[Biochemical parameters predictive of neuronal damage in childhood].
BACKGROUND
Hypoxemia, hypoxia and ischemia may induce deletereous effects on both metabolism and cellular structure, particularly at neuronal level. Early estimation of the potential severity of an acute cerebral hypoxic ischemic injury or other pathological conditions would be useful on making preventive or therapeutic decisions. On the basis of the physiopathological mechanisms involved in the brain damage related to hypoxic ischemic encephalopathy of the newborn, a number of metabolic parameters had been studied in the aim to provide an early and reliable marker of tissue injury for both diagnostic and prognostic purposes.


OBJECTIVE
To provide a current revision about the diagnostic and prognostic value of various biochemical parameters determined in different body fluids and studied in the last years, the attention focusing in the hypoxic ischemic encephalopathy of the newborn. Design. For methodological purposes the exposition is structured in the following sections: 1. creatine kinase isoenzymes; 2. lactate; 3. lactate dehydrogenase, aspartate aminotransferase and hidroxybutirate dehydrogenase; 4. excitatory amino acids; 5. glial fibrillary acidic protein; 6. cytokines; 7. neuron specific enolase; 8. oxypurines; 9. cyclic adenosine monophosphate; 10. Others.


CONCLUSIONS
The current role of the above mentioned biochemical parameters as predictors of brain damage and the future perspectives on this topic are discussed.
Castro-Gago
M
M
Departamento de Pediatría; Complejo Hospitalario Universitario de Santiago de Compostela, Santiago de Compostela, 15706, España. pdcastro@uscmail.usc.es
Rodríguez-Núñez
A
A
Novo-Rodríguez
M I
MI
Eirís-Puñal
J
J
D001219:Aspartate Aminotransferases / Q000097:blood; D001238:Asphyxia Neonatorum / Q000150:complications* / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis*; D001925:Brain Damage, Chronic / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism*; D002543:Cerebral Hemorrhage / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D002556:Cerebrospinal Fluid Proteins / Q000032:analysis; D003402:Creatine Kinase / Q000032:analysis; D052276:Creatine Kinase, BB Form; D000242:Cyclic AMP / Q000134:cerebrospinal fluid; D016207:Cytokines / Q000134:cerebrospinal fluid; D018846:Excitatory Amino Acids / Q000134:cerebrospinal fluid; D005312:Fetal Blood / Q000737:chemistry; D005316:Fetal Distress / Q000097:blood; D005311:Fetal Hypoxia / Q000150:complications* / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000134:cerebrospinal fluid; D006801:Humans; D006884:Hydroxybutyrate Dehydrogenase / Q000097:blood; D019271:Hypoxanthine / Q000032:analysis; D020925:Hypoxia-Ischemia, Brain / Q000150:complications* / Q000378:metabolism; D007231:Infant, Newborn; D007234:Infant, Premature; D007527:Isoenzymes / Q000032:analysis; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D019344:Lactic Acid / Q000032:analysis; D010751:Phosphopyruvate Hydratase / Q000134:cerebrospinal fluid; D011237:Predictive Value of Tests; D011379:Prognosis; D012680:Sensitivity and Specificity; D019820:Xanthine / Q000032:analysis
D015415:Biomarkers; D002556:Cerebrospinal Fluid Proteins; D016207:Cytokines; D018846:Excitatory Amino Acids; D005904:Glial Fibrillary Acidic Protein; D007527:Isoenzymes; D019820:Xanthine; D019271:Hypoxanthine; D019344:Lactic Acid; D000242:Cyclic AMP; D007770:L-Lactate Dehydrogenase; D006884:Hydroxybutyrate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D052276:Creatine Kinase, BB Form; D010751:Phosphopyruvate Hydratase