3.9 Article

Change in plasma gelsolin level after traumatic brain injury

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JOURNAL OF TRAUMA AND ACUTE CARE SURGERY
卷 72, 期 2, 页码 491-496

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/TA.0b013e318226ec39

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Gelsolin; traumatic brain injury; mortality; prognosis

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BACKGROUND: Plasma gelsolin depletion has been associated with poor outcome of critically ill patients. However, there is a paucity of data available on circulating plasma gelsolin concentration in traumatic brain injury (TBI). Thus, we sought to investigate change in plasma gelsolin level after TBI and to evaluate its relation with disease outcome. METHODS: Fifty 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. RESULTS: Twenty-six patients (27.7%) died from TBI in a month. After TBI, plasma gelsolin level in patients decreased during the 6-hour period immediately, was at the nadir in 24 hours, increased gradually thereafter, and was substantially lower than that in healthy controls during the 7-day period. A multivariate analysis showed plasma gelsolin level was an independent predictor for 1-month mortality (odds ratio, 0.941; 95% confidence interval, 0.895-0.989; p = 0.017) and positively associated with Glasgow Coma Scale (GCS) score (t = 6.538, p < 0.001). A receiver operating characteristic curve identified that a baseline plasma gelsolin level <52.7 mg/L predicted 1-month mortality with 88.5% sensitivity and 79.4% specificity (area under the curve, 0.869; 95% confidence interval, 0.783-0.930). The predictive value of the gelsolin concentration was thus similar to that of GCS scores (p = 0.185). However, gelsolin did not statistically significantly improve the area under the curve of GCS scores (p = 0.517). CONCLUSIONS: Decreased plasma gelsolin level is associated with GCS scores and an independent prognostic marker of mortality after TBI. Reversing plasma gelsolin deficiency may be an effective treatment for TBI. (J Trauma. 2012; 72: 491-496. Copyright (C) 2012 by Lippincott Williams & Wilkins)

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