Transfusion · 2026
Pathogen-reduced plasma, cryoprecipitate reduced for therapeutic plasma exchange.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Tupin Florian, Mouriaux Clarisse, Hechler Beatrice, Kaastrup Kaja, Yegneswaran Subra, Corash Laurence, Mangin Pierre H
Аннотация
BACKGROUND: Therapeutic plasma exchange (TPE) for thrombotic thrombocytopenic purpura (TTP) and auto-immune disorders involves repeated patient exposure to allogenic plasma with the risk of transfusion-transmitted infection (TTI). Amotosalen-UVA Pathogen Reduction technology is FDA approved to manufacture pathogen-reduced plasma, cryoprecipitate reduced (PRPCR), a form of cryoprecipitate poor plasma (CPP) with potentially improved TPE outcomes and reduced TTI risk.
METHODS: PRPCR was manufactured from pathogen-reduced (PR) plasma. Thrombin generation, fibrinogen, Factors II, V, VII, VIII, IX, X, XI, XIII, VWF, ADAMTS13, Protein C, Protein S, α-2 plasmin inhibitor (α-2 PI), IgG, IgM, and IgA were measured. Microfluidic chamber assays at variable shear rates characterized PRPCR-mediated platelet adhesion and aggregation.
RESULTS: Compared to PR plasma, fibrinogen, Factor VIII, and VWF levels were depleted in PRPCR. Factors II, V, VII, IX, X, XI, XIII, thrombin generation, Protein C, Protein S, α-2 PI, ADAMTS13, and immunoglobulins were conserved. At low wall shear rates (300 s-1) PRPCR supported platelet adhesion. Perfusion of plasma-free blood containing PRPCR flowed over immobilized VWF binding peptide (100 μg/mL) and showed absence of platelet adhesion. Perfusion of plasma-free blood containing PRPCR flowed over immobilized collagen (200 μg/mL) at high wall shear rate (1500 s-1) and demonstrated no platelet thrombus formation.
CONCLUSIONS: PRPCR retained hemostatic capacity, anti-thrombotic proteins, and ADAMTS13, but collagen induced platelet aggregation was negligible at high shear due to depletion of functional high molecular weight VWF. PRPCR is a CPP option for TPE with reduced platelet-mediated thrombotic risk and TTI risk, but with retention of plasma hemostatic capacity and immunoglobulins.
METHODS: PRPCR was manufactured from pathogen-reduced (PR) plasma. Thrombin generation, fibrinogen, Factors II, V, VII, VIII, IX, X, XI, XIII, VWF, ADAMTS13, Protein C, Protein S, α-2 plasmin inhibitor (α-2 PI), IgG, IgM, and IgA were measured. Microfluidic chamber assays at variable shear rates characterized PRPCR-mediated platelet adhesion and aggregation.
RESULTS: Compared to PR plasma, fibrinogen, Factor VIII, and VWF levels were depleted in PRPCR. Factors II, V, VII, IX, X, XI, XIII, thrombin generation, Protein C, Protein S, α-2 PI, ADAMTS13, and immunoglobulins were conserved. At low wall shear rates (300 s-1) PRPCR supported platelet adhesion. Perfusion of plasma-free blood containing PRPCR flowed over immobilized VWF binding peptide (100 μg/mL) and showed absence of platelet adhesion. Perfusion of plasma-free blood containing PRPCR flowed over immobilized collagen (200 μg/mL) at high wall shear rate (1500 s-1) and demonstrated no platelet thrombus formation.
CONCLUSIONS: PRPCR retained hemostatic capacity, anti-thrombotic proteins, and ADAMTS13, but collagen induced platelet aggregation was negligible at high shear due to depletion of functional high molecular weight VWF. PRPCR is a CPP option for TPE with reduced platelet-mediated thrombotic risk and TTI risk, but with retention of plasma hemostatic capacity and immunoglobulins.