Assessment of the pro-thrombotic state in patients with bronchial asthma

Abstract

Inflammation has a central role in the pathophysiology of asthma. As noted in the definition of asthma, airway inflammation involves an interaction of many cell types and multiple mediators with the airways that eventually results in the characteristic pathophysiological features of the disease: bronchial inflammation and airflow limitation that result in recurrent episodes of cough, wheeze, and shortness of breath. In recent years, our understanding of the involvement of coagulation and anticoagulant pathways, the fibrinolytic system, and platelets in the pathophysiology of asthma has increased considerably. Asthma is associated with a procoagulant state in the bronchoalveolar space, further aggravated by impaired local activities of the anticoagulant protein C system and fibrinolysis. Protease-activated receptors have been implicated as the molecular link between coagulation and allergic inflammation in asthma. Patients with asthma show evidence of up-regulation of pulmonary coagulation via an increase in TF activity. Although limited activation of coagulation can assist in epithelial repair, pulmonary coagulation resulting from a crosstalk between epithelial, endothelial, and inflammatory cells can have a major impact on asthma pathophysiology