• Ahmet Zulfikar Akelma, Aydin Celik, Osman Ozdemir, Fatma Kavak Akelma, Ayhan Abaci, Cem Hasan Razi, Fatih Mehmet Kislal, and Okhan Akin.
• Deparment of Pediatrics, Fatih University Medical School, Ankara, Turkey. akelma@gmail.com
• Am J Emerg Med. 2013 Mar 1;31(3):524-8.

IntroductionThe aim of this study was to evaluate the role of S100B protein and neuron-specific enolase (NSE) in children with carbon monoxide (CO) poisoning.MethodsIn this prospective, case-controlled study, children with CO poisoning were recruited. Patient demographics features and Glasgow Coma Scale (GCS) were recorded. Blood samples were collected from all children with CO poisoning at their admission to the hospital and at 3 and 6 hours after admission. Levels of NSE and S100B were measured. The control group consisted of age-matched healthy children.ResultsA total of 30 children with CO poisoning (mean age, 7.88 ± 3.75 years; 17 boys) and 30 healthy children (mean age, 8.16 ± 3.05 years; 7 boys) were enrolled in the study. Mean carboxyhemoglobin level (%) measured at admission was 30.05 ± 8.00. Serum NSE levels of the children with CO poisoning were significantly higher than those of children from the control group at 0 hour and also at 3 and 6 hours (P < .001, P = .001, and P = .005, respectively). Serum S100B protein levels were similar between the 2 groups at 0 and 3 and 6 hours (P > .05). Serum NSE levels of patients with CO poisoning demonstrated a negative correlation with the admission GCS scores. No correlation was found between GCS scores and S100B protein levels.ConclusionWe have shown that NSE levels increase in CO-associated hypoxic brain damage in accordance with clinical findings. We have also found that, contrary to the studies conducted on adults, S100B protein levels do not increase in response to hypoxic brain damage.Copyright © 2013 Elsevier Inc. All rights reserved.

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