Marcadores moleculares de la asfixia perinatal / Molecular markers of perinatal asphyxia

Introducción: la asfixia perinatal es un problema de salud que puede acarrear alteraciones del neurodesarrollo en los recién nacidos. Las determinaciones en suero de enolasa específica de neurona, lactato deshidrogenasa y aspartato amino transferasa han sido utilizadas como marcadores de asfixia perinatal. Objetivos: evaluar el valor de las determinaciones en suero de lactato deshidrogenasa, aspartato amino transferasa y enolasa específica de neurona como marcadores moleculares de la asfixia perinatal. Métodos: se realizó un estudio observacional descriptivo de corte transversal. Se trabajó con una muestra intencional de 41 recién nacidos asfícticos, clasificados con distintos grados de encefalopatía hipóxico-isquémica según los criterios de Sarnat. Se tomaron muestras de suero al momento del nacimiento y a las 72 horas siguientes. Las determinaciones en suero de enolasa específica de neurona se realizaron por ELISA. Se cuantificó lactato deshidrogenasa y aspartato amino transferasa por espectrofotometría. Resultados: todos los pacientes presentaron valores elevados en suero, de los tres analitos, a las 24 y 72 horas de nacidos. Los valores enzimáticos no variaron significativamente entre las 24 y 72 horas de nacidos sin tomar en cuenta el grado de encefalopatía hipóxico-isquémica. Existe correlación positiva entre los valores enzimáticos a las 24 y a las 72 horas de enolasa específica de neurona y lactato deshidrogenasa. No fue posible diferenciar el grado de encefalopatía hipóxico-isquémica a través de los niveles en suero de estas enzimas. Conclusiones: los valores de estas determinaciones enzimáticas contribuyen a describir desde el punto de vista bioquímico el cuadro del neonato con asfixia perinatal(AU)

Introduction: perinatal asphyxia is a health problem which may cause neurodevelopmental alterations in newborns. Serum determinations of neuron-specific enolase, lactate dehydrogenase, and aspartate aminotransferase have been used as markers of perinatal asphyxia. Objectives: evaluate the value of serum determinations of lactate dehydrogenase, aspartate aminotransferase and neuron-specific enolase as molecular markers of perinatal asphyxia. Methods: a cross-sectional observational descriptive study was conducted of 41 asphyxiated newborns classified as different grades of hypoxic-ischemic encephalopathy according to Sarnat's scale. Serum samples were taken at birth and 72 hours later. Serum determinations of neuron-specific enolase were obtained by ELISA. Lactate dehydrogenase and aspartate aminotransferase were quantified by espectrophotometry. Results: all the patients had high serum values of the three analytes 24 and 72 hours after birth. Enzyme values did not vary significantly from 24 to 72 hours after birth, not considering the grade of hypoxic-ischemic encephalopathy. A positive correlation was found between enzyme values for neuron-specific enolase and lactate dehydrogenase at 24 and 72 hours. It was not possible to differentiate the grade of hypoxic-ischemic encephalopathy via the serum levels of these enzymes. Conclusions: the values of these enzyme determinations contribute to describe the status of neonates with perinatal asphyxia from a biochemical point of view(AU)

Free oxygen radicals--predictors of neonatal outcome following perinatal asphyxia.

The study was undertaken to evaluate the role of free oxygen radicals in asphyxiated neonates. Thirty term neonates appropriate for gestational age and with severe birth asphyxia (Apgar score of 3 or less at 1 minute of life) formed the study subjects. The levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), creatine phosphokinase (CPK) and lipid peroxidase (LPO) in the CSF of these neonates were estimated between 12 and 48 hrs of life. Enzyme estimation was performed by standard methods and the results were analysed statistically using Multivariate Logistic Regression analysis and non parametric tests namely Kruskal Wallis test and Wilcoxon's rank sum test. Out of the thirty babies, 14 were observed to be neurologically normal, 9 had significant morbidity and 7 died. The SOD levels ranged from 12.4 to 140 units/ml, GPx from 128 to 1933 nmol/min/dl, CPK from 2 to 2098 IU/dl and LPO from 5.4 to 30.8 umol/hr/dl. The SOD and GPx levels had an inverse relationship whereas rise in LPO and CPK levels were directly proportional to the extent of neurological damage and ultimate clinical outcome. CPK levels higher than 140 IU/ml were lethal and associated with 100% mortality whereas all normal neonates had CPK below 37 IU/ml. The levels of antioxidant enzymes can reliably and significantly predict mortality and morbidity whereas level of an enzyme cannot confidently confer normalcy. Hence antioxidant enzyme levels with a cut off value can be a useful marker and serve as a prognostic indicator in times to come.