• Xiao-Qiao Dong, Man Huang, Song-Bin Yang, Wen-Hua Yu, and Zu-Yong Zhang.
• Department of Neurosurgery, The First Hangzhou Municipal People's Hospital, Nanjing Medical University, Hangzhou, China. huyueyu2008@163.com
• J Trauma. 2011 Nov 1;71(5):1194-8.

BackgroundHigh serum copeptin levels are associated with injury severity after traumatic brain injury (TBI). However, not much is known regarding its relation with mortality. Thus, we sought to evaluate its relation with disease mortality.MethodsFifty healthy controls and 94 patients with acute severe TBI were included. Plasma samples were obtained on admission and at days 1, 2, 3, 5, and 7. Its concentration was measured by enzyme-linked immunosorbent assay.ResultsTwenty-six patients (27.7%) died from TBI in a month. After brain injury, plasma copeptin level in patients increased during the 6-hour period immediately, peaked in 24 hours, plateaued at day 2, decreased gradually thereafter, and was substantially higher than that in healthy controls during the 7-day period. A forward stepwise logistic regression selected plasma copeptin level (odds ratio, 1.008; 95% confidence interval, 1.002-1.014; p = 0.010) as an independent predictor for 1-month mortality of patients. A multivariate linear regression showed that plasma copeptin level was negatively associated with Glasgow Coma Scale (GCS) score (t = -7.161; p < 0.001). A receiver operating characteristic curve identified plasma copeptin cutoff level (451.8 pg/mL) that predicted 1-month mortality with the optimal sensitivity (88.5%) and specificity (75.0%) values (area under curve, 0.874; 95% confidence interval, 0.789-0.933; p < 0.001). The area under curve of plasma copeptin level was similar to that of GCS score (p = 0.299). However, copeptin did not statistically significantly improve the area under curve of GCS score (p = 0.413).ConclusionsIncreased plasma copeptin levels are associated with mortality after TBI.

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