摘要
目的探讨肺结核并发医院感染患者免疫球蛋白E(IgE)、转铁蛋白(TRF)和血清肿瘤坏死因子-α(TNF-α)水平的变化、病原菌分布及耐药性,为临床治疗提供参考依据。方法调查2012年1月-2014年12月于医院治疗的50例肺结核发生医院感染患者临床资料,检测患者治疗前后细胞因子水平及感染病原菌分布,数据采用SPSS 18.0软件进行统计分析。结果肺结核发生医院感染患者治疗后TNF-α、IgE、TRF分别为(101.25±35.53)ng/L、(381.35±69.40)IU/ml、(45.8±18.5)μmol/L,明显优于治疗前,治疗前后TNF-α、IgE、TRF存在明显差异(P<0.05);共分离出病原菌72株,以革兰阴性菌为主,共42株占58.3%,革兰阴性菌对亚胺培南的耐药性低,均<10.0%。结论测定TNF-α、TRF、LgE水平对肺结核患者的诊断与预后具有一定的临床意义,可据此判断其医院医院感染程度,在临床治疗中,应根据抗药性的试验结果合理选择药物进行治疗。
OBJECTIVE To investigate the changes of immune globulin E（IgE）,transferrin（TRF）and serum tumor necrosis factor-α（TNF-α）in tuberculosis patients complicated with nosocomial infections and analyze the pathogenic bacteria distribution and drug resistance,so as to provide reference for clinical treatment.METHODS A total of 50 cases of tuberculosis infection patients with tuberculosis in our hospital from Jan.2012 to Dec.2014 in our hospital were studied.The cytokines level and pathogenic bacteria distribution were analyzed before and after treatment.Data were analyzed by SPSS 18.0.RESULTS After treatment,the observation group of patients with tuberculosis and nosocomial infection had TNF-α（101.25±35.53）ng/L,IgE（381.35±69.40）IU/ml and TRF（45.8±18.5）μmol/L which were significantly better than before treatment.There were significant differences between TNF-α,IgE and TRF before and after treatment（P〈0.05）;A total of 72 strains of bacteria were isolated,mainly gram-negative bacteria in 42 strains,accounting for 58.3%.The drug resistance rate of gram-negative bacteria to imipenem was less than 10.0%.CONCLUSION The determination of TNF-a,TRF and LgE levels in patients with pulmonary tuberculosis has certain clinical significance to the diagnosis and prognosis,which could be used accordingly for the judgment of infection degree.In clinical treatment,the resistance of the test results should be used for the rational choice of drugs for treatment.
出处
《中华医院感染学杂志》
CAS
CSCD
北大核心
2016年第16期3651-3653,共3页
Chinese Journal of Nosocomiology
基金
山东省自然科学基金资助项目(2015338479)
关键词
病原菌
医院感染
肺结核
肿瘤坏死因子-Α
Pathogenic bacteria
Nosocomial infection
Tuberculosis
Tumor necrosis factor-α
