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The Value of Serum Caspase-3 NSE and O2UCc in Early Prediction of Delayed Encephalopathy Caused by Acute Carbon Monoxide Poisoning |
BAI Yanyan, LI Ruibo, ZHAO Rui, et al |
The First Hospital of Yulin City, Shaanxi Yulin 719000, China |
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Abstract Objective: To investigate the value of cysteine aspartic protease-3 (caspase-3), neuron-specific enolase (NSE) and early cerebral oxygen utilization (O2UCc) in early prediction of delayed encephalopathy caused by acute carbon monoxide poisoning. Methods: A total of 125 patients with acute carbon monoxide poisoning admitted to our hospital from January 2019 to December 2020 were selected. According to whether delayed encephalopathy of carbon monoxide poisoning occurred within 60 days after poisoning, the patients were divided into encephalopathy group (34 cases) and control group (91 cases). Serum caspase-3, NSE and O2UCc levels of the two groups were compared within 24h after admission, and the value of each index in predicting delayed encephalopathy in patients with acute carbon monoxide poisoning was analyzed by receiver operating curve (ROC). Logistic multivariate model was used to analyze the relationship between caspase-3, NSE, O2UCc and delayed encephalopathy caused by carbon monoxide poisoning. Results: The measured values of caspase-3 and NSE in encephalopathy group were significantly higher than those in control group, while the measured values of O2UCc in encephalopathy group were significantly lower than those in control group, with statistical significance (P<0.05). The sensitivity of caspase-3, NSE, O2UCc, caspase-3+NSE+O2UCc to predict delayed encephalopathy of acute carbon monoxide poisoning were 63.41%, 57.52%, 62.77% and 92.33%, respectively. The specificity was 85.28%, 80.66%, 82.94%, 78.58%, and the area AUC under ROC curve was 0.802, 0.797, 0.798, 0.936, respectively. Logistic regression model showed that aging, prolonged CO exposure time, consciousness disturbance ≥10h, severe poisoning, increased caspase-3, increased NSE and decreased O2UCc were independent risk factors for delayed encephalopathy of acute carbon monoxide poisoning (P<0.05). Conclusion: Early caspase-3 and NSE levels were significantly increased and O2UCc levels were significantly decreased in patients with acute carbon monoxide poisoning delayed encephalopathy, and there was a significant relationship with the occurrence of delayed encephalopathy in patients with acute carbon monoxide poisoning.
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