1,625 research outputs found
Laboratory reporting of hemostasis assays: the final post-analytical opportunity to reduce errors of clinical diagnosis in hemostasis?
No full textThe advent of modern instrumentation, with associated improvements in test performance and reliability, together with appropriate internal quality control (IQC) and external quality assurance (EQA) measures, has led to substantial reductions in analytical errors within hemostasis laboratories. Unfortunately, the reporting of incorrect or inappropriate test results still occurs, perhaps even as frequently as in the past. Many of these cases arise due to a variety of events largely outside the control of the laboratories performing the tests. These events are primarily preanalytical, related to sample collection and processing, but can also include post-analytical events related to the reporting and interpretation of test results. The current report provides an overview of these events, as well as guidance for prevention or minimization. In particular, we propose several strategies for the post-analytical reporting of hemostasis assays, and how this may provide the final opportunity to prevent serious clinical errors in diagnosis. This report should be of interest to both the laboratory scientists working in hemostasis and clinicians that request and attempt to interpret the test results. Laboratory scientists are ultimately responsible for these test results, and there is a duty to provide both accurate and precise results to enable clinicians to manage patients appropriately and to avoid the need to recollect and retest. Also, clinicians will not be in a position to best diagnose and manage their patient unless they gain an appreciation of these issues
Laboratory testing and/or monitoring of the new oral anticoagulants/antithrombotics: for and against.
No full textLaboratory testing and/or monitoring of the new oral anticoagulants/antithrombotics: for and against
Problems in laboratory testing: hemophilia and beyond.
No full textProblems in laboratory testing: hemophilia and beyond
Laboratory testing in the era of direct or non-vitamin k antagonist oral anticoagulants: a practical guide to measuring their activity and avoiding diagnostic errors.
No full textA new generation of antithrombotic agents has recently emerged. These provide direct inhibition of either thrombin (factor IIa [FIIa]) or FXa, and are increasingly replacing the classical anticoagulants (heparin and coumarins such as warfarin) in clinical practice for a variety of conditions. These agents have been designated several acronyms, including NOACs, DOACs, and TSOACs, respectively, referring to new (novel; non-vitamin K antagonist) oral anticoagulants, direct oral anticoagulants, and target-specific oral anticoagulants, and currently include dabigatran (FIIa inhibitor), and rivaroxaban, apixaban, edoxaban, and betrixaban (FXa inhibitors). The pervading mantra that NOACs do not require laboratory monitoring is countered by ongoing recognition that laboratory testing for drug effects is needed in many situations. Moreover, since these agents "do not require" laboratory monitoring, some clinicians inappropriately take this to mean that they do not affect hemostasis tests. This review aims to briefly review the laboratory studies that have evaluated the NOACs against a wide range of laboratory assays to assess utility for qualitative or quantitative measurements of these drugs, as well as interferences that may cause misdiagnosis of hemostatic defects. Point of care testing, including use of alternate samples such as urine and serum, is also under development but is not covered extensively in this review. The main aims of this article are to provide practical guidance to general laboratory testing for NOACs, as well as to help avoid diagnostic errors associated with hemostasis testing performed on samples from treated patients, as these currently comprise major challenges to hemostasis laboratories in the era of the NOACs
Coagulation update: what's new in hemostasis testing?
No full textThe current report provides a personal perspective summarising some interesting recent developments in hemostasis, as well as providing a brief glimpse into some possible imminent changes to come. We briefly review routine coagulation tests, and what changes may take place related to the new emerging anticoagulants. We also briefly review the old and new global tests of hemostasis, including thrombin generation and thromboelastography. Also briefly discussed within the diagnostics of bleeding and thrombotic disorders are the role of microparticles, the rise and fall of thrombophilia testing, the 'disappearance' of fibrinolysis pathway tests, and the absence of tests related to the endothelium, in part reflecting upon Virchow's triad. © 2011 Elsevier Ltd
The new oral anticoagulants and the future of haemostasis laboratory testing
No full textThe tests currently employed within most haemostasis laboratories to monitor anticoagulant therapy largely comprise the prothrombin time (PT)/International Normalised Ratio (INR) and the activated partial thromboplastin time (APTT). These are respectively used to monitor Vitamin K antagonists (VKAs) such as warfarin, and unfractionated heparin. Additional tests that laboratories may also employ for assessing or monitoring unfractionated heparin include thrombin time (TT) and the anti-Xa assay, which can also be used to monitor low molecular weight heparin. Several new anti-thrombotic agents have recently emerged, or are in the final process of clinical evaluation. These novel drugs that include Dabigatran etexilate and Rivaroxaban would not theoretically require monitoring; however, testing is useful in specific situations. The tests currently used to monitor VKAs and heparin are typically either too sensitive or too insensitive to the new drugs to be used as ‘typically performed in laboratories’, and may thus require some methodological adjustments to increase or decrease their sensitivity. Alternately, different tests may be better employed in these assessments. Whatever the case, laboratories may soon be performing a reduced or possibly increased number of tests, the same kind of tests but perhaps differently, or conceivably different assay panels. Specific laboratory guidance on the choice of the appropriate test to be ordered according to the drug being administered, as well as on appropriate interpretation of test results, will also be necessary. The current report reviews the current state of play and provides a glimpse to the possible future of the coagulation laboratory
