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Bcs xp coagulometer

Manufactured by Siemens
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Sourced in Hungary, Germany

The BCS-XP coagulometer is a laboratory instrument used for the analysis of blood coagulation. It measures the time it takes for a blood sample to clot, providing information about the patient's blood clotting ability. The BCS-XP performs automated coagulation testing, analyzing the sample and generating results.

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Lab products found in correlation

N antiserum to human antithrombin 3, by Siemens (2 mentions) Enzygnost f1 2, by Siemens (1 mentions) Liaphen fibrinogen, by Hyphen Biomed (1 mentions) Hemoclot thrombin time, by Hyphen Biomed (1 mentions) Multifibren u, by Siemens (1 mentions) Innovin reagent, by Siemens (1 mentions) Multifibren u reagent, by Siemens (1 mentions) Bnii instrument, by Siemens (1 mentions) Cobas 6000 system, by Roche (1 mentions)

7 protocols using bcs xp coagulometer

1

Novel Antithrombin Mutations and Thrombosis

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Between January 2016 and December 2021, nine novel AT mutations were detected in our center. Clinical data were collected retrospectively from the patients. Information on the type and date of the first thrombotic event were obtained from medical records. Inherited thrombophilia (protein C and S deficiencies, APC resistance, dysfibrinogenemia) was investigated by routine laboratory methods with a BCS-XP coagulometer (Siemens, Marburg, Germany). For diagnosing AT deficiency hc-anti-FXa and p-anti-FXa (Labexpert Antithrombin H + P, Labexpert Ltd., Debrecen, Hungary; reference intervals 80–120% and 82–118%, respectively) were detected with a Siemens BCS-XP coagulometer. AT antigen was measured by immunonephelometry (Siemens, N Antiserum to Human Antithrombin III, reference interval 0.19–0.31 g/L).
Kállai J., Gindele R., Pénzes-Daku K., Balogh G., Bogáti R., Bécsi B., Katona É., Oláh Z., Ilonczai P., Boda Z., Róna-Tas Á., Nemes L., Marton I, & Bereczky Z. (2024). Clinical and Molecular Characterization of Nine Novel Antithrombin Mutations. International Journal of Molecular Sciences, 25(5), 2893.
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2

Coagulation Factor Quantification Protocol

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Citrated blood samples were centrifuged to isolate plasma and frozen in aliquots at −70 °C, if not tested immediately. Plasma levels of functional Fg were measured by the Clauss method using the HemosIL Fibrinogen activity (IL QFA Thrombin) on an ACL Top Analyzer or Multifibren U (Siemens, Marburg, Germany) on a BCS® XP coagulometer. Levels of total Fg antigen were measured by a latex immunoassay (Liaphen Fibrinogen, Hyphen BioMed, Neuville sur Oise, France) on a BCS® XP coagulometer (Siemens, Germany).
Prothrombin time (PT; Owren method, Axis-Shield, Oslo, Norway), activated partial thromboplastin time (APTT; Actin FSL reagent) and thrombin time (Hemoclot Thrombin Time, Hyphen BioMed, France) were assessed in citrated plasma on an ACL Top Analyzer analyzer. Prothrombin fragments (F1+2) were measured by an enzyme immunoassay (Enzygnost® F1+2, monoclonal, Siemens Healthcare Diagnostics, Marburg, Germany.
Szanto T., Lassila R., Lemponen M., Lehtinen E., Neerman-Arbez M, & Casini A. (2021). Whole Blood Thromboelastometry by ROTEM and Thrombin Generation by Genesia According to the Genotype and Clinical Phenotype in Congenital Fibrinogen Disorders. International Journal of Molecular Sciences, 22(5), 2286.
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3

Coagulation Assays for FXI Activity

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Medpace Reference Laboratories (Cincinnati, OH) performed the routine clinical laboratory analyses. Coagulation assays, which were performed by Hemostasis Reference Laboratory Inc. (Hamilton, ON, Canada), included measurement of FXI activity levels using a 1-stage aPTT-based clotting assay on a BCS-XP coagulometer, quantification of FXI antigen levels using enzyme-linked immunosorbent assay, and determination of prothrombin time (PT) and INR using Innovin reagent (Siemens Healthcare Diagnostics, Deerfield, IL) on the BCS-XP coagulometer.
Walsh M., Bethune C., Smyth A., Tyrwhitt J., Jung S.W., Yu R.Z., Wang Y., Geary R.S., Weitz J, & Bhanot S. (2021). Phase 2 Study of the Factor XI Antisense Inhibitor IONIS-FXIRx in Patients With ESRD. Kidney International Reports, 7(2), 200-209.
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4

