ABSTRACT
Resumen Introducción: Las calcificaciones vasculares forman parte del trastorno mineral óseo en la enfermedad renal crónica y constituye una de las principales causas de mortalidad. Existe plausibilidad y asociación experimental entre el trastorno bioquímico con la calcificación vascular, sin embargo, no existe evidencia suficiente de su asociación clínica. Objetivo: Determinar la asociación de las alteraciones bioquímicas del trastorno mineral óseo (calcio >10 mg/dl, fósforo >5 mg/dl, paratohormona >300 pg/ml) con las calcificaciones vasculares valoradas de acuerdo al score de Kauppila. Material y métodos: Estudio observacional, transversal y analítico. Se incluyeron 97 pacientes con ERC estadio V, en terapia de hemodiálisis, 69% prevalente (establecido en >6 meses) con un tiempo promedio de 5,3 años. Se estableció asociación estadística según test Chi2 de Pearson y regresión logística. Resultados: El 60,8% presentó algún grado de calcificación vascular con un score de Kauppila >1 y el 43,3% presentó un score ≥3, que fue predominante en la población prevalente en hemodiálisis (78,6%). Sin embargo, no se encontró asociación estadística con el trastorno bioquímico mineral óseo en el análisis bivariado por Chi2 ni por regresión logística. Conclusiones: Una valoración transversal de la alteración bioquímica del trastorno mineral óseo no permite establecer su asociación con las calcificaciones vasculares. Es necesario establecer previamente el balance positivo prospectivo de calcio y de fósforo para demostrar esta asociación.
Abstract Introduction: Vascular calcifications are part of the mineral bone disorder in chronic kidney disease and they are one of the main causes of mortality. There is plausibility and experimental association between metabolic disorder and vascular calcification; however, there is no enough evidence for their clinical connection. Objective: To determine the association of biochemical alterations of mineral bone disorder (calcium: >10 mg/dL; phosphorus: >5 mg/dL; paratohormone: >300 pg/mL) with vascular calcifications evaluated according to the Kauppila score. Methods: An observational, cross-sectional, analytical study was performed. 97 stage V CKD patients undergoing hemodialysis were included; 69% were prevalent cases (diagnosed within >6 months) with an average time of 5.3 years. A statistical association was established according to Pearson's Chi2 test and logistic regression. Results: A level of vascular calcification was found with a Kauppila score of >1 in 60.8% of patients and of ≥3 in 43.3% of them, being predominant in the prevalent dialysis population (78.6%). However, no statistical association was found with mineral bone disorder in the chi-squared bivariate analysis or the logistic regression. Conclusions: A cross-sectional test of the biochemical alteration in mineral bone disorder does not allow to find an association with vascular calcifications. It is necessary to establish a prospective calcium-phosphorus positive balance first to prove this association.
ABSTRACT
Introducción: Las hojas de Manihot esculenta Crantz (yuca) han sido usadas alrededor del mundo y a lo largo del tiempo con el fin de disminuir la respuesta antiinflamatoria. Objetivo: Evaluar la actividad antiinflamatoria del extracto etanólico de la hoja de Manihot esculenta crantz en ratas. Métodos: Se realizó un estudio tipo experimental. La población de estudio fueron 60 ratas albinas sp. Rattus novergicus, distribuidas en 4 grupos de 15 ratas cada uno. Se usó una solución homogénea de extracto etanólico de hojas de Manihot esculenta crantz para su administración vía intraperitoneal. Se utilizó carragenina como inductor inflamatorio, que fue administrado por vía intradérmica; para la medición del edema plantar, se hizo uso del Digital Water Plethysmometer (LE7500). Se administró al grupo control negativo solución de tween 80/agua (1:10) a dosis de 1ml/10g., al grupo control positivo betametasona 4mg/Kg y a los grupos de tratamiento 1 y 2 Manihot esculenta crantz, 2 mg/kg y 4 mg/kg, respectivamente. Se utilizó la prueba de ANOVA de 1 cola y la prueba post-hoc de Tukey, para las comparaciones entre los grupos. Resultados: En el 37,67% del grupo de tratamiento 2 se observó una reducción del edema a las 3 horas de administrar Manihot esculenta crantz (p <0,05). En otras mediciones se encontró una tendencia no significativa en ambos grupos de administración de Manihot esculenta crantz a la reducción del edema plantar. Conclusión: El extracto etanólico de Manihot sculenta a partir de la dosis de 4 mg/kg parece tener actividad antiinflamatoria en la reducción del edema plantar en el modelo animal utilizado.
