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Increased factor XI but not factor XII is associated with enhanced inflammation and impaired fibrin clot properties in patients with eosinophilic granulomatosis with polyangiitis


1, 2, 3, 4

 

  1. Krakow Centre for Medical Research and Technologies, John Paul II Hospital, Krakow, and Department of Thromboembolic Diseases Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
  2. Krakow Centre for Medical Research and Technologies, John Paul II Hospital, Krakow, and Department of Thromboembolic Diseases Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
  3. 2nd Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
  4. Krakow Centre for Medical Research and Technologies, John Paul II Hospital, Krakow, and Department of Thromboembolic Diseases Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland. mmundas@cyf-kr.edu.pl

CER17008
2024 Vol.42, N°4
PI 0822, PF 0827
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PMID: 38079326 [PubMed]

Received: 21/07/2023
Accepted : 02/10/2023
In Press: 04/12/2023
Published: 29/04/2024

Abstract

OBJECTIVES:
In eosinophilic granulomatosis with polyangiitis (EGPA) a prothrombotic state, including formation of denser fibrin networks with reduced lysability has been observed. Little is known about the intrinsic pathway in EGPA. We investigated whether coagulation factors (F)XI and FXII are associated with eosinophil-driven prothrombotic state.
METHODS:
In 34 consecutive EGPA patients with remission we assessed FXI and FXII levels along with plasma fibrin clot permeability (Ks), fibrin clot morphology using scanning electron microscopy, and efficiency of fibrinolysis, expressed as lysis time (t50%) and maximum rate of increase in D-dimer levels (D-Drate).
RESULTS:
Increased FXI level (>130%, the upper reference limit) was found in 8 (23.5%) patients. Compared to patients with FXI levels ≤130%, those with increased FXI had higher eosinophil count (+365%) and reduced percentage of neutrophils (-20.4%), along with reduced Ks (-20.5%). In patients with FXI>130% clots were composed of thinner fibrin fibers (-17.5%). FXI was not associated with C-reactive protein and fibrinogen levels or anti-neutrophil cytoplasmic antibodies titers. There were no correlations between FXI and FXII levels as well as between FXII and eosinophil count (all p>0.05).
CONCLUSIONS:
To our knowledge, this study is the first to show association between FXI and a prothrombotic state in EGPA. Given clinical trials on FXI inhibition as an antithrombotic option, our findings suggest that this therapeutic approach could be useful in diseases with hypereosinophilia.

DOI: https://doi.org/10.55563/clinexprheumatol/kzi1u4

Rheumatology Article