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Thrombin Hemostatic

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261. Prevention of Peri-operative Venous Thromboembolism in Paedatric Patients

for comment on accuracy, evidence base and recommendations made, from which each response was addressed in subsequent draft versions. The draft guideline was then submitted for review to the APA council members and each response addressed. A final draft was submitted to council for editorial input and quality check. 31 10. References 1. Andrew M, Vegh P, Johnston M, Bowker J, Ofosu F, Mitchell L. Maturation of the Hemostatic System During Childhood. Blood. 1992;80(8):1998–2005. 2. Andrew M, David M, Adams (...) Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e737S–801S. 46. Andrew M, Mitchell L, Vegh P, Ofosu F. Thrombin regulation in children differs from adults in the absence and presence of heparin. Thromb Haemost. 1994 Dec;72(6):836–42. 47. Dix D, Andrew M, Marzinotto V, Charpentiel K, Bridge S, Monagle P, et al. The use of low molecular weight heparin in pediatric patients: a prospective cohort

2017 Association of Paediatric Anaesthetists of Great Britain and Ireland

263. Management of Bleeding in Patients on Oral Anticoagulants

. How- ever, noninvasively measured blood pressure may not alwaysre?ectintra-arterialpressure.Continuousinvasive measurement of mean arterial pressure is considered superiorforassessment,andavalue 50 ng/mL, and for patients requiring an invasive procedure with high bleeding risk and a DOAC level>30 ng/mL (17). Anti-Xa¼ anti–factor Xa; aPTT¼ activated partial thromboplastin time; DOAC¼ direct-acting oral anticoagulant; PT¼ prothrombin time; TT¼ thrombin time. TABLE 2 Suggestions for Laboratory (...) –factor Xa; aPTT¼ activated partial thromboplastin time; DOAC¼ direct-acting oral anticoagulant; ECA¼ ecarin chromogenic assay; ECT¼ ecarin clotting time; PT¼ prothrombin time; TT¼ thrombin time. Tomaselli et al. JACC VOL. -,NO. -,2017 2017 ACC ECDP on Management of Bleeding in Patients on Oral Anticoagulants -,2017:-–- 8may worsen the coagulopathy and perpetuate the bleeding.Thereisnoevidencetosupporttheuseofone crystalloid solution over another (24); however, caution should be given

2017 American College of Cardiology

265. Management of Patients on Non?Vitamin K Antagonist Oral Anticoagulants in the Acute Care and Periprocedural Setting: A Scientific Statement From the American Heart Association Full Text available with Trip Pro

for indepen- dent peer review and approved for publication by the AHA Manuscript Oversight Committee on April 29, 2016. PHARMACOLOGY OF NOACS NOACs act through direct inhibition of thrombin or inhi- bition of factor Xa (Figure 1). Dabigatran etexilate me- sylate is a competitive direct thrombin inhibitor. Rivar- oxaban, apixaban, and edoxaban inhibit factor Xa and prothrombinase activity, thus inhibiting the conversion of prothrombin to thrombin. Thrombin catalyzes the con- version of fibrinogen to fibrin (...) ; activates factors V, VIII, XI, and XIII; and activates platelets. Therefore, inhibiting thrombin decreases thrombus formation. In contrast with warfarin, NOACs have a rapid onset of action, a shorter half-life, and more predictable pharmacokinet- ics. Routine therapeutic monitoring was not done in the major NOAC efficacy trials and is at present not recom- mended in usual clinical practice. Information pertaining to NOAC dose, time to peak effect, and time to offset of effect is outlined in Table 1

2017 American Heart Association

267. Myths and Realities: Is My Cirrhotic Patient Auto-anticoagulated?

a hemostatic plug; second, they promote the generation of thrombin. Platelet activation occurs during endothelial damage. Platelets undergo a remarkable shape change to extend pseudopods to form a platelet plug in the damaged vessel. They then adhere to the vessel wall when complexed with von Willebrand Factor (vWF), which is subsequently degraded by ADAMTS13. Platelet activation also brings activated clotting factors to [1]. Platelet Function in the context of Cirrhosis: Platelet function is changed both (...) abnormal processing and glycosylation of factors such as fibrinogen (Table 1), which can affect their function and potentially be prothrombotic. It is well accepted that the summation of these abnormalities culminates in impaired hemostasis. However, thrombin production is surprisingly well preserved in compensated cirrhosis. Coagulation Cascade: the fibrinolysis players In addition to synthesizing coagulation factors that promote a hemostatic plug, the liver also produces the inhibitors

2017 Clinical Correlations

268. A decreased and less sustained desmopressin response in hemophilia A carriers contributes to bleeding Full Text available with Trip Pro

