DOCSLIB.ORG

BLOOD RESEARCH June 2014 ARTICLE

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
BLOOD RESEARCH June 2014 ARTICLE VOLUME 49ㆍNUMBER 2 REVIEW BLOOD RESEARCH June 2014 ARTICLE Hypercoagulable states: an algorithmic approach to laboratory testing and update on monitoring of direct oral anticoagulants Megan O. Nakashima, Heesun J. Rogers Department of Laboratory Medicine, Cleveland Clinic, Cleveland, OH, United States p-ISSN 2287-979X / e-ISSN 2288-0011 Abstract http://dx.doi.org/10.5045/br.2014.49.2.85 Hypercoagulability can result from a variety of inherited and, more commonly, acquired Blood Res 2014;49:85-94. conditions. Testing for the underlying cause of thrombosis in a patient is complicated both by the number and variety of clinical conditions that can cause hypercoagulability as well Received on May 31, 2014 as the many potential assay interferences. Using an algorithmic approach to hyper- Revised on June 17, 2014 coagulability testing provides the ability to tailor assay selection to the clinical scenario. Accepted on June 19, 2014 It also reduces the number of unnecessary tests performed, saving cost and time, and preventing potential false results. New oral anticoagulants are powerful tools for manag- Correspondence to ing hypercoagulable patients; however, their use introduces new challenges in terms of Heesun J. Rogers, M.D., Ph.D. test interpretation and therapeutic monitoring. The coagulation laboratory plays an essen- Department of Laboratory Medicine, Cleveland Clinic, 9500 Euclid Avenue tial role in testing for and treating hypercoagulable states. The input of laboratory pro- (L-11), Cleveland, OH 44195, United States fessionals is necessary to guide appropriate testing and synthesize interpretation of Tel: ＋216-445-2719 results. Fax: ＋216-444-4414 E-mail: [email protected] Key Words Hypercoagulability, Algorithmic approach, Antiphospholipid syndrome, Ⓒ 2014 Korean Society of Hematology Direct oral anticoagulant, Venous thromboembolism setting of a strong family history, VTE in an unusual vascular INTRODUCTION site (cerebral, hepatic, mesenteric, or renal veins), neonatal purpura fulminans, warfarin-induced skin necrosis, and re- Hypercoagulability, also known as thrombophilia, de- current pregnancy loss [5, 6]. scribes a group of hereditary and acquired conditions which confer a propensity to develop thrombi in the veins, arteries, 1. Clinical history and sources of interference or both. Based on current knowledge, antiphospholipid syn- Many assays used in the laboratory evaluation of hyper- drome is the most prevalent hypercoagulable state, followed coagulability are affected by concurrent clinical conditions by factor V Leiden (FVL) mutation, prothrombin gene and medications. Whenever possible, a thorough clinical G20210A mutations, elevated factor VIII, and hyperhomocy- history including site of thrombosis, previous bleeding or steinemia. Less common disorders include deficiencies in thrombotic events, other medical disorders (i.e., liver, auto- antithrombin, protein C, or protein S. immune, or cardiovascular disease), pregnancy, medications The prevalence of thrombosis is higher in individuals with (including but not limited to anticoagulants), and family a personal and/or family history of thrombosis than in the history should be elicited. These are essential for appropriate general population. Acquired and hereditary risk factors for test selection and interpretation of results; sources of interfer- thrombophilia are summarized in Table 1 [1, 2]. Although ence for specific assays are described in the following patients with hypercoagulable risk factors are at a great risk sections. Tests should be performed at least 4–6 weeks after for developing a thrombotic event, not all patients with an acute thrombotic event or discontinuation of anti- hypercoagulable risk factors will develop clinically relevant coagulant/thrombolytic therapies including warfarin, hep- thrombosis; conversely, not all patients with thrombosis will arin, direct thrombin inhibitors (DTIs), direct factor Xa in- have an identifiable hypercoagulable state [2-4]. hibitors, and fibrinolytic agents [1, 4, 5]. If abnormal results Diagnostic thrombophilia testing is indicated in patients are found during acute illness or anticoagulant therapy, test- with idiopathic or recurrent venous thromboembolism ing should be repeated in a new specimen when the patient (VTE), first VTE at a young age (＜40 years), VTE in the is stable and after anticoagulant therapy is discontinued. