ObjectivesCommercially available cyanoacrylates are known to release formaldehyde during degradation. However, it is unknown whether venous adhesive cyanoacrylates used in the treatment of saphenous veins release formaldehyde. Formaldehyde is a known contact allergen, carcinogen and sensitiser.MethodsVenaSeal®, VenaBlock®, Glubran® Tiss 2, Histoacryl®, and Supaglue® were investigated in vitro. All adhesive agents were polymerised in phosphate-buffered saline, sealed in glass bottles and incubated at 37°C for up to 12 weeks. Headspace-gas chromatography mass spectrometry was used to measure formaldehyde release at set time intervals.ResultsPeak levels of formaldehyde were detected in all cyanoacrylate samples within 2 weeks of incubation, with peak levels ranging from 0.05% to 0.17% w/w. These peak concentrations emerged as early as 2 weeks post-polymerisation and remained consistently elevated throughout the 12-week observation period. Glubran Tiss 2 demonstrated the lowest formaldehyde release at 0.05% w/w, while VenaSeal exhibited the highest, reaching a peak of 0.17% w/w at 2 weeks, similar to commercial SupaGlue. Notably, VenaSeal maintained formaldehyde levels above 0.1% w/w for the duration of the 12-week testing period.ConclusionFormaldehyde is released during the post-polymerisation degradation of medical cyanoacrylates. Despite all products containing n-butyl cyanoacrylate (n-BCA), formaldehyde release varied-likely due to undisclosed formulation differences. VenaSeal released the highest level (0.17% w/w) compared to other products tested, suggesting that formulation influences degradation behaviour.

The activated partial thromboplastin time (APTT) assay is essential for evaluating coagulation. However, prolonged APTT may result from pathological conditions or contamination with unfractionated heparin (UFH), which can occur due to improper phlebotomy or use of heparinized lines—even in patients not on UFH therapy. Distinguishing between true pathology and heparin contamination is critical for patient care and appropriate laboratory reporting. This study assessed the effectiveness of Antihepca HRRS (AHCa, a Heparin Resistant Recalcifying Solution (HRRS)), in neutralizing heparin interference in APTT testing. APTT results using AHCa HRRS and standard 0.025 M CaCl 2 were compared in 33 heparinized and 41 non-heparinized patient samples on Sysmex CN-6000 and Stago Start Max analyzers. Additionally, 30 random plasma samples with prolonged APTT were tested, and heparin-spiked plasmas were used to determine AHCa HRRS's neutralization limit. AHCa HRRS fully corrected prolonged APTT in samples containing up to 0.6 IU/mL UFH. In the 33 heparinized samples, AHCa HRRS reduced all APTT results to <40 s, eliminating the need for urgent reporting. Among the 30 prolonged APTT samples, 8 were corrected by AHCa HRRS (indicating heparin), 20 remained prolonged (suggesting other causes), and 1 was inconclusive. In non-heparinized samples, AHCa HRRS caused only minor APTT shortening (∼5%), confirming minimal impact on true results. Overall, AHCa HRRS effectively neutralizes UFH interference in APTT testing without compromising accuracy in non-heparinized samples. It offers a practical alternative to conventional calcium reagents and thrombin time for identifying heparin contamination in clinical laboratories.

Background: Direct oral anticoagulants (DOACs) cause unwanted interference in various hemostasis assays, including lupus anticoagulant (LA) testing, where false positive and false negative identification may occur. DOAC Stop (DS) is an activated charcoal (AC) product used to specifically and effectively adsorb DOACs from test plasma. This process normally requires plasma treatment, centrifugation and plasma separation prior to tests, but inexperienced operators may also inadvertently transfer residual AC particles, thereby potentially adversely affecting clot detection. Methods: We hypothesized that residual DS might not be problematic for mechanical clot detection. We therefore investigated the potential impact of DS and a new DS liquid (DS-L) product on clotting tests using a mechanical clot detection system. Varying concentrations of DS were added to normal and abnormal plasmas with and without DOAC presence. Clotting tests including PT, APTT and dRVVT were performed directly in the analyzer without plasma/DS centrifugation. Results: DS up to double the recommended treatment level had only minor effects on all test results, despite completely obscuring visibility in the plasma/reagent mix. This confirms that the centrifugation step may be able to be omitted when using mechanical detection systems. Conclusions: Should DS carryover into treated plasmas occur, this should not cause issues with testing performed on mechanical clot-sensing devices. Moreover, we hypothesize that DS can be used directly in these systems, without the need for centrifugation, thereby simplifying its many potential applications.