Assessment Tool (ISTH-BAT). DDAVP (0.3 μg/kg) was administered either IV or subcutaneously (SC), and blood was drawn at baseline and 1, 2, and 4 hours postadministration. Blood was assessed for factor VIII (FVIII) level, von Willebrand factor (VWF) antigen (VWF:Ag), VWF activity (VWF:RCo or VWF:GPIbM), thromboelastography (TEG), and thrombin generation assay (TGA) at all points, and for VWF propeptide (VWFpp):Ag ratio and ABO blood type at baseline. Carriers were older than control patients (median age (...) with those with normal bleeding scores (P = .036). Hemophilia A carriers have a lower and less sustained FVIII response to DDAVP, suggesting an impaired ability to respond to hemostatic stress, which contributes to bleeding.© 2018 by The American Society of Hematology.

2018 Blood advances

269. Prothrombin conversion is accelerated in the antiphospholipid syndrome and insensitive to thrombomodulin Full Text available with Trip Pro

, we demonstrate that in APS, the hemostatic balance shifts toward a more prothrombotic phenotype due to elevated prothrombin conversion but unchanged thrombin inactivation rates. Within the group of APS patients, increased TG and prothrombin conversion are associated with a history of thrombosis.© 2018 by The American Society of Hematology. (...) Prothrombin conversion is accelerated in the antiphospholipid syndrome and insensitive to thrombomodulin Antiphospholipid syndrome (APS) is a condition in which the presence of antibodies against phospholipid-binding proteins is associated with thrombophilia and/or pregnancy morbidity. Although antiphospholipid antibodies have anticoagulant characteristics in vitro, they are associated with thromboembolic complications. Thrombin generation (TG) is a sensitive global test of coagulation

2018 Blood advances

270. Factor XIII in plasma, but not in platelets, mediates red blood cell retention in clots and venous thrombus size in mice Full Text available with Trip Pro

imposing deleterious hemostatic consequences are 2 critical unresolved questions. FXIII is present in multiple compartments, including plasma (FXIIIplasma) as a heterotetramer of A2 and B2 subunits and platelets (FXIIIplt) as an A2 homodimer. We determined the role of the FXIII compartment and level in clot contraction, composition, and size in vitro and using in vivo models of hemostasis and venous thrombosis. Reducing overall FXIII levels decreased whole blood clot weight but did not alter thrombin

2018 Blood advances

271. Prognostic value of D-dimer and markers of coagulation for stratification of abdominal aortic aneurysm growth Full Text available with Trip Pro

Prognostic value of D-dimer and markers of coagulation for stratification of abdominal aortic aneurysm growth Abdominal aortic aneurysm (AAA) is associated with high morbidity and mortality and is an established cause of unbalanced hemostasis. A number of hemostatic biomarkers have been associated with AAA; however, the utility of hemostatic biomarkers in AAA diagnosis and prognosis is unclear. The aim of the present study was to characterize the potential prognostic value of D-dimer (...) and markers of altered hemostasis in a large cohort of patients with AAAs characterized by either fast or slow aneurysm growth (frequency matched for baseline diameter) and subaneurysmal dilations. We measured plasma concentrations of thrombin-antithrombin (TAT) complex, platelet factor 4 (PF4), and D-dimer in 352 patients with either fast-growing AAAs (>2 mm/y), slow-growing AAAs (<2 mm/y), subaneurysmal aortic dilations, or nonaneurysmal aortas. Plasma D-dimer and TAT were significantly elevated in both

2018 Blood advances

272. New/Novel Oral Anticoagulants (NOACs): Management of Bleeding

effect 1 ? Not relevant ? Not relevant Thrombin time ? Normal indicates no dabigatran present ? If increased, indicates some anticoagulant effect ? Not relevant ? Not relevant Calibrated anti-Xa ? Not relevant ? 30 ng/mL = likely significant anticoagulant effect 1 ? 30 ng/mL = likely significant anticoagulant effect 1 1 There are no data to establish a hemostatic threshold below which drug levels are unlikely to affect hemostasis. These estimates are extrapolated from observations in clinical trials (...) New/Novel Oral Anticoagulants (NOACs): Management of Bleeding © 2016 Thrombosis Canada Page 1 of 1 NOVEL ORAL ANTICOAGULANTS (NOACS): MANAGEMENT OF BLEEDING OBJECTIVE: To assist clinicians in the management of bleeding in patients receiving direct oral anticoagulants (NOACs). BACKGROUND: Two oral Factor Xa inhibitors (apixaban and rivaroxaban) and an oral thrombin inhibitor (dabigatran) are approved for clinical use in Canada based on findings from large randomized trials. Like all other

