S-100 [beta] and neuron-specific enolase levels in carbon monoxide-related brain injury

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. 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. 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. 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.