International Journal of Laboratory HematologyVolume 45, Issue 4 p. 603-606 LETTER TO THE EDITOR Mixing factor Xa and thrombin inhibiting direct oral anticoagulants produces a synergistic prolonging effect on most clotting tests Thomas Exner, Thomas Exner orcid.org/0000-0002-3933-7669 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorLisa Ellwood, Lisa Ellwood orcid.org/0000-0003-4259-3695 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorManita Dangol, Manita Dangol orcid.org/0000-0002-1315-5760 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorEmmanuel J. Favaloro, Corresponding Author Emmanuel J. Favaloro [email protected] orcid.org/0000-0002-2103-1661 Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Sydney, New South Wales, Australia School of Dentistry and Medical Sciences, Faculty of Science and Health, Charles Sturt University, Wagga, New South Wales, Australia School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Westmead Hospital, Sydney, New South Wales, Australia Correspondence Emmanuel J. Favaloro, Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia. Email: [email protected]Search for more papers by this author Thomas Exner, Thomas Exner orcid.org/0000-0002-3933-7669 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorLisa Ellwood, Lisa Ellwood orcid.org/0000-0003-4259-3695 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorManita Dangol, Manita Dangol orcid.org/0000-0002-1315-5760 Haematex Research Pty Ltd, Sydney, New South Wales, AustraliaSearch for more papers by this authorEmmanuel J. Favaloro, Corresponding Author Emmanuel J. Favaloro [email protected] orcid.org/0000-0002-2103-1661 Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Sydney, New South Wales, Australia School of Dentistry and Medical Sciences, Faculty of Science and Health, Charles Sturt University, Wagga, New South Wales, Australia School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Westmead Hospital, Sydney, New South Wales, Australia Correspondence Emmanuel J. Favaloro, Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Westmead, Sydney, NSW 2145, Australia. Email: [email protected]Search for more papers by this author First published: 21 February 2023 https://doi.org/10.1111/ijlh.14043Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat REFERENCES 1Lippi G, Mattiuzzi C, Favaloro EJ. 10-year evolution in worldwide usage of anticoagulant drugs. Semin Thromb Hemost. 2022; 2023(3): 314-316. doi:10.1055/s-0042-1756702 2Gosselin RC, Adcock DM, Bates SM, et al. International Council for Standardization in Haematology (ICSH) recommendations for laboratory measurement of direct Oral anticoagulants. Thromb Haemost. 2018; 118(3): 437-450. 3Bonar R, Favaloro EJ, Mohammed S, Pasalic L, Sioufi J, Marsden K. The effect of dabigatran on haemostasis tests: a comprehensive assessment using in-vitro and ex-vivo samples. Pathology. 2015; 47(4): 355-364. 4Bonar R, Favaloro EJ, Mohammed S, et al. The effect of the direct factor Xa inhibitors apixaban and rivaroxaban on haemostasis tests: a comprehensive assessment using in vitro and ex vivo samples. Pathology. 2016; 48(1): 60-71. doi:10.1016/j.pathol.2015.11.025 5Exner T, Ellwood L, Rubie J, Barancewicz A. Testing for new oral anticoagulants with LA resistant Russels viper venom reagents. Thromb Haemost. 2013; 109: 762-765. 6Sennesaal AL, Exner T, Chatelain B, et al. An optimized dRVVT-based assay to estimate the intensity of anticoagulation in patients treated with direct oral anticoagulants. Thromb Res. 2017; 157: 29-37. 7Exner T, Joseph J, Low J, Connor D, Ma D. A new factor Xa-based clotting method with improved specificity for procoagulant phospholipid. Blood Coagul Fibrinolysis. 2003; 14: 773-779. 8Exner T, Michalopoulos N, Pearce J, Xavier R, Ahuja M. Simple method for removing DOACs from plasma samples. Thromb Res. 2018; 163: 117-122. 9Sniecinski MR, Nielsen GV, Tanaka K. Searching for an alternative anticoagulant for cardiopulmonary bypass:does two plus two equal two? Anesth Analg. 2022; 135(1): 49-51. 10Nadtochiy SM, Stefanos T, Angona RE, et al. Rivaroxaban reduces the dabigatran dose required for anticoagulation during simulated cardiopulmonary bypass. Anaesth Analg. 2022; 135: 52-59. 11Douketis DJ, Foster AG, Crowther AM. Clinical risk factors and timing of recurrent venous thromboembolism during the initial 3 months of anticoagulant therapy. Arch Intern Med. 2000; 160(22): 3431-3436. 12Arachchillage DRJ, Besser M, Maclean R, Baglin T, van Veen JJ. Combined factor IIa and Xa inhibitor therapy for thrombosis whilst on therapeutic anticoagulant. Thromb Res. 2016; 143: 137-140. Citing Literature Volume45, Issue4August 2023Pages 603-606 ReferencesRelatedInformation

