Neuron-specific enolase and S100B protein in children with carbon monoxide poisoning: children are not just small adults

Abstract

Introduction

The aim of this study was to evaluate the role of S100B protein and neuron-specific enolase (NSE) in children with carbon monoxide (CO) poisoning.

Methods

In 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.

Results

A 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.

Conclusion

We 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.

Introduction

Carbon monoxide (CO) is a colorless, tasteless, odorless, nonirritating gas produced primarily by incomplete combustion of any hydrocarbons fuels and may be responsible for more than half of all fatal poisonings worldwide. Common sources include motor vehicle exhaust gases in a poorly ventilated garage or in areas near garages and combustion appliances, for example, heating units, wood, and coal, in which partial combustion of oils, kerosene, and others occurs. Carbon dioxide poisoning results in generalized hypoxia in the body, and the central nervous system is the most sensitive area to this poisoning. Especially, CO poisoning can cause severe neurologic and psychiatric sequelae [1], [2]. Carbon dioxide poisoning, especially during the winter, is common in our region basically because of the use of stoves, charcoal burners, or gas-driven water heaters in small spaces with poor ventilation [3]. Organs such as the brain, heart, skeletal muscles, and kidneys, which have particularly higher oxygen demand, are the most sensitive tissues to acute CO poisoning. Prompt and accurate identification and appropriate treatment of hypoxia-induced organ injuries are essential.

Neuron-specific enolase (NSE) is a glycolytic enzyme that is localized primarily to the neuronal cytoplasm in the central nervous system. In previous studies, serum concentrations of NSE have been assessed as markers of neuronal damage in patients with a variety of conditions including traumatic and hypoxic brain damage, status epilepticus, and cardiac arrest [4], [5], [6], [7], [8]. S100B is a calcium-binding protein localized to astroglial cells. S100B has previously been studied in cardiac arrest, stroke, subarachnoid hemorrhage, and traumatic and hypoxic brain damage [7], [8], [9], [10].

Both NSE and S100B protein are released as a result of neuronal and astroglial cell death after hypoxic or traumatic brain damage. Increased NSE and S100B protein levels mediated by traumatic brain damage have been reported in children [11]. In addition, several studies performed on adults reported that S100B protein and NSE might act as an indicator of CO-induced hypoxic brain damage [4], [12], [13], [14].

Pediatric patients account for a significant percentage of all CO poisoning cases [15]. However, the role of the S100B protein and NSE in children with CO poisoning remains unknown. Considering that children are not just small adults, we decided to investigate this issue and assessed serum S100B protein and NSE levels and their correlation with clinical and laboratory parameters to evaluate the degree of brain damage that occurs as a result of CO poisoning in children. In this study, we hypothesized that serum NSE and S100B protein levels would increase in children sustaining CO poisoning.