The impact of beta-blocker therapy on anemia after traumatic brain injury

被引:5
|
作者
Glass, Nina E.
Kaltenbach, Lisa A.
Fleming, Sloan B.
Arbogast, Patrick G.
Cotton, Bryan A.
机构
[1] NYU, Dept Surg, Sch Med, New York, NY 10016 USA
[2] Vanderbilt Univ, Med Ctr, Dept Biostat & Pharmacol, Nashville, TN USA
[3] Univ Texas Hlth Sci Ctr, Dept Surg, Houston, TX USA
[4] Univ Texas Hlth Sci Ctr, Ctr Translat Injury Res, Houston, TX USA
关键词
ERYTHROID COLONY FORMATION; HEAD-INJURY; IMPROVED OUTCOMES; HYPERCATECHOLAMINE STATE; ADRENERGIC AGONISTS; IMPROVED SURVIVAL; CELL TRANSFUSION; ERYTHROPOIESIS; EXPOSURE; HYPOXIA;
D O I
10.1111/j.1537-2995.2012.03609.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND: An increase in endogenous catecholamine levels after traumatic brain injury (TBI) is well described. Animal studies suggest that postinjury anemia is exacerbated by a persistent hyperadrenergic state. This study aims to determine if beta-blocker (BB) exposure affects anemia after TBI. STUDY DESIGN AND METHODS: We reviewed a Level I trauma registry for patients with TBI, examining markers of anemia between patients who received BB with those who did not. RESULTS: A total of 174 patients were exposed to BB (BB+) and 245 were not exposed (BB-). The mean age in the BB+ group was 50 years (vs. 36 years in BB-group, p < 0.001). The mean injury severity score was 33.6 for the BB+ group (vs. 30.8 for BB-group, p = 0.01). While BB+ patients were more likely to receive a transfusion (60.9% vs. 35.1%, p < 0.001), BB+ patients reached their nadir hemoglobin (Hb) at a later day of hospitalization and their rate of decrease in Hb was significantly slower (both p < 0.001). Choosing Hb cutoffs for anemia of both 7 and 10 g/dL, Kaplan-Meier demonstrated a significant delay in time to anemia. CONCLUSION: This study suggests beta-blockade delays anemia after TBI. Elaboration of this effect may demonstrate an additional benefit of beta-blockade after head injury.
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页码:2155 / 2160
页数:6
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