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. 86 Megan O. Nakashima and Heesun J. Rogers Table 1. Acquired and hereditary risk factors for thrombophilia. Acquired factors Hereditary factors Major surgery/trauma Activated protein C resistance/factor V Leiden Immobilization (e.g., hip/knee replacement, prolonged cast, Prothrombin gene G20210A mutation stroke, bedridden because of illness) Protein C deficiencya) Solid or hematologic malignancies Protein S deficiencya) Pregnancy Antithrombin deficiencya) Oral contraceptives Hyperhomocysteinemiaa) Estrogen replacement therapy Elevated factor VIII activitya) Antiphospholipid antibody syndrome Dysfibrinogenemiaa) Heparin-induced thrombocytopenia Paroxysmal nocturnal hemoglobinuria Obesity Nephrotic syndrome Smoking a)Can be hereditary or acquired. Fig. 1. Comprehensive hypercoa- gulability testing panel using a diagnostic algorithm. Abbreviat- ions: aPTT, activated partial throm- boplastin time; B2GP1, beta2 glycoprotein 1; CRP, C-reactive protein; DRVVT, dilute Russell’s Viper Venom test; MTHFR, me- thylenetetrahydrofolate reductase; PL, phospholipid; PNP, platelet neutralization procedure; PT, pro- thrombin time; SNP, single nu- cleotide polymorphism. Alternatively, thrombophilia testing may be delayed until all hypercoagulable defects. Selection of the most informative acute clinical conditions have subsided. The exception is tests may differ depending on location and type (venous DNA analysis for genetic mutations, which is not generally or arterial) of thrombosis. Fig. 1 outlines a testing algorithm affected by other medical issues or anticoagulant therapy. to maximize diagnostic potential in patients with thrombo- philia while avoiding unnecessary and potentially expensive 2. Algorithmic approach to laboratory testing tests. Testing should be performed in a step-wise manner No single laboratory test is yet available that can identify beginning with high-yield screening tests followed by appro- Blood Res 2014;49:85-94. bloodresearch.or.kr Hypercoagulability: algorithmic approach 87 priate specific confirmatory tests. These comprehensive pan- phospholipid (e.g., DRVVT confirmatory ratio, hexagonal els generate multiple test results that can each be affected phospholipid neutralization ratio, platelet neutralization). (4) by a variety of clinical conditions and drugs. Comprehensive Presence of specific factor inhibitors (especially factor VIII narrative interpretation by coagulation specialists is neces- inhibitors) and anticoagulant drugs (heparin or DTI) should sary to synthesize test results, correctly interpret them ac- be excluded [10, 11, 13-15]. In addition to the ISTH guideline cording to the patient’s clinical condition, and provide appro- (2009) and updated British Committee for Standards in priate guidance to clinicians [2, 7]. In some patients with Haematology (2012) guidelines, the Clinical and Laboratory thrombophilia, it may be best to test for all recognized heredi- Standards Institute recently published the first LA guideline tary risk factors, both common and uncommon [5, 7, 8]. [11, 16, 17]. Although all guidelines aim to standardize and harmonize methodologies and improve the quality of LA testing, identifying LA remains a diagnostic challenge. SPECIFIC HYPERCOAGULABLE Paradoxically, LAs prolong clot-based assays in vitro while DISORDERS AND LABORATORY STUDIES predisposing to thrombosis in vivo. In fact, approximately 30% of LA patients will experience thrombosis. In approx- 1. Antiphospholipid syndrome imately 15% of patients with deep vein thrombosis (DVT), Antiphospholipid syndrome (APS) is the most common clotting is attributable to LA [2, 18]. Because no single test cause of acquired thrombophilia. Antiphospholipid anti- is available to detect LA, laboratory testing for LA consists bodies (APAs) are acquired autoantibodies directed against of a panel of assays following a diagnostic algorithm (Fig. phospholipid-protein complexes and are present in 3–5% 1). To maximize diagnostic potential, at least 2 assays based of the general population. APAs are associated with increased on different principles should be performed to evaluate for risk of both arterial and venous thrombosis and recurrent each of the 4 ISTH criteria. If fewer than 4 diagnostic criteria pregnancy loss [9, 10]. APAs can arise spontaneously (pri- are met but clinical suspicion for LA exists, the panel is mary) or in association with another condition (secondary). interpreted as indeterminate and should be repeated at a Also known as lupus anticoagulants (LA) because of their later date [9-11, 19]. prevalence in patients with systemic lupus erythematosus Acute thrombotic events or acute phase responses with (SLE), APAs are extremely heterogeneous and can be directed elevated factor VIII can cause false-negative results. Throm- against a wide variety of anionic phospholipids, including bin time
