The Role of Plasma Granulocyte Colony Stimulating Factor and Bone Marrow Dysfunction after Severe Trauma

The Role of Plasma Granulocyte Colony Stimulating Factor and Bone Marrow Dysfunction after Severe Trauma
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DOI:
10.1016/j.jamcollsurg.2012.08.028
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发表时间:
2013-01-01
影响因子:
5.2
通讯作者:
Livingston, David H.
Livingston, David H.
中科院分区:
医学2区
文献类型:
--
作者:
Cook, Kristin M.;Sifri, Ziad C.;Livingston, David H.

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背景:严重创伤患者普遍存在骨髓功能障碍,表现为造血祖细胞(HPC)向外周血释放。粒细胞集落刺激因子(G-CSF)是一种强大的HPC动员刺激因子。我们假设创伤后血浆G-CSF水平升高,并与创伤后贫血和感染相关。研究设计:83例严重创伤患者在多个时间点采集血液,测定G-CSF水平和HPC动员,并与健康志愿者的血液进行比较。数据按年龄、性别、损伤严重程度评分(ISS)和患者是否休克进行分类。记录血红蛋白和输血要求以及医院获得的感染数据。结果:创伤后患者血浆G-CSF值较对照组升高50倍(1640.4+/-304.3 pg/mLvs33.0+/-6.8pg/mLp<0.001)。出现休克的患者G-CSF值是非休克患者的5倍,是对照组的75倍(2528.7+/-536.4 pg/mlvs 728.0+/-191.0 pg/mLvs33.0+/-6.8pg/mLp<0.001)。年龄、性别和ISS对G-CSF水平没有影响。HPC的动员持续时间长达10天,涉及多种细胞类型。较高的G-CSF水平还与伤后3周较低的血红蛋白水平和较高的输血量以及较高的医院获得性肺炎和细菌血症的发生率有关。结论:创伤后血浆G-CSF水平显著升高,且在休克时升高更明显。G-CSF的升高也与HPC的长时间动员有关。人类严重创伤后G-CSF的升高可能在创伤后骨髓功能障碍、贫血和感染的发生中起重要作用。《华尔街日报》2013;216:57--。(C)2013年由美国外科医师学会颁发)
BACKGROUND: Bone marrow dysfunction is common in severely injured trauma patients, with release of hematopoietic progenitor cells (HPC) into the peripheral blood. Granulocyte colony stimulating factor (G-CSF) is a potent stimulator of HPC mobilization. We hypothesized that plasma G-CSF levels are elevated after trauma and correlate with postinjury anemia and infection.STUDY DESIGN: Blood from 83 severely injured patients was collected at several time points for determination of G-CSF levels and HPC mobilization and compared with that from healthy volunteers. Data were categorized by age, sex, Injury Severity Score (ISS), and whether the patient was in shock. Hemoglobin and transfusion requirements and hospital-acquired infection data were recorded. Data are expressed as mean +/- SEM.RESULTS: After trauma, there is a 50-fold increase in plasma levels of G-CSF in trauma patients compared with controls (1,640.4 +/- 304.3 pg/mL vs 33.0 +/- 6.8 pg/mL, p < 0.001). Patients who presented in shock had 5-times higher G-CSF levels than nonshock trauma patients and a 75-fold increase compared with controls (2,528.7 +/- 536.4 pg/mL vs 728.0 +/- 191.0 pg/mL vs 33.0 +/- 6.8 pg/mL, p < 0.001). Age, sex, and ISS had no effect on G-CSF levels. Mobilization of HPC was sustained for up to 10 days after injury and involved multiple cells types. Higher G-CSF levels were also associated with lower hemoglobin levels and greater transfusion requirements 3 weeks after injury and a higher incidence of hospital-acquired pneumonia and bacteremia.CONCLUSIONS: Plasma G-CSF is markedly elevated after injury and is greater in patients who present in shock. The rise in G-CSF was also associated with prolonged mobilization of HPC. Elevation of G-CSF in humans after severe trauma may play a significant role in the development of post-traumatic bone marrow dysfunction, anemia, and infection. (J Am Coll Surg 2013;216:57-64. (C) 2013 by the American College of Surgeons)