Blood Coagulation and Asthma Exacerbation in Children

Wiparat Manuyakorn1, Dara Mairiang, Nongnuch Sirachainan

  • 1Department of Pediatrics, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.

Insights

Pediatric asthma exacerbations show increased blood coagulation markers like von Willebrand factor (vWF) and PAI-1, alongside decreased protein C. This suggests a role for blood clotting in severe asthma attacks.

Area of Science:

  • Pulmonary Medicine
  • Hematology
  • Pediatric Critical Care

Background:

  • Asthma exacerbations are linked to airway inflammation and bronchoconstriction.
  • Emerging evidence suggests activation of coagulation pathways within asthmatic airways.

Purpose of the Study:

  • To investigate systemic blood coagulation markers during asthma exacerbations in children.
  • To compare coagulation status in children with asthma during exacerbation versus stable states.

Main Methods:

  • Enrollment of pediatric patients (5-15 years) experiencing asthma exacerbation.
  • Measurement of key coagulation markers: von Willebrand factor (vWF), plasminogen activator inhibitor type-1 (PAI-1), protein C, D-dimer, prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complex (TAT), and C-reactive protein (CRP).
  • Comparison of marker levels during exacerbation and stable asthma states.

Main Results:

  • Significantly elevated median levels of vWF, PAI-1, and CRP were observed during asthma exacerbations compared to stable states (p < 0.001, p < 0.03, p < 0.015, respectively).
  • Protein C levels were significantly lower during exacerbations (p = 0.01).
  • No significant differences in D-dimer, F1 + 2, or TAT levels were found between exacerbation and stable states, though D-dimer correlated with exacerbation severity (R = 0.466, p = 0.027).

Conclusions:

  • Asthma exacerbations in children are associated with increased endothelial activation and elevated PAI-1 levels.
  • These findings highlight a potential role for systemic blood coagulation activation in the pathophysiology of asthma exacerbations.
Abstract

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