Load more

Recommended publications
  • Syllabus: Page 23
    The University of Texas at El Paso College of Health Sciences Clinical Laboratory Science Program CLSC 3364 Hematology II Course Outline Spring What do you see? What is in your Head? Video or audio recordings will not be permitted. Instructor M. Lorraine Torres, Ed. D, MT (ASCP) College of Health Sciences Room 423 Phone: 747-7282 E-Mail: [email protected] Office Hours TR 3:00 – 4:00 p.m., Friday 2 – 3 p.m. or by appointment Class Schedule Monday and Wednesday 11:00 – 12:30 A.M. HSCI 135 Course Description This course is a sequel to Hematology I. It will include but is not limited to the study of the white blood cells with emphasis on white cell formation and function and the etiology and treatment of white blood cell disorders. This course will also encompass an introduction to hemostasis and laboratory determination of hemostatic disorders. Prerequisite; CLSC 3356 & CLSC 3257. Topical Outline 1. Maturation series and biology of white blood cells 2. Disorders of neutrophils 3. Reactive lymphocytes and Infectious Mononucleosis 4. Acute and chronic leukemias 5. Myelodysplastic syndromes 6. Myeloproliferative disorders 7. Multiple Myeloma and related plasma cell disorders 8. Lymphomas 9. Lipid (lysosomal) storage diseased and histiosytosis 10. Hemostatic mechanisms, platelet biology 11. Coagulation pathways 12. Quantitative and qualitative vascular and platelet disorders (congenital and acquired) 13. Disorders of plasma clotting factors 14. Interaction of the fibrinolytic, coagulation and kinin systems 15. Laboratory methods REQUIRED TEXTBOOKS: same books used for Hematology I Keohane, E.M., Smith, L.J. and Walenga, J.M. 2016. Rodak’s Hematology: Clinical Principles and applications.
    [Show full text]
  • The Role of the Laboratory in Treatment with New Oral Anticoagulants
    Journal of Thrombosis and Haemostasis, 11 (Suppl. 1): 122–128 DOI: 10.1111/jth.12227 INVITED REVIEW The role of the laboratory in treatment with new oral anticoagulants T. BAGLIN Department of Haematology, Addenbrooke’s Hospital, Cambridge University Hospitals NHS Trust, Cambridge, UK To cite this article: Baglin T. The role of the laboratory in treatment with new oral anticoagulants. J Thromb Haemost 2013; 11 (Suppl. 1): 122–8. tion of thromboembolism in patients with atrial fibrilla- Summary. Orally active small molecules that selectively tion. For some patients, these drugs offer substantial and specifically inhibit coagulation serine proteases have benefits over oral vitamin K antagonists (VKAs). For the been developed for clinical use. Dabigatran etexilate, majority of patients, these drugs are prescribed at fixed rivaroxaban and apixaban are given at fixed doses and doses without the need for monitoring or dose adjustment. do not require monitoring. In most circumstances, these There are no food interactions and very limited drug inter- drugs have predictable bioavailability, pharmacokinetic actions. The rapid onset of anticoagulation and short half- effects, and pharmacodynamic effects. However, there life make the initiation and interruption of anticoagulant will be clinical circumstances when assessment of the therapy considerably easier than with VKAs. As with all anticoagulant effect of these drugs will be required. The anticoagulants produced so far, there is a correlation effect of these drugs on laboratory tests has been deter- between intensity of anticoagulation and bleeding. Conse- mined in vitro by spiking normal samples with a known quently, the need to consider the balance of benefit and risk concentration of active compound, or ex vivo by using in each individual patient is no less important than with plasma samples from volunteers and patients.