We aimed to review the interfering effect of DOACs on tests for haemostatic function and then to discuss overcoming these with activated carbon (AC) products, thereby eliminating DOAC issues from test plasmas. Recent relevant articles were reviewed and are discussed. Laboratory tests for DOACs, lupus anticoagulant, factor assays and APC Resistance were carried out in such publications with and without an AC product on various instruments using reagents approved for diagnostic use in well-regulated clinical laboratories. All reports on this plasma pre-treatment by AC products agree that they extract DOACs from plasma samples with minimal effect on underlying clotting tests. The specific extraction of DOACs significantly reduced false positive lupus anticoagulant detection and provided more reliable results in clotting factor assays, APC resistance and other thrombophilia tests. Dabigatran and edoxaban seem to be adsorbed more thoroughly by AC from plasmas than rivaroxaban and apixaban. In summary, most of the AC products reviewed here appear to remove DOACs from test plasmas without significantly affecting underlying clotting tests and permit correct diagnosis of various haemostatic conditions despite the initial presence of DOACs. The application of such agents as a sample pre-treatment to overcome the effects of DOACs for routine coagulation testing is supported by the emerging literature.

Introduction: Clotting test results are currently not useful for estimating direct oral anti-coagulant (DOAC) concentrations because baseline results vary. DOAC Stop is a DOAC extracting agent with no effect on clotting factors. We investigated if aPTT (activated partial thromboplastin time) and dRVVT (dilute Russells viper venom time) results might correlate better with DOAC concentrations if results after DOAC extraction were used to estimate a "before/after" value (Correction Ratio). Materials and methods: We used activated partial thromboplastin time (aPTT, PTT-LA) and dilute Russells viper venom time clotting test (dRVVT) results previously recorded on DOAC patient plasmas (25 dabigatran, 15 apixaban, 19 rivaroxaban) without known thrombotic risk factors before and after DOAC extraction. DOAC concentrations had been determined by standard chromogenic assays. Results: Correlations between aPTT and dabigatran, apixaban, and rivaroxaban concentrations were initially poor (0.64, 0.15 and 0.39 respectively). However, they improved significantly to 0.94, 0.89 and 0.80 when the ratios of initial aPTT to the aPTT obtained after DOAC extraction were plotted against DOAC concentration. Still better correlations (0.99, 0.97, 0.95) and much higher sensitivities to the DOACs were obtained when dRVVT (LA Confirm) tests were used following this procedure on the same samples. Conclusions: The correlations of aPTT and dRVVT tests with DOAC concentrations were significantly improved by using the ratio of result "before" to those "after" DOAC extraction. The results indicate that dRVVT (especially LA Confirm) and similar tests might be useful for determining DOAC concentrations more reliably and with better sensitivity than currently possible with clotting tests.

Background The aim of the study was to investigate the specificity of an activated charcoal-based product (DOAC Stop™) initially intended for the specific extraction of direct oral anticoagulants (DOACs) from test plasmas on a range of other anticoagulants. Methods Test plasmas were prepared by adding various anticoagulants to pooled normal plasma at concentrations prolonging an activated partial thromboplastin time (APTT) test by a factor of 1.5-3. These plasmas were treated with DOAC Stop™ for 5 and 20 min. Then APTTs were repeated and residual anticoagulant concentrations estimated from dose-response curves. Results The activated charcoal (AC)-based product was found to extract DOACs efficiently. It also bound the intravenous anticoagulants argatroban and lepirudin, but it had no effect on heparin, enoxaparin or danaparoid in plasma. Among other APTT-inhibiting agents that might be present in test plasmas from patients, it extracted protamine, aprotinin and polymyxin. It had no effect on annexin V, thrombomodulin, a typical lupus anticoagulant, a factor VIII antibody, activated protein C or its activator, but it did bind some cationic inhibitors of the APTT with molecular weight below approximately 30 kDa. Conclusions The AC-based product extracted DOACs efficiently with no effect on heparin-type anticoagulants. It did bind argatroban and hirudin-type anticoagulants, which might occur in plasmas from some inpatients, and APTT results obtained after its use should be interpreted after due consideration of patient medications.

