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Holstein, Katharina; Matysiak, Anna; Witt, Leonora; Sievers, Bianca; Beckmann, Lennart; Haddad, Munif; Renné, Thomas; Voigtlaender, Minna; Langer, Florian
Annals of hematology, 07/2020, Letnik: 99, Številka: 7Journal Article
In haemophilia, thrombin generation and fibrin deposition upon vascular injury critically depend on the tissue factor (TF)-driven coagulation pathway. TF expression by monocytes/macrophages and circulating microvesicles contributes to haemostasis, thrombosis and inflammation. Inflammation is a hallmark of blood-induced joint disease. The aim of this study is to correlate TF production by whole-blood monocytes with inflammatory markers and clinical parameters in patients with moderate-to-severe haemophilia A or B ( n = 43) in comparison to healthy males ( n = 23). Monocyte TF antigen and microvesicle-associated TF procoagulant activity (MV TF PCA) were measured immediately after blood draw (baseline) and following incubation of whole blood with buffer or lipopolysaccharide (LPS) using two-colour flow cytometry and chromogenic FXa generation assay, respectively. Patients with HIV or uncontrolled HBV/HCV infections were excluded. TF was hardly detectable and not different in baseline and buffer-treaded samples from both groups. Stimulation with LPS, however, induced monocyte TF production, with increased TF-specific mean fluorescence intensity ( P = 0.08) and MV TF PCA ( P < 0.05) in patients compared to controls. Patients also had elevated hs-CRP and IL-6 serum levels ( P < 0.001), which correlated with LPS-induced TF parameters. Further exploratory analyses revealed that the presence of systemic (low-grade) inflammation and boosted LPS-induced monocyte TF production were mainly restricted to patients with clinically controlled HBV and/or HCV infection ( n = 16), who were older and also had a significantly worse orthopaedic joint score than patients with no history of viral hepatitis ( P < 0.01). Our study delineates a previously unrecognised link between systemic inflammation and inducible monocyte TF production in patients with haemophilia A or B.
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