    [Show full text]
  • Approach to Coagulopathy in the Icu Dic and Thrombotic Emergencies
    APPROACH TO COAGULOPATHY IN THE ICU DIC AND THROMBOTIC EMERGENCIES NEIL KUMAR, MD UNIVERSITY OF ROCHESTER MEDICAL CENTER Disclosures u I have no financial disclosures u I am NOT A HEMATOLOGIST Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies Coagulation u Coagulation is the process in which blood clots u Fibrinolysis is the process in which clot dissolves u Hemostasis is the stopping of bleeding or hemorrhage. u Ideally, hemostasis is a balance between coagulation and fibrinolysis Coagulation (classic pathways) Michael G. Crooks Simon P. Hart Eur Respir Rev 2015;24:392-399 Coagulation (another view) Gando, S. et al. (2016) Disseminated intravascular coagulation Nat. Rev. Dis. Primers doi:10.1038/nrdp.2016.37 Coagulation (yet another view) u Inflammation and coagulation intersect with platelets in the middle u An example of this is Disseminated Intravascular Coagulation. Gando, S. et al. (2016) Disseminated intravascular coagulation Nat. Rev. Dis. Primers doi:10.1038/nrdp.2016.37 Outline u Review of hemostasis and coagulopathy u Discuss laboratory markers for coagulopathy u Discuss an approach to a few specific coagulopathies and thrombotic emergencies PT / INR u Prothrombin Time u Test of Extrinsic Pathway u Take plasma (blood without cells) and re-add calcium u Calcium was removed with citrate in tube u Add tissue factor u See how long it takes to clot and normalize PT to get INR Coagulation (classic pathways) Michael G.
    [Show full text]
  • Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants
    biomedicines Review Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants Osamu Kumano 1,2,* , Kohei Akatsuchi 3 and Jean Amiral 1 1 Research Department, HYPHEN BioMed, 155 Rue d’Eragny, 95000 Neuville sur Oise, France; [email protected] 2 Protein Technology, Engineering 1, Sysmex Corporation, Kobe 651-2271, Japan 3 R&D Division, Sysmex R&D Center Americas, Inc., Mundelein, IL 60060, USA; [email protected] * Correspondence: [email protected]; Tel.: +81-78-991-2203 Abstract: Anticoagulant drugs have been used to prevent and treat thrombosis. However, they are associated with risk of hemorrhage. Therefore, prior to their clinical use, it is important to assess the risk of bleeding and thrombosis. In case of older anticoagulant drugs like heparin and warfarin, dose adjustment is required owing to narrow therapeutic ranges. The established monitoring methods for heparin and warfarin are activated partial thromboplastin time (APTT)/anti-Xa assay and pro- thrombin time – international normalized ratio (PT-INR), respectively. Since 2008, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), have been widely prescribed to prevent and treat several thromboembolic diseases. Although the use of DOACs without routine monitoring and frequent dose adjustment has been shown to be safe and effective, there may be clinical circumstances in specific patients when measurement of the anticoagulant effects of DOACs Citation: Kumano, O.; Akatsuchi, K.; is required. Recently, anticoagulation therapy has received attention when treating patients with Amiral, J. Updates on Anticoagulation coronavirus disease 2019 (COVID-19). In this review, we discuss the mechanisms of anticoagulant and Laboratory Tools for Therapy drugs—heparin, warfarin, and DOACs and describe the methods used for the measurement of Monitoring of Heparin, Vitamin K their effects.
