Evaluation of DOAC Filter, a new device to remove direct oral anticoagulants from plasma samples.

INTRODUCTION: Directs oral anticoagulants (DOACs) can interfere with coagulation assays, especially in thrombophilia workup. To avoid these interferences, a new device, DOAC Filter, allows the removal of DOACs from citrated plasma. This study aims to confirm that DOAC Filter efficiently removes DOACs and to ascertain that coagulation assays are not impacted by filtration. METHODS: Directs oral anticoagulants Filter (Diagnostica Stago, France) is a filtration cartridge in which DOAC molecules are trapped by noncovalent binding, while plasma is filtered through a solid phase. Normal pool plasma (NPP) spiked with DOACs up to 300 ng/mL, with dabigatran etexilate (n = 27), rivaroxaban (n = 35), apixaban (n = 33), and edoxaban (n = 27) or 120 ng/mL for betrixaban (n = 4), and 18 plasma's samples from DOAC-treated patients were used to assess efficacy. The potential impact of DOAC Filter on coagulation assays was evaluated with NPP and plasma's samples from positive and negative lupus anticoagulant (LA) patients. RESULTS: Directs oral anticoagulants concentrations measured after filtration were below the limit of detection (LoD) of DOAC-specific assays for all plasmas tested, except for one apixaban plasma sample, with postfiltration concentration slightly higher than anti-Xa assay LoD (25.1 ng/mL). Coagulation assays results varied between -4 and +8% after filtration and between -6 and +8% for LA plasmas. Such limited variations are not expected to have any clinical impact. CONCLUSION: Directs oral anticoagulants Filter efficiently removes DOACs from plasma and achieves concentrations below DOAC-specific assays LoD, except in the case of one apixaban sample. The integrity of plasma is respected, and the cartridge seems not to impact LA diagnosis.

Factor VII Deficiency: From Basics to Clinical Laboratory Diagnosis and Patient Management.

Factor VII (FVII) deficiency is a rare inheritable bleeding disorder affecting 1/500 000 individuals. Clinical manifestations are heterogeneous, from asymptomatic to severe and potentially fatal bleeding. These clinical manifestations do not correlate well with FVII plasma levels. For this reason, FVII-deficient patient management during surgery or for long-term prophylaxis remains challenging. Laboratory testing for FVII activity is, however, the first-line method for FVII deficiency diagnosis and is helpful for managing patients in combination with clinical history. Additional testing consists of FVII immunoassay and genetic testing. Genetic abnormalities on the FVII gene are heterogeneous and can translate into quantitative or qualitative defects. Some of the latter can react differently with different thromboplastins; this can be misleading for the laboratory as no consensus exists at present on an FVII deficiency diagnosis methodology. Indeed, no single test is able to predict accurately the bleeding risk. This review provides a broad picture of inherited and acquired FVII deficiency with a particular focus on laboratory diagnosis.