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Relationship between platelet activation and cytokines in systemic inflammatory response syndrome patients with

S Nomura1, H Kagawa, Y Ozaki

  • 1The First Department of Internal Medicine, Kansai Medical University, Osaka, Moriguchi, Japan. fwkg4681@mb.infoweb.ne.jp

Thrombosis Research
|October 9, 1999
PubMed

Insights

Activated platelets and platelet-derived microparticles (PMP) may predict pre-disseminated intravascular coagulation in patients with systemic inflammatory response syndrome (SIRS). Treatment with panipenem/betamipron (PAPM/BP) reduced PMP levels and inflammatory cytokines.

Area of Science:

  • Hematology
  • Immunology
  • Critical Care Medicine

Background:

  • Systemic inflammatory response syndrome (SIRS) involves complex immune dysregulation.
  • Platelet activation and platelet-derived microparticles (PMP) are implicated in inflammatory conditions.
  • Hematological malignancies can exacerbate SIRS and associated complications.

Purpose of the Study:

  • To investigate the role of platelet activation and PMP in SIRS patients with hematological malignancies.
  • To assess the impact of panipenem/betamipron (PAPM/BP) treatment on immune markers and platelet activation.

Main Methods:

  • Phenotypic analysis of lymphocyte subsets (T cells, NK cells).
  • Measurement of serum cytokine levels (IL-1beta, IL-6, IL-8, TNF-alpha, IFN-gamma).
  • Quantification of soluble receptors (sIL-2R, sVCAM-1, sTM) and platelet activation markers (CD62P, CD63, PMP).

Main Results:

  • PAPM/BP treatment significantly decreased total and activated T cells, and NK cells.
  • IL-6 and IL-8 levels were significantly reduced post-treatment, while IL-1beta remained unchanged.
  • Platelet activation markers (CD62P, CD63) and PMP levels significantly decreased after PAPM/BP treatment and correlated with IL-6 and IL-8.

Conclusions:

  • Activated platelets and PMP may serve as predictive markers for pre-disseminated intravascular coagulation in SIRS.
  • PAPM/BP treatment effectively modulates inflammatory cytokine profiles and reduces platelet activation markers.
  • These findings highlight the potential of targeting platelet activation in managing SIRS-related complications.

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