    [Show full text]
  • 15-7022 Quick Guide 115X200 2015.Indd
    H A E M O S T A S tPA FDP I S -1 D-Dimer PAI Plasminogen Plasmin Fibrin T M Fibrinogen IIa PC IIa T A APC PS II PS AP T V C A Activated Va Xa Platelet vWF X A T XI IXa VIIIa APC PS VIII XIa IX T A Activation pathways Inhibition pathways Coagulation PAI-1 AT All rights reserved - 04/2013 Ref. 27646 VIIa AT AGO - Fibrinolysis Xa TFPI T S APC PS Xa TFPI A TF © 2009 DIAGNOSTIC 4614 Diagnostica Stago S.A.S. RCS Nanterre B305 151 409 9, rue des Frères Chausson 92600 Asnières sur Seine (France) AT THE HEART OF HAEMOSTASIS Ph.: +33 (0)1 46 88 20 20 Quick Guide Fax: +33 (0)1 47 91 08 91 [email protected] At the Heart of Haemostasis www.stago.com To Haemostasis Screening assays in Haemostasis Anticoagulant therapy monitoring (1): Vitamin K antagonists Anticoagulant therapy monitoring (2): Heparin Assays for other anticoagulant therapy (3) Disseminated Intravascular Coagulation (DIC) Thrombophilia D-Dimer assay for the exclusion of venous thromboembolism (VTE) Lupus anticoagulants / Antiphospholipid antibodies For more information, visit our website at www.stago.com Screening assays in Haemostasis 1) Questionnaire l Personal and familial history l Treatments l Diseases l Clinical symptoms 2) Physical examination 3) Pre-operative Haemostasis screening assays l Prothrombin time (PT) n Screening test for the extrinsic and common pathways of coagulation (factors II, V, VII, X). Limited sensitivity to fibrinogen. n Usual normal ranges: 12 - 13 sec (may vary between reagents, please refer to manufacturer’s insert) l Activated Partial Thromboplastin Time (aPTT) n Screening test for the intrinsic and common coagulation pathways of coagulation (factors VIII, IX, XI, XII, V and II).
    [Show full text]
  • Collaborative Study on Monitoring Methods to Determine Direct Thrombin Inhibitors Lepirudin and Argatroban
    Collaborative Study On Monitoring Methods To Determine Direct Thrombin Inhibitors Lepirudin And Argatroban On behalf of the Control of Anticoagulation Subcommittee of the Scientific and Standardization Committee of the International Society of Thrombosis and Haemostasis E. Gray 1 and J Harenberg * SUMMARY Background: Direct thrombin inhibitors are now used clinically for the prophylaxis and treatment of thrombosis and related cardiovascular diseases. Although all these inhibitors bind to thrombin, their modes of action are different. Routine anticoagulant monitoring tests such as the APTT are used to estimate the activity of these inhibitors. However, no studies have been carried out to assess the suitability of these tests. Methods: An international collaborative study was carried out utilising a panel of plasmas spiked with lepirudin and argatroban to evaluate the robustness and the sensitivity of the different monitoring methods. Results: Thirteen laboratories took part in the trial. The point-of-care TAS-analyser, using cards with high or low concentrations of ecarin reagents gave the lowest intra- and inter- laboratory variation. APTT using local or common APTT reagents also showed acceptable within and between-laboratory variations. The chromogenic anti-IIa activity and the wet ecarin clotting time gave higher inter-laboratory variations. The ELISA for lepirudin had the highest inter-laboratory variation. Conclusion: APTT and the TAS-analyser with ECT-cards gave the most reproducible results compared to other methods. Further studies will evaluate the validity for patient samples. INTRODUCTION Direct and indirect serine protease inhibitors are used clinically for inhibition of blood coagulation (1). Direct inhibitors such as hirudin and fondaparinux inhibit individual serine proteases such as thrombin and factor Xa.
    [Show full text]
  • Ecarin Based Coagulation Testing Gosselin, Robert C; Douxfils, Jonathan
    Institutional Repository - Research Portal Dépôt Institutionnel - Portail de la Recherche University of Namurresearchportal.unamur.be RESEARCH OUTPUTS / RÉSULTATS DE RECHERCHE Ecarin based coagulation testing Gosselin, Robert C; Douxfils, Jonathan Published in: European Medical Journal Hematology DOI: Author(s)10.1002/ajh.25852 - Auteur(s) : Publication date: 2020 Document Version PublicationPeer reviewed date version - Date de publication : Link to publication Citation for pulished version (HARVARD): Gosselin, RC & Douxfils, J 2020, 'Ecarin based coagulation testing', European Medical Journal Hematology, vol. Permanent95, no. 7, link pp. 863-869. - Permalien https://doi.org/10.1002/ajh.25852 : Rights / License - Licence de droit d’auteur : General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal ? Take down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. BibliothèqueDownload
