Platelet function and fibrinolytic activity in patients with bronchial asthma

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Tutluoglu B., Gurel Ç. , Ozdas S. , Musellim B., Erturan S., Anakkaya A., ...More

CLINICAL AND APPLIED THROMBOSIS-HEMOSTASIS, vol.11, pp.77-81, 2005 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 11
  • Publication Date: 2005
  • Doi Number: 10.1177/107602960501100109
  • Page Numbers: pp.77-81


Platelets have the capacity to release mediators with potent inflammatory or anaphylactic properties. Platelet factor-4 (PF4) and beta-thromboglobulin (BTG) are two of these mediators. On the otter hand, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) are two important mediators of fibrinolysis. Borh mediators are secreted mainly by vascular endothelium. Plasma levels of PF4, BTG, PAI-1, and tPA may show changes in chronic inflammatory diseases such as asthma. This study examined the role of thrombocytes and the function of the endothelium in asthmatic patients during an attack and during a stable phase. Eighteen patients with known allergic asthma who came to our emergency department with an asthma attack and 14 control subjects were included in the study. Blood samples were taken after starting therapy with salbutamol inhalation. Lung function tests were performed after receiving the first emergency therapy for asthma. Plasma levels of PF4, BTG, PA-1, tPA were determined before starting steroid therapy and after receiving 1 week of steroid therapy. Plasma levels of PF4 among patients with an asthma attack were significantly higher than those of controls (150.5 +/- 8.92 IU/mL vs. 92.5 +/- 7.63 IU/mL, p<0.001). A further increase in plasma PF4 levels was detected after steroid therapy (163.5 +/- 9.16 IU/mL). Plasma BTG levels of patients on admission were not statistically different from those in the control group (140.4 +/- 6.34 IU/ml, vs. 152.2 +/- 8.71 IU/mL). An increase was detected after therapy (171.6 +/- 7.27 IU/mL) and post-treatment plasma levels were statistically meaningful versus the controls. Plasma levels of tPA and PAI were statistically higher than those in controls in asthmatic patients on admission (6.01 +/- 2.72 vs. 5.4 +/- 2.3 ng/mL for tPA and 75.2 +/- 27.2 ng/mL vs. 32.7 +/- 14.3 ng/mL for PAI-1). Further increases were detected in two parameters after 1 week of therapy with steroids (tPA levels were 6.85 +/- 2.96 ng/mL and PAI-1 levels were 83.5 +/- 29.6 ng/mL). There seems to be an increased activity of platelets during an asthma attack. Elevated PAI-1 and tPA levels may also indicate the activated endothelium in asthma. Increases of plasma levels of PAI-1 and tPA after steroid therapy need further investigation because elevated PAI-1 levels enhance airway remodeling.