouse, an animal model of the disease, and discusses growth hormone and novel FGF23 related therapies.

Poscondicionamiento con ozono en un modelo de isquemia-reperfusión renal. Pruebas funcionales y morfológicas / Ozone postconditioning in renal ischaemia-reperfusion model. Functional and morphological evidences

Antecedentes: La isquemia-reperfusión es causa fundamental de complicaciones renales. La lesión más frecuente es la necrosis tubular aguda (NTA). En modelos de isquemia-reperfusión se ha demostrado que el precondicionamiento oxidativo con ozono ejerce un efecto modulador del estado redox de las células renales, al estimular los mecanismos antioxidantes endógenos. Trabajos más recientes, que han empleado el postcondicionamiento isquémico, han obtenido resultados similares. Objetivos: Evaluar el efecto del poscondicionamiento oxidativo con ozono sobre la morfología y la función renal en un modelo de isquemia-reperfusión en ratas. Métodos: Se utilizaron 40 ratas Wistar hembras con un peso entre 150 y 200 g, divididas al azar en cuatro grupos (control negativo, control positivo, oxígeno y ozono). Los grupos control positivo, oxígeno y ozono fueron sometidos a 60 minutos de isquemia y 10 días de reperfusión. Durante la reperfusión al grupo oxígeno se le administraron 26 mg/kg de peso corporal de oxígeno y al grupo ozono, 0,5 mg/kg de peso corporal de ozono, por vía rectal. Al final del experimento se tomaron muestras de orina y de sangre para las pruebas de función renal y se extrajeron los riñones para el estudio histológico. Resultados: El grupo ozono no mostró diferencias significativas en los valores de fracción de filtración y proteinuria con respecto al grupo control negativo. Los valores de intensidad de filtrado glomerular, flujo plasmático renal y creatinina mostraron una mejoría ligera en comparación con los grupos oxígeno y control positivo. El grupo ozono mostró de forma significativa un menor daño histológico global que los grupos control positivo y oxígeno. Conclusiones: El poscondicionamiento con ozono tuvo un efecto protector (AU)

Background: Ischaemia-reperfusion is one of the main causes of kidney complications. The most frequent lesion is acute tubular necrosis. Ozone oxidative preconditioning exerts a modulatory effect of redox state of renal cells in models of ischaemia-reperfusion, by stimulating endogenous antioxidant mechanisms. Similar results have been obtained in more recent studies using ischaemic postconditioning. Objectives: To evaluate the effect of ozone oxidative postconditioning on renal function and morphology in an ischaemia-reperfusion rat model. Methods: We used forty female Wistar rats weighing between 150g-200g randomly divided into 4 groups (negative control, positive control, oxygen and ozone). The groups: positive control, oxygen and ozone were subjected to 60 minutes of ischaemia and 10 days of reperfusion. During reperfusion, the oxygen group was given 26mg/kg body weight of oxygen, and the ozone group 0.5mg/kg body weight of ozone, rectally. At the end of the experiment urine and blood samples were taken for renal function tests and kidneys were removed for histological study. Results: The ozone group showed no significant differences for filtration fraction and proteinuria compared to the negative control group. The glomerular filtrate rate, renal plasma flow and creatinine showed a slight improvement in comparison with oxygen and positive control groups. The ozone group showed significantly less overall histological damage than the positive control and oxygen groups. Conclusions: Ozone postconditioning showed to have a protective effect in preserving renal function and morphology (AU)

Ozone postconditioning in renal ischaemia-reperfusion model. Functional and morphological evidences.

BACKGROUND: Ischaemia-reperfusion is one of the main causes of kidney complications. The most frequent lesion is acute tubular necrosis. Ozone oxidative preconditioning exerts a modulatory effect of redox state of renal cells in models of ischaemia-reperfusion, by stimulating endogenous antioxidant mechanisms. Similar results have been obtained in more recent studies using ischaemic postconditioning. OBJECTIVES: To evaluate the effect of ozone oxidative postconditioning on renal function and morphology in an ischaemia-reperfusion rat model. METHODS: We used forty female Wistar rats weighing between 150g-200g randomly divided into 4 groups (negative control, positive control, oxygen and ozone). The groups: positive control, oxygen and ozone were subjected to 60 minutes of ischaemia and 10 days of reperfusion. During reperfusion, the oxygen group was given 26mg/kg body weight of oxygen, and the ozone group 0.5mg/kg body weight of ozone, rectally. At the end of the experiment urine and blood samples were taken for renal function tests and kidneys were removed for histological study. RESULTS: The ozone group showed no significant differences for filtration fraction and proteinuria compared to the negative control group. The glomerular filtrate rate, renal plasma flow and creatinine showed a slight improvement in comparison with oxygen and positive control groups. The ozone group showed significantly less overall histological damage than the positive control and oxygen groups. CONCLUSIONS: Ozone postconditioning showed to have a protective effect in preserving renal function and morphology.

Acute administration of grape seed proanthocyanidin extract modulates energetic metabolism in skeletal muscle and BAT mitochondria.

Proanthocyanidin consumption might reduce the risk of developing several pathologies, such as inflammation, oxidative stress and cardiovascular diseases. The beneficial effects of proanthocyanidins are attributed to their antioxidant properties, although they also can modulate gene expression at the transcriptional level. Little is known about the effect of proanthocyanidins on mitochondrial function and energy metabolism. In this context, the objective of this study was to determine the effect of an acute administration of grape seed proanthocyanidin extract (GSPE) on mitochondrial function and energy metabolism. To examine this effect, male Wistar rats fasted for fourteen hours, and then they were orally administered lard oil containing GSPE or were administered lard oil only. Liver, muscle and brown adipose tissue (BAT) were used to study enzymatic activity and gene expression of proteins related to energetic metabolism. Moreover, the gastrocnemius muscle and BAT mitochondria were used to perform high-resolution respirometry. The results showed that, after 5 h, the GSPE administration significantly lowers plasma triglycerides, free fatty acids, glycerol and urea concentrations. In skeletal muscle, GSPE lowers FATP1 mRNA levels and increases mitochondrial oxygen consumption, using pyruvate as the substrate, suggesting a promotion of glycosidic metabolism. Furthermore, GSPE increased the genetic expression of key genes in energy metabolism such as peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC1α), and modulated the enzyme activity of proteins, which are involved in the citric acid cycle and electron transport chain (ETC) in BAT. In conclusion, GSPE affects mainly the skeletal muscle and BAT mitochondria, increasing their oxidative capacity rapidly after acute supplementation.