The predictive value of elevation in specific serum enzymes for subsequent development of hypoxic-ischemic encephalopathy or intraventricular hemorrhage in full-term and premature asphyxiated newborns.
Serum lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT), and hydroxybutyrate dehydrogenase (HBDH) activities are significantly elevated in asphyxiated newborns within the first days of life. The approach of the present study was to evaluate firstly if serum levels of these enzymes correlate with the development of hypoxic-ischemic encephalopathy (HIE) and periventricular-intraventricular hemorrhage (PIVH) in full-term and premature asphyxiated newborns, and secondly if postnatally elevated enzyme activities could be predictive for these disorders. ASAT, LDH and HBDH activities were measured in 98 asphyxiated newborns. Blood samples were taken serially at five fixed times: 0 (cord), 12, 24, 72, and 144 hours post partum. All newborns were examined for the development of HIE and PIVH using standardized scoring systems. Fifty percent of the newborns were full-term and 50% were premature. Ten of the full-term (20.4%) and 21 (42.8%) of the premature newborns developed HIE. Nineteen newborns (19.4%) suffered PIVH (full-term/premature, 7/12). The full-term asphyxiated newborns with HIE or PIVH showed significantly elevated ASAT, LDH, and HBDH activities within the first 72 hours of life. In case of the premature asphyxiated newborns, the enzyme activities did not differ significantly between the study groups. The overall predictive values showed a high sensitivity (HIE/PIVH, 90.0%/71.4%), a high specificity (71.0%/88.1%), an acceptable negative predictive value (44.9%/50.0%), and a high positive predictive value (96.5%/94.9%) for the development of HIE and PIVH in full-term asphyxiated newborns. It is concluded that measurements of ASAT, LDH, and HBDH activities are reliable predictors for the development of HIE and PIVH in full-term asphyxiated newborns.(ABSTRACT TRUNCATED AT 250 WORDS)
Lackmann
G M
GM
Department of Pediatrics, Städtisches Klinikum Fulda, Teaching Hospital, University of Marburg, Germany.
Töllner
U
U
D001238:Asphyxia Neonatorum / Q000209:etiology*; D001921:Brain / Q000201:enzymology* / Q000503:physiopathology*; D002545:Brain Ischemia / Q000150:complications* / Q000503:physiopathology*; D002543:Cerebral Hemorrhage / Q000503:physiopathology*; D002552:Cerebral Ventricles / Q000503:physiopathology*; D006801:Humans; D006884:Hydroxybutyrate Dehydrogenase / Q000097:blood* / Q000378:metabolism; D000860:Hypoxia / Q000150:complications* / Q000503:physiopathology*; D007231:Infant, Newborn; D007234:Infant, Premature; D013997:Time Factors
D006884:Hydroxybutyrate Dehydrogenase