Introduction: Manihot esculenta Crantz (yucca) leaves have been used around the world and over time in order to decrease the anti-inflammatory response. Objective: To evaluate the anti-inflammatory activity of the ethanolic extract of the Manihot esculenta Crantz leaf in rats. Methods: An experimental study was conducted. The study population included 60 albino rats sp. Rattus novergicus, distributed in 4 groups of 15 rats each. A homogeneous solution of ethanolic extract of Manihot esculenta Crantz leaves was used for intraperitoneal administration. Carrageenan was used as an inflammatory inducer that was administered intradermally; for the measurement of plantar edema, the Digital Water Plethysmometer (LE7500) was used. Tween 80 / water solution (1:10) was administered to the negative control group at a dose of 1mL./100g., To the betamethasone positive control group 4mg / Kg and to treatment groups 1 and 2 Manihot esculenta Crantz, 2 mg / kg and 4 mg / kg, respectively. The 1-tail ANOVA test and the Tukey post hoc test were used for comparisons between the groups. Results: In 37.67% of treatment group 2 a reduction in edema was observed 3 hours after administering Manihot esculenta Crantz (p <0.05). In both administration groups of Manihot esculenta Crantz there was a nonsignificant trend to reduce plantar edema with values close to significance. Conclusion: The Manihot esculenta Crantz ethanolic extract at a 4 mg / kg dose probably have anti-inflammatory activity in this animal model of acute inflamation.
ABSTRACT
Compelling evidence indicates that exposure to urban airborne particulate matter (PM) affects health. However, how PM components interact with PM-size to cause adverse health effects needs elucidation, especially when considering soil and anthropogenic sources. We studied PM from Mexicali, Mexico, where soil particles contribute importantly to air pollution, expecting to differentiate in vitro effects related to PM-size and composition. PM samples with mean aerodynamic diameters ≤2.5µm (PM(2.5)) and ≤10µm (PM(10)) were collected in Mexicali (October 2005-March 2006) from a semi-urban (expected larger participation of soil sources) and an urban (predominately combustion sources) site. Samples were pooled by site and size, analyzed for elemental composition (particle-induced X-ray emission) and tested in vitro for: induction of human erythrocytes membrane disruption (hemolysis) (colorimetrically); inhibition of cell proliferation (ICP) (crystal violet) and TNFα/IL-6 secretion (ELISA) using J774.A1 murine monocytic cells; and DNA degradation using Balb/c3T3 cell naked DNA (electrophoretically). Results of PM elemental composition principal component analysis were used in associating cellular effects. Sixteen elements identified in PM grouped in two principal components: Component(1) (C(1)): Mg, Al, Si, P, Cl, K, Ca, Ti, V, Cr, Fe, and Component(2) (C(2)): Cu, Zn. Hemolysis was predominately induced by semi-urban-PM(10) (p<0.05) and was associated with urban-PM(10)C(1) (r=0.62, p=0.003). Major ICP resulted with semi-urban PM(2.5) (p<0.05). TNFα was mainly induced by urban samples regardless of size (p<0.05) and associated with urban-PM(2.5)C(2) (r=0.48, p=0.02). Both PM(10) samples induced highest DNA degradation (p<0.05), regardless of location. We conclude that PM-size and PM-related soil or anthropogenic elements trigger specific biological-response patterns.
