BACKGROUND: Recently, copeptin has been identified as a plasma prognosis marker in acute ischemic stroke and intracerebral hemorrhage (ICH). This study investigated the prognostic value of copeptin in the patients with aneurysmal subarachnoid hemorrhage(aSAH). METHODS: In this retrospective study, 243 consecutive patients were included. Upon admission, plasma copeptin levels were measured by enzyme-linked immunosorbent assay. The end points were mortality and poor functional outcome (Glasgow Outcome Scale score of 1-3) after 3 months. RESULTS: In 243 patients, 112 (46.1%) were male and median age was 58 years (IQR 49-68). Median copeptin plasma levels were 21.0 pmol/l (IQR 13.2-31.2). Copeptin levels increased with increasing severity of aSAH as defined by the World Federation of Neurological Surgeons (WFNS) score. Patients with a poor outcome and nonsurvivors had significantly increased copeptin levels on admission (P < .001 both). In the multivariate analysis, for each 1 pmol/l increase of plasma concentration of copeptin, the adjusted risk of poor outcomes and mortality would be increased by and 6% (1.06 [1.02-1.10], P < .001) and 9% (1.09 [1.03-1.13], P < .001), respectively. Receiver operating characteristics to predict functional outcome and mortality demonstrated areas under the curve of copeptin of 0.74 (95% confidence interval [CI], 0.67-0.81) and 0.81 (95% CI, 0.74-0.87), which was comparable with the WFNS score(P > .05) but superior to C-reactive protein and IL-6 (P < .01). CONCLUSIONS: The data shows that copeptin levels may reliably predict short-term prognosis at its onset in aSAH patients.
BACKGROUND: Recently, copeptin has been identified as a plasma prognosis marker in acute ischemic stroke and intracerebral hemorrhage (ICH). This study investigated the prognostic value of copeptin in the patients with aneurysmal subarachnoid hemorrhage(aSAH). METHODS: In this retrospective study, 243 consecutive patients were included. Upon admission, plasma copeptin levels were measured by enzyme-linked immunosorbent assay. The end points were mortality and poor functional outcome (Glasgow Outcome Scale score of 1-3) after 3 months. RESULTS: In 243 patients, 112 (46.1%) were male and median age was 58 years (IQR 49-68). Median copeptin plasma levels were 21.0 pmol/l (IQR 13.2-31.2). Copeptin levels increased with increasing severity of aSAH as defined by the World Federation of Neurological Surgeons (WFNS) score. Patients with a poor outcome and nonsurvivors had significantly increased copeptin levels on admission (P < .001 both). In the multivariate analysis, for each 1 pmol/l increase of plasma concentration of copeptin, the adjusted risk of poor outcomes and mortality would be increased by and 6% (1.06 [1.02-1.10], P < .001) and 9% (1.09 [1.03-1.13], P < .001), respectively. Receiver operating characteristics to predict functional outcome and mortality demonstrated areas under the curve of copeptin of 0.74 (95% confidence interval [CI], 0.67-0.81) and 0.81 (95% CI, 0.74-0.87), which was comparable with the WFNS score(P > .05) but superior to C-reactive protein and IL-6 (P < .01). CONCLUSIONS: The data shows that copeptin levels may reliably predict short-term prognosis at its onset in aSAHpatients.