interleukin-8 and Purpura

Plasma levels of interleukin 12 (IL-12), a cytokine consisting of two different polypeptide subunits (p40 and p35), were measured together with interferon gamma (IFN-gamma) and other cytokines in 46 children with septic shock and purpura. The median (range) plasma IL-12 p40 level on admission was 457 (244-2677) pg/ml in non-survivors vs 189 (< 40-521) pg/ml in survivors (P = < 0.001). IL-12 p70 levels were elevated in only nine patients. IL-12 p40 plasma levels were positively correlated with tumour necrosis factor alpha (TNF-alpha), IL-6, IL-8, IL-10 and PRISM-score, whereas they were negatively correlated with C-reactive protein (CRP), whole blood cell (WBC) and serum glucose levels. Twelve (29%) of the patients had detectable levels of IFN-gamma. Thus, circulating levels of IL-12 p40 and to a lesser extent those of IL-12 p70, are elevated in children with septic shock and purpura, and correlate with severity of disease and outcome.

Topics: Adolescent; Blood Glucose; C-Reactive Protein; Child; Child, Preschool; Female; Humans; Infant; Interferon-gamma; Interleukin-10; Interleukin-12; Interleukin-6; Interleukin-8; Male; Purpura; Severity of Illness Index; Shock, Septic; Tumor Necrosis Factor-alpha

Proinflammatory cytokines (tumor necrosis factor [TNF]-alpha and interleukin [IL]-6 and -8), counterinflammatory compounds (IL-10 and soluble TNF receptors p55 and p75 [sTNFR-55 and -75]), and hemostatic parameters were determined in 38 patients with meningococcal septic shock. Eleven patients (29%) died. Serum levels of pro- and counterinflammatory compounds and plasma levels of plasminogen activator inhibitor (PAI)-1 were significantly higher in nonsurvivors. The interval between appearance of petechiae and blood sampling was shorter in nonsurvivors than in survivors (3.6 +/- 2.4 vs. 6.1 +/- 3.3 h; P = 0.4). This interval correlated strongly with the levels of TNF-alpha, IL-6, -8, and -10, sTNFR-55 and -75, and PAI-1. However, with the exception of PAI-1, differences between concentrations of these mediators disappeared after adjustment for the interval. PAI-1 levels correlated with TNF-alpha concentrations (r = .75; P < .001) and were 1.9 (P = .01) times higher in nonsurvivors at a similar TNF-alpha concentration. Thus, an increased PAI-1 response to TNF-alpha may be associated with fatality, probably because of polymorphism of the PAI-1 gene.

Topics: Adolescent; Antigens, CD; Blood Coagulation; Child; Child, Preschool; Cytokines; Female; Fibrinolysis; Humans; Infant; Interleukin-10; Interleukin-6; Interleukin-8; Male; Meningococcal Infections; Plasminogen Activator Inhibitor 1; Prospective Studies; Purpura; Receptors, Tumor Necrosis Factor; Receptors, Tumor Necrosis Factor, Type I; Receptors, Tumor Necrosis Factor, Type II; Shock, Septic; Tumor Necrosis Factor-alpha

The participation of apoptotic cell death of neutrophils in the development of skin lesions of patients with anaphylactoid purpura was examined by the in situ specific labeling of fragmented DNA. In the early stage of the skin lesions, there were few positively stained nuclei in infiltrating cells. The number of positive cells increased markedly in the fully developed stage of the lesions. A number of neutrophils were stained positively. Finally, a few fragmented nuclei were still positive in the late stage of the lesions. It was therefore suggested that fragmentation of neutrophils in the skin lesions from the patients might be due to apoptosis. Inducible nitric oxide synthase and nitrotyrosine were detected in infiltrates, and interleukin-8 was also detected in vascular endothelial cells in those skin lesions. The roles of nitric oxide and interleukin-8 in the apoptosis of neutrophils are discussed.

Topics: Adolescent; Adult; Aged; Anaphylaxis; Apoptosis; Cell Nucleus; Child; Child, Preschool; DNA Fragmentation; Endothelium, Vascular; Female; Humans; Interleukin-8; Leukocyte Count; Male; Middle Aged; Neutrophils; Nitric Oxide Synthase; Purpura; Skin Diseases; Tyrosine

Topics: Altitude Sickness; Angiogenesis Inducing Agents; Animals; Brain Edema; Cytokines; Endothelial Growth Factors; Endothelium, Vascular; Fibroblast Growth Factor 2; Humans; Interferon-alpha; Interleukin-2; Interleukin-8; Lignin; Lymphokines; Macrophage Activation; Neovascularization, Pathologic; Purpura; Retinal Hemorrhage; Transforming Growth Factor beta; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factors