Aim To evaluate a simple method using an adsorbent product (DOAC Stop) for extracting direct oral anti-coagulants (DOACs) from plasmas. Method DOAC Stop was tested on normal and a range of abnormal plasmas initially using activated partial thromboplastin time (APTT) tests and a more DOAC-sensitive Russells viper venom-based clotting test (DOAC Test). Further tests for prothrombin time/International Normalized Ratio (PT/INR), lupus anticoagulants, activated protein C (APC) resistance, antithrombin, plasminogen, protein C and S were carried out on various patient samples. Results DOAC Stop was found to remove all types of DOACs including dabigatran, apixaban, rivaroxaban and edoxaban from test plasmas with minimal effect on any of the (mainly clotting) tests considered in this study. Summary DOAC Stop can be used to identify plasmas containing DOAcs using simple clotting tests. It reduces the false positivity for lupus anticoagulants observed in dilute Russells viper venom time (dRVVT) tests on DOAC-containing plasmas and could be useful for eliminating unwanted effects of DOACs on routine coagulation testing.

Background The dilute Russell's viper venom time (dRVVT) has been suggested for the assessment of the intensity of anticoagulation of all direct oral anticoagulants (DOACs). This study aimed to compare the performance of an optimized liquid-stable dRVVT-based DOAC assay (DRVV-DOAC) on clinical samples before and after mixing these with normal pooled plasma (NPP). Methods Forty-one apixaban, 25 dabigatran, 56 rivaroxaban and 49 vitamin K antagonists (VKAs) plasma samples were included for retrospective analysis. Plasma DOAC concentrations were determined by liquid chromatography coupled with tandem mass-spectrometry. INR was determined for all VKA samples. DRVV-DOAC was performed with an original ready-to-use reagent (Haematex Research™) where plasma samples were tested neat and in a 1:1 mix with NPP. Results Plasma concentrations ranged from 1 to 406 ng/ml for apixaban, 0 to 386 ng/ml for dabigatran and 0 to 719 ng/ml for rivaroxaban. INR ranged from 2.2 to 6.1. DRVV-DOAC correlated well with plasma concentrations (r2 = 0.70, 0.94, 0.63 (non-mixed procedure) and 0.77, 0.97, 0.86 (mixed procedure) for apixaban, dabigatran and rivaroxaban, respectively). DRVV-DOAC measurements in the normal range ruled out dabigatran and rivaroxaban concentrations above 30 and 50 ng/ml, but performance was lower for apixaban. DRVV-DOAC was sensitive to VKA samples but poorly reflected INR values. When VKA samples were mixed with NPP, DRVV-DOAC measurements decreased to values close to baseline clotting time. Conclusions DRVV-DOAC is a quick method which showed increased sensitivity compared with other phospholipid-rich dRVVT reagents already investigated. Mixing samples with NPP improved the specificity but reduced sensitivity, especially for apixaban.

Professor Jerry Koutts was a larger-than-life figure in the arena of Australian Haematology, while also enjoying international recognition. He was an innovator in the diagnosis of inherited bleeding disorders and founded (in the early 1980s) the Clinical Haematology Department at Westmead Hospital, in Sydney's then growing western suburbs, and at that time a brand new public teaching hospital planned to be the largest such facility in the Sydney landscape.

