S-100β and neuron-specific enolase levels in carbon monoxide–related brain injury
Received 23 August 2008; received in revised form 24 October 2008; accepted 26 October 2008. published online 26 October 2009.
Abstract
Introduction
Carbon monoxide (CO) toxicity may cause persistent injuries in tissues sensitive to hypoxia. Neuropsychiatric sequelae may be observed in about 67% of cases after severe CO exposure.
Aim
The aims of this study were to demonstrate the usefulness of S-100β and neuron-specific enolase (NSE) in CO intoxications, show the degree of neurological response, and determine the indications for hyperbaric oxygen treatment (HBOT) as biochemical markers.
Results
The S-100β and NSE levels of the sera of 30 patients were studied upon admittance and at the third and sixth hours. S-100β levels were found to be high in all 3 analyses. There was no significant change in NSE levels. When the S-100β levels were compared with Glasgow Coma Scale levels, a strong negative correlation was found for all hours (r = −0.7, −0.8; P = .00). The correlation between S-100β and carboxyhemoglobin levels at the initial hour was found to be statistically significant (r = 0.4; P = .01). The S-100β levels in patients receiving HBOT showed a considerable decrease compared with those in patients not receiving the treatment. The same decrease was valid for NSE, although it was insignificant.
Conclusion
S-100β may be useful in evaluating intoxications as an early biochemical marker in CO intoxications, as well as in the differential diagnosis due to other causes, and in determining HBOT indications.
aDepartment of Emergency Medicine, Ataturk University, Medical School, 25090 Erzurum, Turkey
bDepartment of Biochemistry, Ataturk University, Medical School, 25090 Erzurum, Turkey
cDepartment of Medical Education, Ataturk University, Medical School, 25090 Erzurum, Turkey
ABSTRACT