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Updated: Jan 28, 2026

Bronchial Thermoplasty: A Novel Therapeutic Approach to Severe Asthma
Published on: November 4, 2010
好酸球性喘息における鼻ポリープの有無による全身性凝固および線溶系の変化
Nur Aleyna Yetkin1, İnsu Yılmaz1, Merve Özel Yetkin2
1Department of Pulmonology, Faculty of Medicine, Erciyes University, Kayseri, Turkiye.
Abstract:
ObjectiveAsthma with nasal polyps constitutes a distinct eosinophilic phenotype marked by inflammation and altered coagulation. This study aimed to compare systemic coagulation and fibrinolytic profiles in eosinophilic asthma with and without nasal polyps.MethodsSeventy-two participants were enrolled: eosinophilic asthma with nasal polyps (n = 28), eosinophilic asthma without nasal polyps (n = 22), and age-, sex-, and body mass index-matched healthy controls (n = 22). To minimize confounding, participants were devoid of chronic comorbidities or medications affecting coagulation. Asthma patients were stable on maintenance corticosteroids. Blood eosinophil counts and hemostatic biomarkers [tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), α2-antiplasmin, D-dimer, fibrinogen, activated partial thromboplastin time (aPTT), international normalized ratio (INR), Factors V and VIII, and thrombin-antithrombin III complex (TAT)] were measured.ResultsCompared with controls, non-polyp asthma showed higher tPA and fibrinogen levels, whereas the nasal polyp subgroup had shorter aPTT and higher PAI-1. TAT levels were significantly lower in the nasal polyp subgroup than in the non-polyp subgroup (p < 0.05). In the overall asthma group, eosinophils correlated negatively with Factor V and PAI-1. Distinctly, the nasal polyp subgroup showed the lowest aPTT and Factor VIII levels, with eosinophils positively correlating with Factor VIII (r = 0.638, p < 0.001).ConclusionEosinophilic asthma with nasal polyps is characterized by distinct hemostatic alterations, including shorter aPTT, higher PAI-1, and lower TAT levels compared to the non-polyp phenotype. These findings suggest a specific link between type 2 inflammation and systemic hemostasis regulation in this subgroup.
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