Thrombosis research · 2025
Coagulopathy in Dabie bandavirus infection is related to endogenous heparinoids release and mast cells activation.
СтатьяНаблюдательное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Wang Bin, Bai Huan, Yuan Peihong, Li Dengju, Tang Ning
Аннотация
BACKGROUND: The prolonged activated partial thromboplastin time (APTT) and thrombin time in patients infected with Dabie bandavirus (DBV) have been recognized to be poor prognostic indicators and attributed to a heparin-like effect rather than a decrease in coagulation factor levels.
OBJECTIVES: To clarify the correlation between endogenous heparinoids and coagulopathy in patients infected with DBV, and their possible sources.
METHODS: One hundred and twenty-one consecutive patients with confirmed DBV infection were enrolled in this prospective, single-center, observational study. Routine coagulation parameters, levels of syndecan-1, heparan sulphate (HS) and mast cell tryptase (MCT), and thrombin generation (TG) profile of these patients on admission were detected, and their outcomes were recorded.
RESULTS: In the enrolled patients, prolonged APTT was associated with lower TG and higher levels of syndecan-1, HS and MCT (P < 0.05). There was a strong correlation between HS and MCT (r = 0.879, P < 0.001) and a weak correlation between HS and syndecan-1 (r = 0.252, P = 0.006). With the increase of viral load, both of the MCT and HS levels were significantly elevated, and levels of endogenous thrombin potential (ETP) was significantly decreased (P < 0.05). Age, ETP and MCT were independent predictors for 28-day mortality of patients infected with DBV (P < 0.05).
CONCLUSIONS: The coagulopathy in SFTS patients were related to decreased TG, endogenous heparinoids release and mast cells activation caused by DBV infection. Further study is needed to confirm whether blocking mast cells activation has the potential to improve their coagulopathy and prognosis.
OBJECTIVES: To clarify the correlation between endogenous heparinoids and coagulopathy in patients infected with DBV, and their possible sources.
METHODS: One hundred and twenty-one consecutive patients with confirmed DBV infection were enrolled in this prospective, single-center, observational study. Routine coagulation parameters, levels of syndecan-1, heparan sulphate (HS) and mast cell tryptase (MCT), and thrombin generation (TG) profile of these patients on admission were detected, and their outcomes were recorded.
RESULTS: In the enrolled patients, prolonged APTT was associated with lower TG and higher levels of syndecan-1, HS and MCT (P < 0.05). There was a strong correlation between HS and MCT (r = 0.879, P < 0.001) and a weak correlation between HS and syndecan-1 (r = 0.252, P = 0.006). With the increase of viral load, both of the MCT and HS levels were significantly elevated, and levels of endogenous thrombin potential (ETP) was significantly decreased (P < 0.05). Age, ETP and MCT were independent predictors for 28-day mortality of patients infected with DBV (P < 0.05).
CONCLUSIONS: The coagulopathy in SFTS patients were related to decreased TG, endogenous heparinoids release and mast cells activation caused by DBV infection. Further study is needed to confirm whether blocking mast cells activation has the potential to improve their coagulopathy and prognosis.