Tomasz Gawlikowski

Acute CO Poisoning is Associated with Impaired Fibrinolysis and Increased Thrombin Generation

Carbon monoxide (CO) poisoning is a leading cause of unintentional poisoning deaths in many countries. In ex vivo studies, CO released from carbon monoxide‐releasing molecules has been shown to attenuate fibrinolysis via increased alpha‐2‐antiplasmin activity. Hypofibrinolysis is associated with coronary ischaemia, which is also commonly observed in CO poisoning. We examined fibrin clot properties in acutely poisoned CO patients. Ex vivo plasma fibrin clot permeability, turbidimetry and efficiency of fibrinolysis were investigated in 48 patients and controls matched for age and sex. CO‐poisoned patients had 11.6% longer clot lysis time than the controls (p < 0.0001). No intergroup differences in clot permeability or turbidimetric variables were observed. Plasma tissue‐type plasminogen antigen (tPA), plasminogen activator inhibitor‐1 (PAI‐1) antigen and activity and F1.2 prothrombin fragments were higher in the patients than in the controls (all p < 0.0001). Plasma tPA activity was lower in the CO‐poisoned group. Multiple linear regression showed that a thrombin generation marker, F1.2, is the strongest predictor of clot lysis time, followed by PAI‐1 activity and carboxyhaemoglobin levels. In conclusion, this report is the first to demonstrate that acute CO poisoning in human beings is linked to increased thrombin generation and impaired fibrinolysis, which might contribute to ischaemic complications.

Proteins as biomarkers of carbon monoxide neurotoxicity

Abstract Context: Carbon monoxide (CO) poisoning is the most common form of accidental lethal poisoning and is associated with a risk of brain damage in survivors. Objective: The goal of this study was to examine whether Tau protein or S100B protein may be used as a biomarker for acute brain dysfunction. Materials and methods: The determination of Tau and S100B proteins was performed in serum samples collected from 27 CO-poisoned patients and 12 healthy volunteers. Results: The level of Tau protein in the serum of patients (444 ± 227 ng L−1) differed significantly compared with those in the healthy controls (240 ± 61 ng L−1) and correlated with the level of carboxyhemoglobin. A higher concentration of Tau protein was found in patients who had lost consciousness during CO exposure. The concentration of S100B in the serum of CO-poisoned subjects (0.08 ± 0.03 µg L−1) was not statistically different from values obtained for the controls (0.07 ± 0.02 µg L−1). Conclusion: CO poisoning appears to be associated with an elevated level of Tau and S100B proteins in the serum of patients who had suffered a loss of consciousness. The study has shown that Tau protein is a more sensitive biomarker than S100B protein for the earlier stage of neurotoxic effects of CO intoxication.