The missing link between genotype, phenotype and clinics
No full textBroj genetskih testova bilježi eksponencijalan rast u kliničkim laboratorijima, zahvaljujući izvanrednim znanstvenim i tehnološkim dostignućima, uz potporu relativno jeftinih, brzih, pouzdanih i visoko propulzivnih tehnika. Sasvim je neupitno da je genetsko testiranje pomoglo u identi%ciranju molekularne osnove monogenskih bolesti, kao i mnoštva gena upletenih u većinu poligen-skih patologija. To je pak omogućilo individualizaciju liječenja i farmakološke terapije. Međutim, to je isto tako stvorilo jedan paradoks u upravljanom liječenju bolesnika prema kojemu se genetsko testiranje sad često vidi kao panacea, „lijek za sve", pretpostavljajući kako je svaki pojedini genetski po-limor%zam udružen sa speci%čnim, pojedinim fenotipom i/ili kliničkom slikom. Nažalost, više procesa koji reguliraju ekspresiju proteina ostaje i dalje nepoznato, dok njihova biološka osnova još nije konačno prepoznata, pa veza između genotipa, fenotipa i kliničkih nalaza nije uvijek očita te je često još teže ispitati u kojoj će mjeri veza između gena i okoline utjecati na liječenje bolesnika. Cilj ovoga članka je pružiti kritički osvrt na složen i višeslojan odnos koji povezuje gene, biokemiju i kliničke podatke, s naglaskom na prednosti i nedostatke genetskog testiranja kod monogenskih i poligenskih bolesti, te u predviđanju farmakološkog odgovora.Due to outstanding scientific and technological progresses, the number of genetic tests is growing exponentially in clinical laboratories, supported by relatively inexpensive, fast, reliable, high-throughput techniques. It is unquestionable that genetic testing has helped to identify the molecular bases of monogenic disorders as well as a variety of genes involved in most multifactorial pathologies. This in turn has allowed for personalized treatments and pharmacological therapies. However, it has also produced a paradox in the managed care of patients, in that genetic testing is now often perceived as a panacea, with assumptions that each single genetic polymorphism is associated with a specific, individual phenotype and/or clinical picture. Unfortunately, several processes regulating protein expression are still unknown, and their biological background has not been definitely recognized, so that the link between the genotype, the phenotype and the clinics is not always obvious, and it is often even more challenging to address how much the link between genes and environment will impact on the managed care of the patients. The present article aims to critically review the complex and multifaceted relationship linking genes, biochemistry and clinics, highlighting advantages and drawbacks of genetic testing in monogenic disorders, polygenic pathology and in the prediction of the pharmacological response
Laboratory diagnostics and therapy in thrombosis and hemostasis: from bedside to bench to bedside.
No full textLaboratory diagnostics and therapy in thrombosis and hemostasis: from bedside to bench to bedside
Hemostatic properties of the lymph: relationships with occlusion and thrombosis.
No full textLymphatic thrombosis is a rare occurrence, and although its frequency is likely underestimated, its burden remains substantially lower than that of venous or arterial thrombosis. Current evidence suggests that despite measurable levels of fibrinogen, von Willebrand factor and other coagulation factors in the lymph, fibrin generation is substantially inhibited under physiological conditions, essentially making the lymph a hypocoagulable biological fluid. Although factor VIIa-tissue factor-catalyzed activation of factor X is possible in the lymph, fibrin generation is largely counteracted by the unavailability of cell surface anionic phospholipids such as those physiologically present on blood platelets, combined with only low levels of coagulation factors, and the strong inhibitory activity of heparin, antithrombin, and tissue factor pathway inhibitor. Enhanced fibrinolytic activity further contributes to reduce the development and growth of lymph clots. Nevertheless, lymphatic thrombosis is occasionally detected, especially in the thoracic duct, axillary, or inguinal lymphatics. Pathogenetic mechanisms are supported by the release of thromboplastin substances from the injured lymphatic endothelium accompanied by chronic obstruction of lymph flow in the presence of a hypercoagulable milieu, thereby mirroring the Virchow triad that otherwise characterizes venous thrombosis. In theory, any source of lymphatic vessel occlusion, such as internal obliteration, external compression, or increased lymphatic pressure, might predispose to localized lymphatic thrombosis. The leading pathologies that can trigger thrombosis in the lymphatic vessels include cancer (due to external compression, neoplastic obliteration of the lymphatic lumen by metastatic cells, or lymphatic dysfunction after lymph node dissection), infections (especially lymphatic filariasis or sustained by Chlamydia trachomatis, Mycobacterium tuberculosis, Treponema pallidum, or Streptococcus pyogenes), congestive heart failure, chronic edema and inflammation of the distal lower limb, complications of central venous catheterization, coronary artery bypass grafting, thoracic outlet syndrome, and amyloidosis. © 2012 by Thieme Medical Publishers, Inc
Hemophilia, cancer and cardiovascular disease.
No full textHemophilia, cancer and cardiovascular disease
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