    [Show full text]
  • Impact of Dabigatran on a Large Panel of Routine Or Specific Coagulation Assays Laboratory Recommendations for Monitoring of Dabigatran Etexilate
    New Technologies, Diagnostic Tools and Drugs © Schattauer 2012 1 Impact of dabigatran on a large panel of routine or specific coagulation assays Laboratory recommendations for monitoring of dabigatran etexilate Jonathan Douxfils1*; François Mullier1,2*; Séverine Robert1; Christian Chatelain3; Bernard Chatelain2*; Jean-Michel Dogné1* 1Department of Pharmacy, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for LIfe Sciences (NARILIS), University of Namur, Belgium; 2Hematology Laboratory, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for LIfe Sciences (NARILIS), CHU Mont-Godinne, Université Catholique de Louvain, Belgium; 3Hematology Department, Namur Thrombosis and Hemostasis Center, CHU Mont-Godinne, Université Catholique de Louvain, Belgium Summary and TGA were the most sensitive tests but are not available 24 hours a Due to low bioavailability and high inter-individual variability, monitor- day. In addition, HTI showed a linear correlation with a good reproduci- ing of dabigatran may be required in specific situations to prevent the bility. Dabigatran induced a concentration-dependent delay and in- risk of bleedings or thrombosis. The aim of the study was to determine hibition of tissue factor-induced TGA. Cut-offs related with higher risk which coagulation assay(s) could be used to assess the impact of dabig- of bleedings or thrombosis were defined for each reagent of aPTT and atran on secondary haemostasis. Dabigatran was spiked at concen- HTI. In conclusion, aPTT could be used for the monitoring of dabigatran trations ranging from 4.7 ng/ml to 943.0 ng/ml in pooled citrated and as screening test for the risk of overdose. However, because of its human platelet-poor plasma.
    [Show full text]
  • Autoimmune Heparin‐Induced Thrombocytopenia
    Journal of Thrombosis and Haemostasis, 15: 2099–2114 DOI: 10.1111/jth.13813 REVIEW ARTICLE Autoimmune heparin-induced thrombocytopenia A. GREINACHER,* K. SELLENG* andT. E. WARKENTIN† *Institut fur€ Immunologie und Transfusionsmedizin, Universitatsmedizin€ Greifswald, Greifswald, Germany; and †Department of Pathology and Molecular Medicine, Department of Medicine, and McMaster Centre for Transfusion Research, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada To cite this article: Greinacher A, Selleng K, Warkentin TE. Autoimmune heparin-induced thrombocytopenia. J Thromb Haemost 2017; 15: 2099–114. in the setting of HIT-associated DIC, known as ‘APTT Summary. Autoimmune heparin-induced thrombocytope- confounding’. Thus, non-APTT-adjusted therapies with nia (aHIT) indicates the presence in patients of anti-plate- drugs such as danaparoid and fondaparinux, or even let factor 4 (PF4)–polyanion antibodies that are able to direct oral anticoagulants, such as rivaroxaban or apixa- activate platelets strongly even in the absence of heparin ban, are suggested therapies, especially for long-term (heparin-independent platelet activation). Nevertheless, as management of persisting HIT. In addition, emerging seen with serum obtained from patients with otherwise data indicate that high-dose intravenous immunoglobulin typical heparin-induced thrombocytopenia (HIT), serum- can interrupt HIT antibody-induced platelet activation, induced platelet activation is inhibited at high heparin leading to rapid platelet count recovery. concentrations (10–100 IU mLÀ1 heparin). Furthermore, upon serial dilution, aHIT serum will usually show hep- Keywords: autoimmunity; heparin-induced thrombocy- arin-dependent platelet activation. Clinical syndromes topenia; high-dose intravenous immunoglobulin; platelet- associated with aHIT include: delayed-onset HIT, persist- activating antibodies; platelet factor 4 (PF4).
