Evaluation of the Atellica COAG 360 coagulation analyzer in a specialized coagulation laboratory

Strandberg, Karin; Augustsson, Cecilia

doi:10.1002/jcla.24276

Cited by 3 publications

(3 citation statements)

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Section: Methodsmentioning

confidence: 99%

“…Plasma samples with or without concizumab were analysed in triplicates at the Malmö coagulation laboratory (University and Regional Laboratories Region Skåne, Malmö, Sweden) on an Atellica COAG 360 analyser (Siemens Healthineers) using commercially available diagnostic kits and calibrators according to instructions provided by the manufacturer. 15 The PT Quick and PT Owren assays were used to assess normal human plasma (NHP) with and without concizumab. assay for HA with inhibitors (HAwI) plasma added to 16,000 ng/mL concizumab.…”

Section: Coagulation Assaysmentioning

confidence: 99%

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Minimal interference of concizumab with standard clinical coagulation laboratory assays – An in vitro study

Augustsson,

Strandberg,

Kjalke

2024

Haemophilia

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IntroductionNon‐factor replacement therapies are emerging as prophylactic treatment options in haemophilia A or B (HA/HB) with and without inhibitors. Concizumab is an anti‐tissue factor pathway inhibitor (TFPI) monoclonal antibody preventing factor (F)Xa inhibition and enhancing thrombin generation. Based on experience with other non‐factor therapies and extended half‐life products, there is a focus on potential interference with common clinical coagulation assays used to monitor patients treated with concizumab.AimTo evaluate the impact of concizumab on standard clinical coagulation assays.MethodsPlasma samples (normal, HA/HB with/without inhibitors) in the presence/absence of added concizumab (250–16,000 ng/mL) were analysed in clinical assays including activated partial thromboplastin time (aPTT), prothrombin time (PT), FVIII and FIX one‐stage clot and chromogenic substrate assay, assays for detecting FVIII or FIX inhibitors and other assays for coagulation factors.ResultsConcizumab did not impact PT assays, but resulted in a small shortening of aPTT (up to 5 s in haemophilia plasma and 0.4 s in normal plasma). Concizumab had no, or only a minor impact on FVIII and FIX activity assays or Bethesda inhibitor assays. FXI and FXII activity in normal plasma, as measured by single factor aPTT‐based assay, was significantly increased in the presence of concizumab (+11% each). This was also the case for FVII and FX measured by PT‐based assays using plasma with 25% of FVII or FX (+64% and +22%, respectively).ConclusionThe presence of concizumab did not, or only slightly, influence the outcome of standard clinical coagulation assays relevant for HA and HB.

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Section: Methodsmentioning

confidence: 99%

Section: Coagulation Assaysmentioning

confidence: 99%

Minimal interference of concizumab with standard clinical coagulation laboratory assays – An in vitro study

Augustsson,

Strandberg,

Kjalke

2024

Haemophilia

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“…Coagulation parameters were assayed on an automated analyzer, Atellica COAG 360 (Siemens Healthineers, Erlangen, Germany) with reagents and methods explained previously. 6 LA was measured using Siemens dilute Russell viper venom time (dRVVT) reagents. Mixing studies were performed using hepes-buffered normal plasma (Precision Biologic, Dartmouth, Canada).…”

Section: Investigationsmentioning

confidence: 99%

A nonneutralizing antibody as cause of prothrombin deficiency in a patient with follicular lymphoma

Augustsson,

Taxbro,

Strandberg

et al. 2024

Clinical Case Reports

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Key Clinical MessageAcquired inhibitors of blood coagulation are rare but of clinical importance. Prothrombin is a vitamin K‐dependent protein, and acquired antibodies toward prothrombin are often associated with the presence of lupus anticoagulant. We describe a previously healthy 70‐year‐old man presenting with both hemorrhage and thrombosis as well as a prolonged prothrombin time. At arrival at the hospital, he was diagnosed with deep venous thrombosis, and an enlarged lymph node in the left groin was noted (revealed as follicular lymphoma grade 1 by biopsy). Prothrombin activity and antibody titer were followed for 5 months with 15 sampling time points to monitor the treatment outcome of the patient. Diagnostic work‐up identified prothrombin deficiency as cause of bleeding. A nonneutralizing calcium‐dependent antiprothrombin antibody was found, suspected to increase the clearance of prothrombin, which has previously only occasionally been reported. Lupus anticoagulant was ruled out and thrombosis was judged to be caused by a combination of malignant disease and stagnant venous flow following enlarged lymph nodes in the groin. This report illustrates how investigation of prolonged global coagulation tests, triggered the diagnosis of a rare but critical condition, immune‐mediated prothrombin deficiency. The diagnosis is challenging and involves proper differential diagnosis.

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