IntroductionCarbon monoxide (CO) poisoning is a health problem that frequently occurs in Turkey and worldwide. In Turkey, it accounts for 30% of the poisoning cases that end with death (1).This colorless, odorless, tasteless, and nonirritating gas is produced as a result of the incomplete burning of organic matter that can easily be absorbed by the lungs. CO poisoning can cause cerebral, cardiac, and general ischemia. The poisoning can be diagnosed according to the blood carboxyhemoglobin (COHb) levels. There is a weak correlation between blood COHb levels and organ damage. Poisonings higher than 60% end with death and at lower levels clinical findings range from mild to severe. It is not always possible to identify this using the COHb level (2). Biochemical markers other than COHb are being studied to identify the clinical outcomes of this poisoning with neurotoxic and cardiotoxic effects in particular (3).Copeptin is excreted from the posterior hypophysis simultaneously with vasopressin and reflects the amount of vasopressin in circulation. Copeptin is more stable than vasopressin in plasma and serum. Studies conducted have reported that copeptin and vasopressin levels float parallel to each other both in healthy individuals and in the critically ill patient population. Recently copeptin has been investigated as a diagnostic and prognostic factor in many diseases like pneumonia, heart failure, and hemorrhagic and septic shock and it has been identified that its levels rise in correlation with the severity of the disease (4-7).The aim of this study is to identify the copeptin levels in patients presenting to the emergency department with CO poisoning and to investigate its correlation with neurological damage.Background/aim: The aim of this study is to identify the copeptin levels in patients presenting with carbon monoxide (CO) poisoning to the emergency department and to investigate its correlation with the neurological effects. Materials and methods:The study group consisted of patients presenting with CO poisoning and carboxyhemoglobin levels >10%. Blood samples for copeptin levels were obtained twice, first at presentation then at the fourth hour of observation. The data were analyzed using SPSS 16 for Windows. Results:The median copeptin levels of the patient group were identified as 0.63 (0.39-1.06) ng/mL at hour 0 and 0.41 (0.31-0.49) at hour 4. The copeptin levels of the control group were 0.34 (0.25-0.42) ng/mL and were significantly lower than those of the patient group (P < 0.000). According to our results, 0.345 ng/mL for plasma copeptin level as the best cut-off level may be used with sensitivity of 94.0% and specificity of 60%. The copeptin levels at hour 0 were statistically significantly higher in the neurologically affected patients than those not affected (P < 0.001). Conclusion:In this study it was shown that blood copeptin levels increase in patients presenting to the emergency department with CO poisoning.

Aim: Trauma is a leading cause of emergency admissions. In this study, we investigated the effect of Pycnogenol ® on spatial learning and memory (SLM) function in rats subjected to closed head injury.

No abstract