title: Relationship between platelet activation and cytokines in systemic inflammatory response syndrome patients with hematological malignancies.
abstract: We investigated the significance of platelet activation and platelet-derived microparticles (PMP) in 14 patients with systemic inflammatory response syndrome (SIRS) and hematological malignancies. In the phenotypic analysis of lymphocytes, there was a significant decrease of total and activated T cells after panipenem/betamipron (PAPM/BP) treatment (p<0.05). The percentages of helper/inducer T cells and suppressor/cytotoxic T cells were insignificantly decreased after PAPM/BP treatment. The number of natural killer (NK) cells of potent activity was significantly decreased after treatment (p<0.05). The levels of the cytokines interleukin (IL)-1beta, IL-6, and IL-8 in the patients were increased before treatment. IL-1beta concentrations were not changed after treatment. In contrast, the IL-6 and IL-8 levels were significantly decreased (p<0.05) after treatment, while tumor necrosis factor (TNF)-alpha and interferon gamma remained almost normal. We found an increase of soluble IL-2 receptor (sIL-2R) and soluble vascular cell adhesion molecule-1 (sVCAM-1) levels in the patients before treatment. After treatment, the sIL-2R concentrations tended to be decreased and sVCAM-1 levels showed a significant decrease (p<0.01). In contrast, soluble thrombomodulin (sTM) level did not change. Regarding the platelet activation markers, CD62P, CD63, and PMP levels in the patients were increased before treatment. CD62P and CD63 tended to be decreased after treatment, whereas PMP levels were significantly reduced from 1,056+/-103 to 762+/-64/10(4) platelets (p<0.05). Furthermore, CD62P, CD63, and PMP correlated with the levels of IL-6 and IL-8. These results suggest that activated platelets and PMP may be predictive markers in pre-disseminated intravascular coagulation and hypercytokine conditions related to SIRS.
authors.affiliation: The First Department of Internal Medicine, Kansai Medical University, Osaka, Moriguchi, Japan. fwkg4681@mb.infoweb.ne.jp
authors.forename: S
authors.initials: S
authors.lastname: Nomura
authors.forename: H
authors.initials: H
authors.lastname: Kagawa
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
authors.forename: M
authors.initials: M
authors.lastname: Nagahama
authors.forename: C
authors.initials: C
authors.lastname: Yoshimura
authors.forename: S
authors.initials: S
authors.lastname: Fukuhara
mesh_terms: D000328:Adult; D000368:Aged; D016207:Cytokines / Q000097:blood*; D005260:Female; D019337:Hematologic Neoplasms / Q000150:complications*; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000209:etiology / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology
chemical_list: D016207:Cytokines