当前位置:主页 > 医学论文 > 外科论文 >

开放性骨折感染患者血清促炎及抗炎因子表达研究

发布时间:2018-07-08 13:27

  本文选题:开放性骨折 + 感染 ; 参考:《中华医院感染学杂志》2017年04期


【摘要】:目的探讨开放性骨折感染患者血清促炎及抗炎因子表达,为开放性骨折感染的临床诊治提供参考。方法选取2014年8月-2015年8月在医院诊治100例开放性骨折患者为骨折组、同期门诊进行健康体检的50例正常人群为对照组,骨折组在入院后隔日、对照组在体检时抽血检测白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-4(IL-4)、白细胞介素-10(IL-10)、可溶性肿瘤坏死因子受体I(sTNF-RI)水平,骨折组同时取创面分泌物行细菌培养。结果骨折组感染者21例,感染发生率为21.00%,培养出病原菌20株,分别为金黄色葡萄球菌12株、大肠埃希菌5株、表皮葡萄球菌2株、肺炎克雷伯菌1株,构成比分别占60.00%、25.00%、10.00%、5.00%;骨折组患者IL-6、TNF-α、IL-4、IL-10、sTNF-RI水平均高于对照组(P0.05);骨折感染患者IL-6、TNF-α、IL-4、IL-10、sTNF-RI水平分别为(35.45±5.71)ng/L、(42.65±7.89)ng/L、(56.11±13.54)pg/ml、(71.83±15.40)μg/L、(3983.55±945.71)ng/L,均高于骨折无感染患者(14.45±3.56)ng/L、(22.43±4.67)ng/L、(30.32±5.21)pg/ml、(50.15±11.01)μg/L、(2168.61±480.32)ng/L,比较差异有统计学意义(P0.05)。结论开放性骨折患者血清促炎及抗炎因子表达均明显升高,骨折感染可加重机体促炎及抗炎反应。
[Abstract]:Objective to investigate the expression of serum proinflammatory and anti-inflammatory factors in patients with open fracture infection and to provide reference for the diagnosis and treatment of open fracture infection. Methods from August 2014 to August 2015, 100 patients with open fracture were treated in hospital as fracture group, and 50 healthy controls were selected as control group. The fracture group was treated every other day after admission. The levels of interleukin-6 (IL-6), tumor necrosis factor- 伪 (TNF- 伪), interleukin-4 (IL-4), interleukin-10 (IL-10) and soluble tumor necrosis factor receptor I (sTNF-RI) were measured in the control group. Results in fracture group, 21 cases were infected, the incidence of infection was 21.000.Twenty strains of pathogenic bacteria were cultured, including 12 strains of Staphylococcus aureus, 5 strains of Escherichia coli, 2 strains of Staphylococcus epidermidis and 1 strain of Klebsiella pneumoniae. 鏋勬垚姣斿垎鍒崰60.00%,25.00%,10.00%,5.00%;楠ㄦ姌缁勬偅鑰匢L-6,TNF-伪,IL-4,IL-10,sTNF-RI姘村钩鍧囬珮浜庡鐓х粍(P0.05);楠ㄦ姌鎰熸煋鎮h,

本文编号:2107586

资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/waikelunwen/2107586.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户30f87***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com