Transfusion · 2026
Retention of critical platelet hemostatic functions of amotosalen-UVA pathogen-reduced cryoprecipitated fibrinogen complex.
СтатьяНазвание и аннотация: Перевод в очереди
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Tupin Florian, Mouriaux Clarisse, Gatmaitan Michelle, Kaastrup Kaja, Yegneswaran Subramanian, Corash Laurence, Mangin Pierre H
Аннотация
BACKGROUND: Cryoprecipitate Anti-Haemophilic Factor (CRYO-AHF) is enriched for fibrinogen, VWF, FVIII, FXIII and fibronectin, but has short post-thaw expiration due to risk of transfusion-transmitted infection (TTI) limiting availability for rapid treatment. Amotosalen-UVA pathogen reduction treatment (A-PRT) to manufacture pathogen-reduced cryoprecipitated fibrinogen complex (PRCFC) allows 5-day post-thaw expiration, reduces TTI risk, and facilitates early treatment of hemorrhage.
AIMS: To evaluate adhesive protein functions in PRCFC and lyophilized PRCFC (LIFC).
METHODS: CRYO-AHF, PRCFC, LIFC, and commercial fibrinogen concentrate (CFC) were evaluated for platelet adhesion and aggregation in variable shear microfluidic assays.
RESULTS: Platelet adhesion kinetics to CRYO-AHF, PRCFC, and LIFC, under low shear flow (300 s-1) were conserved. Platelet adhesion to CFC at low shear was reduced due to absence of functional VWF. αIIbβ3 integrin/fibrinogen and GPIb-IX-V/VWF platelet interactions with CRYO-AHF, PRCFC, and LIFC were confirmed by abciximab and caplacizumab inhibition, respectively. All fibrinogen sources promoted efficient platelet aggregation. Perfusion of reconstituted plasma-free blood (RBC + platelets + various cryoprecipitates) on immobilized VWF-binding peptide (1500 s-1) showed impaired platelet adhesion to CFC compared to PRCFC and CRYO-AHF. Perfusion of reconstituted blood on collagen (3000 s-1) indicated CRYO-AHF, PRCFC and LIFC formed thrombi to similar levels. Platelets treated with A-PRT combined with PRCFC or LIFC retained similar activity to CRYO-AHF for platelet aggregation and thrombus formation on collagen.
CONCLUSIONS: PRCFC and LIFC retained critical hemostatic functions of VWF and fibrinogen to support platelet adhesion and aggregation during physiologic shear. PRCFC and LIFC represent a therapeutic option for early treatment of massive hemorrhage.
AIMS: To evaluate adhesive protein functions in PRCFC and lyophilized PRCFC (LIFC).
METHODS: CRYO-AHF, PRCFC, LIFC, and commercial fibrinogen concentrate (CFC) were evaluated for platelet adhesion and aggregation in variable shear microfluidic assays.
RESULTS: Platelet adhesion kinetics to CRYO-AHF, PRCFC, and LIFC, under low shear flow (300 s-1) were conserved. Platelet adhesion to CFC at low shear was reduced due to absence of functional VWF. αIIbβ3 integrin/fibrinogen and GPIb-IX-V/VWF platelet interactions with CRYO-AHF, PRCFC, and LIFC were confirmed by abciximab and caplacizumab inhibition, respectively. All fibrinogen sources promoted efficient platelet aggregation. Perfusion of reconstituted plasma-free blood (RBC + platelets + various cryoprecipitates) on immobilized VWF-binding peptide (1500 s-1) showed impaired platelet adhesion to CFC compared to PRCFC and CRYO-AHF. Perfusion of reconstituted blood on collagen (3000 s-1) indicated CRYO-AHF, PRCFC and LIFC formed thrombi to similar levels. Platelets treated with A-PRT combined with PRCFC or LIFC retained similar activity to CRYO-AHF for platelet aggregation and thrombus formation on collagen.
CONCLUSIONS: PRCFC and LIFC retained critical hemostatic functions of VWF and fibrinogen to support platelet adhesion and aggregation during physiologic shear. PRCFC and LIFC represent a therapeutic option for early treatment of massive hemorrhage.