Genetic Study of Antithrombin Deficiency

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Between January 2007 and August 2020, a total of 329 non-related AT deficient patients (index patients) and their family members (total n = 446) were diagnosed at the Clinical Center of the University of Debrecen. Blood samples were collected into 0.109 M citrated vacutainer tubes (Beckton Dickinson, Franklin Lakes, NJ, USA) and plasma samples were stored at −80 °C until analysis. AT activity was determined by chromogenic assay based on factor Xa-inhibition in the presence of heparin (Innovance AT, Siemens, Marburg, Germany) and also in the absence of heparin (progressive AT activity, measured by Labexpert Antithrombin H+P, Labexpert Ltd., Debrecen, Hungary) according to the manufacturers’ instructions on Siemens BCS-XP coagulometer. The AT antigen (AT:Ag) concentration was measured by immunonephelometry (Siemens, N Antiserum to Human Antithrombin III).
Gindele R., Pénzes-Daku K., Balogh G., Kállai J., Bogáti R., Bécsi B., Erdődi F., Katona É, & Bereczky Z. (2021). Investigation of the Differences in Antithrombin to Heparin Binding among Antithrombin Budapest 3, Basel, and Padua Mutations by Biochemical and In Silico Methods. Biomolecules, 11(4), 544.
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5

Fibrinogen Dynamics during Cardiac Surgery

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Data were stored on a departmental research platform (Labkey, Seattle, WA, USA). Fibrinogen was measured using the Clauss method (Clauss fibrinogen, C-FIB) and using fibrin-based thrombo-elastometry (FIBTEM-MCF assay, ROTEM®, TEM International GmbH, Munich, Germany). Whole blood was serially sampled in citrated plastic containers (Monovette, Sarstedt AG, Nümbrecht, Germany) at defined time points as follows: baseline level (pre-CPB value) before anesthesia induction; AodX, five minutes after aortic declamping; Protamine, five minutes after protamine administration; and T1, T2, T3, T4, T6, T8, T12, T18, and T24 at 1, 2, 3, 4, 6, 8, 12, 18, and 24 hours after protamine administration, respectively. All samples were immediately sent to the laboratory, pre-heated to 37°C, and analyzed within 15 minutes. C-FIB was determined using the Multifibren U reagent (Dade Behring, Liederbach, Germany) on a BCS-XP coagulometer (Siemens Healthcare, Marburg, Germany). For FIBTEM, tissue factor was used as the activator, and cytochalasin D was added for platelet inhibition. To minimize user-dependent variability, all coagulation and viscoelastic testing was performed by the hemostasis laboratory.
Erdoes G., Dietrich W., Stucki M.P., Merz T.M., Angelillo-Scherrer A., Nagler M., Carrel T, & Eberle B. (2018). Short-term recovery pattern of plasma fibrinogen after cardiac surgery: A prospective observational study. PLoS ONE, 13(8), e0201647.
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6

Comprehensive Thrombophilia Screening Protocol

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The decision for thrombophilia testing followed international recommendations.20 In particular, patients with VTE were tested if they fulfilled any of the following criteria: (1) age (≤60 years), (2) strong family history of VTE, (3) VTE associated with weak provoking factors at a young age, (4) recurrent VTE, and (5) VTE in an unusual site. All enrolled patients were screened for AT, PC, PS deficiencies, FVL, and PT20210A mutations, as well as rare inherited thrombophilias (pseudo‐homozygous FVL and AT resistance). AT, PC, PS activity, and antigen levels as well as activated protein C resistance were measured as previously reported.9, 21 The criteria used for the classification of AT, PC, and PS defects were in line with the current literature.6, 22 Reduced levels of anticoagulant factors (activity and/or antigen) were confirmed in 2 consecutive determinations and in at least 1 first‐degree relative. FVL and PT20210A were detected by GeneXpert HemosIL® F5 and F2 assay (Cepheid, Sunnyvale, CA, USA).23 We measured the activity of factors II, V, VIII, and IX on a BCS®XP coagulometer (Siemens) with the specific factor‐deficient plasma (Siemens). AT resistance (Prothrombin Padua 2 mutation [c.1786C>T; p.Arg596Trp]) was previously detected by direct sequencing of exon 14 of F2 gene.9
Campello E., Spiezia L., Simion C., Tormene D., Camporese G., Dalla Valle F., Poretto A., Bulato C., Gavasso S., Radu C.M, & Simioni P. (2020). Direct Oral Anticoagulants in Patients With Inherited Thrombophilia and Venous Thromboembolism: A Prospective Cohort Study. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 9(23), e018917.
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7

Automated Clinical Laboratory Analyses

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This article is protected by copyright. All rights reserved.
(Alifax). Complement component 3 (C3) and 4 (C4) were analyzed on BNII instrument (Siemens Healthcare) that uses the nephelometric technology. Prothrombin time and plasma fibrinogen concentration were analyzed on BCS-XP coagulometer (Siemens Healthcare).
Albumin/globulin ratio was determined using the CAPILLARYS electrophoresis instrument (Sebia).
Lipid profile analytes including total cholesterol, high density lipoproteins (HDL) and triglycerides were determined by specific colorimetric enzymatic methods on Cobas 6000 system (Roche Diagnostic). Urine pH and urinary specific gravity values were determined by using Atlas instrument (Siemens Healthcare), and urine sediment was analyzed on Iris instrument (Beckman Coulter). The differential count of leukocytes was performed on the automated cell counters Sysmex-XE 2100 (Dasit) (Supplementary Table 1).
Cortelazzo A., De Felice C., Guerranti R., Signorini C., Leoncini S., Zollo G., Leoncini R., Timperio A.M., Zolla L., Ciccoli L, & Hayek J. (2016). Expression and oxidative modifications of plasma proteins in autism spectrum disorders: Interplay between inflammatory response and lipid peroxidation. Proteomics. Clinical applications, 10(11).
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