Cytokine response to diabetic ketoacidosis and its treatment

被引:113
|
作者
Hoffman, WH
Burek, CL
Waller, JL
Fisher, LE
Khichi, M
Mellick, LB
机构
[1] Med Coll Georgia, Dept Pediat, Sect Pediat Endocrinol, Augusta, GA 30912 USA
[2] Johns Hopkins Univ, Dept Pathol, Baltimore, MD 21287 USA
[3] Med Coll Georgia, Off Biostat, Augusta, GA 30912 USA
[4] Med Coll Georgia, Dept Pediat, Pediat Crit Care Sect, Augusta, GA 30912 USA
[5] Med Coll Georgia, Dept Emergency Med, Augusta, GA 30912 USA
关键词
cellular activation; cytokines; diabetic ketoacidosis;
D O I
10.1016/S1521-6616(03)00144-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The objectives of this study were to monitor plasma cytokines as markers of cellular activation and as potential markers for the progression of the acute complications of diabetic ketoacidosis (DKA). Blood samples were obtained prior to, during and after treatment of severe DKA (pH < 7.2) in six children and adolescents. Plasma IL-10, IL-1beta, TNF-alpha, IL-6, IL-8 and IL-2 cytokine levels were assayed by ELISA at each of the time points. Prior to treatment, elevations of multiple cytokines were found, the highest being IL-10. Treatment of DKA resulted in a significant decrease of IL-10 at 6-8 h (p = 0.0062), and further increases in the inflammatory cytokines at 6-8 h and/or 24 h vs 120 h (baseline): IL-1beta (p = .0048); TNF-alpha (p = .0188) and IL-8 (p = .0048). This study strengthens the hypothesis that the metabolic crisis of DKA, and its treatment, have differential effects on cellular activation and cytokine release. The time frame for the increase in inflammatory cytokines correlates with the reported progression of subclinical brain edema, interstitial pulmonary edema and the development of clinical brain edema. (C) 2003 Elsevier Science (USA). All rights reserved.
引用
收藏
页码:175 / 181
页数:7
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