Objective To investigate the biological effects of foam sclerotherapy in vivo. Materials and methods Ultrasound-guided sclerotherapy was performed using a 3% sodium tetradecyl sulphate or polidocanol. A total of 15 mL of foam was injected. Samples were collected from antecubital veins, target saphenous veins and the adjoining deep veins before, immediately after and 1 hour after the procedure. Saphenous vein samples were also taken sequentially at set 15 cm intervals. Clotting times, D-dimer, cell counts and biochemical parameters were measured. D-dimer levels were repeated one week later. Results Forty procedures were performed. Systemic clotting times were not affected by the procedure. Injection of 0.5 mL of foam 5 cm away from the relevant junctions resulted in procoagulant activity in the adjoining deep veins (sodium tetradecyl sulphate) and the target saphenous veins (sodium tetradecyl sulphate and polidocanol). The procoagulant effect in the target veins reached a peak at 15 cm but normalised at 45 cm. D-dimer levels were significantly increased 1 hour after treatment with either agent and remained elevated one week later. Sodium tetradecyl sulphate and to a lesser degree polidocanol induced biochemical changes consistent with haemoconcentration. Conclusion Infusion of foam sclerosants results in a distance-dependent procoagulant activity in the exposed vessels. Foam sclerotherapy results in haemoconcentration and elevation of D-dimer.

Testing for new oral anticoagulants withLA-resistant Russells viper venom reagents.An in vitro study -

In the majority of fatal avalanches, skiers and snowmobilers apply load to the snow cover which triggers the initial failure in a weak layer. Understanding how the stress due to the dynamic surface load transmits through the snow cover can help people avoid situations where they can trigger avalanches. Capacitive sensors were used to measure this stress within the mountain snow cover. The three main variables affecting stress transmission through the snow cover investigated in this paper are the type of loading, depth and snow cover stratigraphy. At specific depths, snowmobiles added more stress than skiers did, thus increasing the probability of initiating a fracture in a weak layer and releasing a slab avalanche. The increased penetration depth of snowmobiles into the snow cover compared to skiers was the primary reason for this increase in stress. A decrease in stress was observed with increasing depth. A decrease in stress was observed with increased snow cover hardness. Supportive surface layers created a ‘bridging effect’ that spread stress out laterally and decreased the depth to which it penetrated.

In the majority of fatal avalanches, skiers and snowmobilers apply load to the snowpack which triggers the initial failure in a weak layer. Understanding how the stress from a dynamic surface load transmits through the snowpack can help people avoid situations where they can trigger slab avalanches. Capacitive sensors were used to measure this stress within the mountain snowpack. The three main variables affecting stress transmission through the snowpack investigated in this paper are the type of loading, depth and properties of the snowpack. A decrease in stress was observed with increasing depth. At specific depths, snowmobiles added more stress than skiers did, thus increasing the probability of initiating a fracture in a weak layer and releasing a slab avalanche. The increased penetration depth of snowmobiles into the snowpack compared to skiers is the primary reason for this increase in stress. Falling skiers added about 3 times more stress than typical skiing. Skiers added about 1.5 times more stress than snowboarders. A decrease in stress was observed with increasing depth. Supportive surface layers created a "bridging effect" that spread stress out laterally and decreased the depth to which it penetrated.

Objective: To investigate the in vitro effects of detergent sclerosants sodium tetradecyl sulphate (STS) and polidocanol (POL) on clot formation and lysis.Materials and methods: clot kinetics were assessed in whole blood by thromboelastography (TEG (R)) and rotational thromboelastometry (ROTEM (R)). Fibrinogen was measured by the Clauss method in plasma and factor XIII (FXIII) by enzyme-linked immunosorbent assay (ELISA). Turbidity measurements were used to assess clot lysis in plasma, and fibrinolysis in non-cross-linked and cross-linked fibrin. D-dimer was measured by VIDAS (R), STA (R) Liatest (R) and AxSYM (R) assays.Results: Strong clots were formed at low sclerosant concentrations (0.075-0.1%). At midrange concentrations (0.15% STS, 0.15-0.3% POL), both agents inhibited the contribution of platelets to clot firmness and formed weak clots prone to lysis. At higher concentrations (STS >= 0.3% and POL >= 0.6%), clot formation was inhibited. STS destroyed FXIII at >= 0.15% and fibrinogen at >= 0.6%. Neither sclerosant had a significant effect on cross-linked fibrin, but STS had a lytic effect on non-cross-linked fibrin. STS caused an artefactual elevation of D-dimer in the VIDAS (R) assay when fibrinogen was present.Conclusion: Detergent sclerosants demonstrated a trimodal effect on clot formation, initiating strong clots at low concentrations, weak clots at midrange concentrations and preventing clot formation at higher concentrations. Neither agent had fibrinolytic activity. (C) 2010 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.

