摘要
目的探讨白介素18(IL-18)的水平动态变化与急性一氧化碳中毒后迟发性脑病(DEACMP)发生机制的关系,寻找其发生时可能引起的细胞因子的变化,为进一步研究DEACMP免疫学机制提供线索。方法选择2009年1月—2011年1月住我院神经内科的DEACMP患者40例为DEACMP组及同期我院门诊体检健康者36例为对照组,应用酶联免疫吸附法分别测定DEACMP患者急性期及恢复期的血清IL-18水平,并与对照者进行比较分析。结果DEACMP患者急性期、恢复期血清IL-18水平〔(29.7±8.4)ng/L、(28.3±7.9)ng/L〕均高于对照组〔(24.1±5.3)ng/L、(24.1±5.3)ng/L〕,差异均有统计学意义(t=3.433,P=0.001;t=2.693,P=0.009)。DEACMP组急性期血清IL-18水平高于恢复期差异有统计学意义(t=2.421,P=0.020)。结论 IL-18可能通过迟发性免疫途径参与DEACMP的发病过程,对疾病的发展可能有一定的影响。
Objective To investigate the relationship between dynamic changes of serum IL - 18 level and mechanism of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) to find potential cytokine variation during DEAC-MP occurrence and to provide evidence for further study on immunological mechanism of DEACMP. Methods 40 DEACMP pa-tients admitted to the Neurology Department of our hospital from January 2009 to January 2011 were selected as DEACMP group and another 36 healthy people underwent physical examination in the same period were selected as control group. Enzyme - linked Immunoassay (ELISA) method was used to detect the levels of IL -18 in acute stage and recovery stage, and the results were compared with the control group. Results The levels of IL - 18 in DEACMP patients [ (29.7 ± 8. 4) ng/L, (28. 3 ± 7.9) ng/L] were significantly higher than the control group [ (24. 1 ±5. 3) ng/L, (24. 1 ±5.3) ng/L] both in acute stage and re-covery stage ( t = 3. 433, P = 0. 001 ; t = 2. 693, P = 0. 009 ). In DEACMP group, the IL - 18 level in acute stage was signifi-cantly higher than that of recovery stage ( t =2. 421, P =0. 020). Conclusion IL - 18 might be involved in the occurrence of DEACMP in a delayed immunologic way, and play a part in its development.
出处
《中国全科医学》
CAS
CSCD
北大核心
2013年第17期1949-1951,共3页
Chinese General Practice
基金
河南省教育厅自然科学研究计划项目(2011B320011)
关键词
一氧化碳中毒
缺氧缺血
脑
白细胞介素18
酶联免疫吸附测定
Carbon monoxide poisoning
Hypoxia - ischemia, brain
Interleukin - 18
Enzyme - linked immu-nosorbent assay