    [Show full text]
  • APUTS) Reporting Terminology and Codes Haematology (V1.0
    AUSTRALIAN PATHOLOGY UNITS AND TERMINOLOGY (APUTS) Reporting Terminology and Codes Haematology (v1.0) 1 12/02/2013 APUTS Report Terminology and Codes - Haematology Page 1 of 2 RCPA Pathology Units and Terminology Standardisation Project - Terminology for Reporting Pathology: Haematology v1 Preferred term Synonym Usage guidance Length Specimen PUTS Unit LOINC Component Property Timing System Scale Method LongName Activated partial thromboplastin time APTT 38 Platelet poor plasma s 14979-9 Coagulation surface induced Time Pt PPP Qn Coag Activated partial thromboplastin time (aPTT) in Platelet poor plasma by Coagulation assay Activated protein C resistance APCR 30 Platelet poor plasma No unit 13590-5 Activated protein C resistance TRto Pt PPP Qn Coag Activated protein C resistance [Time Ratio] in Platelet poor plasma by Coagulation assay Anti Xa levels 14 Platelet poor plasma U/mL 32684-3 Heparin.low molecular weight ACnc Pt PPP Qn LMW Heparin [Units/volume] in Platelet poor plasma Antibody identification Ab 23 Serum/Plasma No unit 888-8 Blood group antibodies identified Prid Pt Ser/Plas Nom Blood group antibodies identified in Serum or Plasma Antithrombin AT, ATIII 12 Platelet poor plasma % 27811-9 Antithrombin actual/Normal RelCCnc Pt PPP Qn Chromo Antithrombin actual/normal in Platelet poor plasma by Chromogenic method Basophils Baso 10 Blood 10*9/L 26444-0 Basophils NCnc Pt Bld Qn Basophils [#/volume] in Blood Blood film examination Film 22 Blood No unit 18314-5 Morphology Imp Pt Bld Nar Morphology [interpretation] in Blood Narrative
    [Show full text]
  • Explaining Chemical Reactions
    Microfluidic Point-Of-Care Ecarin Based Assays for Monitoring Direct Thrombin Inhibitor Therapy Item Type text; Electronic Thesis Authors Alouidor, Benjamin Publisher The University of Arizona. Rights Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. Download date 25/09/2021 21:05:31 Link to Item http://hdl.handle.net/10150/628176 MICROFLUIDIC POINT-OF-CARE ECARIN BASED ASSAYS FOR MONITORING DIRECT THROMBIN INHIBITOR THERAPY by Benjamin J. Alouidor ____________________________ Copyright © Benjamin Alouidor 2018 A Thesis Submitted to the Faculty of the COLLEGE OF MEDICINE In Partial Fulfillment of the Requirements For the Degree of MASTER OF SCIENCE WITH A MAJOR IN MEDICAL PHARMACOLOGY PERFUSION In the Graduate College THE UNIVERSITY OF ARIZONA 2018 2 Table of Contents List of Figures ..................................................................................................................... 4 Abstract ............................................................................................................................... 5 Introduction ......................................................................................................................... 6 Direct Thrombin Inhibitors (DTIs) as Anti-Coagulants ................................................. 6 Pharmacodynamics
    [Show full text]
  • Coagulation Tests
    Coagulation tests Erik Lerkevang Grove, Associate Prof, MD, PhD, FESC Department of Cardiology, Aarhus University Hospital, Denmark Disclosures • None related to this talk. • General disclosures: • Lecture fees from AstraZeneca, Baxter, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, MSD, Sysmex, and Pfizer. • Advisory board meetings for AstraZeneca, Bayer, Boehringer Ingelheim, and Bristol-Myers Squibb. Erik Lerkevang Grove Outline of talk: Coagulation tests • Coagulation system • Coagulation tests: why?, how?, when? • PT/INR • aPTT • ACT • Anti-Xa activity • Point-of-care testing: TEG & ROTEM • Evaluation of coagulation during treatment with NOACs • Conclusions Erik Lerkevang Grove Evaluating the coagulation system – why? • Unexplained bleeding • Pre- and perioperative testing • Monitoring of anticoagulant treatment • Research Erik Lerkevang Grove Coagulation system: traditional concept Hvas AM, Grove EL, Kristensen SD ESC Textbook of Intensive & Acute Cardiovascular Care, Oxford University Press, 2015 Coagulation system: current concept Modified from De Caterina et al, EHJ 2007. Prothrombin time (PT) and INR • PT measures the time [reference value: 11-13 seconds] it takes plasma to clot when exposed to tissue factor and reflects the ‘extrinsic’ and ‘common’ pathways of coagulation. • International normalized ratio (INR) [ref: 0.8-1.2] = (PT-patient/PT- normal)^ISI • Clinical use: bleeding, liver synthetic function, DIC, warfarin treatment. Erik Lerkevang Grove Activated partial thromboplastin time (aPTT) • The aPTT measures the time
    [Show full text]