It has been widely accepted that microparticles expose phosphatidylserine which in turn binds annexin V. It was the objective of this study to compare the antigenic characteristics and phospholipid-dependent procoagulant activity of annexin V positive and -negative subpopulations of platelet-derived microparticles. Annexin V positive and -negative microparticles were identified and characterised using flow cytometry and procoagulant activity was measured by a phospholipid-dependent assay (XACT). In unstimulated platelet-poor plasma, 80% of platelet-derived microparticles failed to bind annexin V. Varying the assay constituents (buffer, calcium and annexin V concentration) did not alter annexin V binding. The proportion of microparticles that bound annexin V was dependent upon the agonist, with physiological agonists such as collagen resulting in fewer annexin V binding microparticles than non-physiological agonists such as ionophore. CD42b (glycoprotein Ib) expression was significantly decreased and CD62p and CD63 expression were significantly increased in annexin V positive compared to annexin V negative subpopulations. There was no significant difference in CD41, CD61, CD42a and CD40L expression between annexin V positive and -negative subpopulations. A significant correlation between annexin V binding and XACT was found (p=0.033). Annexin V inhibited greater than 95% of phospholipid activity, suggesting that annexin V binding was a true reflection of procoagulant activity. The majority of platelet-derived microparticles in unstimulated plasma failed to bind annexin V and showed significantly increased levels of CD42b compared to annexin V positive events. Phospholipid-dependent procoagulant activity is limited to the annexin V positive subpopulation and is agonist-dependent. The significance of annexin V negative microparticles is unclear, however, it is possible that they possess other activities aside from procoagulant phospholipid activity.

OBJECTIVE:To investigate the effects of Sodium Tetradecyl Sulphate (STS) and Polidocanol (POL) on fibrinolytic mechanisms.MATERIALS AND METHODS:Measurements were done with serial dilutions of sclerosants in whole blood (WB), platelet rich (PRP) and platelet poor plasma (PPP). Control experiments were done in 5% bovine serum albumin (BSA), spiked with the enzyme/inhibitor. Plasminogen was measured with a chromogenic assay. Alpha-2-antiplasmin (AP) activity, plasmin-alpha-2-antiplasmin (PAP) complexes, plasminogen activator inhibitor-1 (PAI-1) activity, tissue plasminogen activator (t-PA) total antigen, t-PA activity, t-PA/PAI-1 complexes, thrombin activatable fibrinolysis inhibitor (TAFI) antigen and activated TAFI (TAFIa) were measured by ELISA.RESULTS:At high concentrations (>0.3%), STS destroyed plasminogen, PAI-1, t-PA/PAI-1 complexes and total t-PA antigen but increased t-PA activity. At low concentrations (<0.3%), both agents reduced PAP complexes while increasing AP activity. Low concentration STS increased PAI-1 activity, t-PA/PAI-1 complexes, TAFI and TAFIa. Low concentration POL mildly increased the total t-PA antigen and TAFI.CONCLUSION:At low concentrations, both agents demonstrated a prothrombotic, antifibrinolytic (increase in PAI-1, total t-PA antigen, AP, TAFI and TAFIa) activity. At high concentrations, STS demonstrated non-prothrombotic (destruction of PAI-1, t-PA/PAI-1 complexes), antifibrinolytic (destruction of plasminogen, increase in AP) activity while POL had minimal effect.

The objective of this study was to validate a simple factor Xa-based clotting test developed to monitor procoagulant phospholipids (PPLs) and platelet-derived microparticles (PMPs). This assay is easily automated, giving it a major advantage over the more laborious and expensive flow cytometry, electron microscopy and ELISA techniques in general usage at present. The intra-assay and inter-assay variation coefficients were less than 5% at both low and high levels of PPLs. The test is not affected by other clotting factors is assured by the use of a phospholipid-free animal plasma, which provides excess factor V, fibrinogen and prothrombin. This test was evaluated in apparently healthy volunteers and in selected patient groups associated with increased levels of PMPs in the circulation (diabetes mellitus, sickle cell disease, thyroid cancer and patients with multiple trauma). The study showed that XaCT has a high discriminating power for PPLs and that the patient groups have significantly highly increased PPLs activities when compared with healthy volunteers. Although of a preliminary nature, the test has shown that it has the sensitivity for discriminating severity of disease, as it could detect patients in sickle cell crisis and differentiate between type 1 and 2 diabetes. In conclusion, the combination of reliability, reproducibility and easy performance makes the XaCT assay a simple test to screen for PPLs in plasma samples.