2016 Thrombosis Interest Group of Canada

273. New/Novel Oral Anicoagulants (NOACs): Coagulation Tests

effect 1 ? Not relevant ? Not relevant Thrombin time ? Normal indicates no dabigatran present ? If increased, indicates some anticoagulant effect ? Not relevant ? Not relevant Calibrated anti-Xa ? Not relevant ? 30 ng/mL = likely significant anticoagulant effect 1 ? 30 ng/mL = likely significant anticoagulant effect 1 1 There are no data to establish a hemostatic threshold below which drug levels are unlikely to affect hemostasis. These estimates are extrapolated from observations in clinical trials (...) New/Novel Oral Anicoagulants (NOACs): Coagulation Tests © 2016 Thrombosis Canada Page 1 of 1 NOVEL ORAL ANTICOAGULANTS (NOACS): MANAGEMENT OF BLEEDING OBJECTIVE: To assist clinicians in the management of bleeding in patients receiving direct oral anticoagulants (NOACs). BACKGROUND: Two oral Factor Xa inhibitors (apixaban and rivaroxaban) and an oral thrombin inhibitor (dabigatran) are approved for clinical use in Canada based on findings from large randomized trials. Like all other

2016 Thrombosis Interest Group of Canada

274. New/Novel Oral Anticoagulants (NOACS): Comparison and Frequently-Asked Questions

of the procedure; consideration can also be given to the use of the pro-hemostatic tranexamic acid mouthwash before and after the procedure. Alternatively, the patient can skip one day’s dose of the NOAC before the procedure and resume the NOAC on the evening after the procedure. For the management of patients who require other procedures or surgery, see the Clinical Guide: New/Novel Oral Anticoagulants (NOACs): Peri-Operative Management. What if the patient has a prosthetic heart valve? In patients (...) of action Direct factor IIa (thrombin) inhibitor Direct factor Xa inhibitor Direct factor Xa inhibitor Renal clearance 80% 33% (active drug) 25% Half-life: Normal to mild impairment (CrCl >50 mL/min) 7-17 hours 7-11 hours 8-12 hours Moderate renal impairment (CrCl 30-49 mL/min) 17-20 hours 7-11hours 8-12 hours Severe renal impairment (CrCl 50 110 or 150 mg twice daily Consider 110 mg dose in patients at increased risk for bleeding or in the elderly (e.g. age = 80 years) Measure CrCl every 12 months 30

2015 Thrombosis Interest Group of Canada

275. Detection of A and B Subunits of Factor XIII and Detection of an Anti-Factor XIII by ELISA

precursor cells. On average, 50% of FXIII-B is found in its free form, and helps stabilize FXIII-A by preventing it from being rapidly eliminated from circulation. Plasma thrombin, with its fibrin cofactors (fibrinogen) and Ca 2+ ions, initiates the activation of FXIII during the final stage of the coagulation cascade. Thrombin cleaves the FXIII-A activation peptide and, in the presence of Ca 2+ , A and B subunits dissociate, and the FXIII-A 2 dimer transforms into an active transglutaminase, activated (...) deficiency have been reported worldwide [Wada et al., 2013]. Clinically, FXIII-B deficiency is characterized by mild bleeding caused by the presence of small quantities of plasma FXIII-A (< 10%) and normal concentrations of intracellular FXIII-A (Table 1). For this reason, the diagnosis of congenital FXIII-B deficiency may easily be missed. However, when there are other concurrent hemostatic disorders, severe or deadly hemorrhagic episodes may be observed [Schroeder and Kohler, 2013]. Treatment

2015 Canadian Agency for Drugs and Technologies in Health - Rapid Review

276. Reducing the Risk - Thrombosis and Embolism during Pregnancy and the Puerperium

be avoided antenatally and intrapartum because of the risk of anaphylactoid reaction. Oral thrombin and Xa inhibitors Non-vitamin K antagonist oral anticoagulants (NOACs) should be avoided in pregnant women. [New 2015] Use of NOACs is not currently recommended in women who are breastfeeding. [New 2015] Anti-embolism stockings The use of properly applied anti-embolism stockings (AES) of appropriate size and providing graduated compression with a calf pressure of 14–15 mmHg is recommended in pregnancy

2015 Royal College of Obstetricians and Gynaecologists

277. Evaluation of hemostasis in patients with end-stage renal disease. Full Text available with Trip Pro

PFA-ADP-test (p<0.05), while no patient on peritoneal dialysis and no HC offered this modification. Thrombin generating potential was significantly lower in patients on hemodialysis, while clot lysis time revealed a hypofibrinolytic state in patients on hemo- and peritoneal dialysis compared to HC (p<0.001). In conclusion, patients with end-stage renal disease have complex hemostatic changes with both hyper- and hypocoagulable features, which are dependent on use and type of dialysis (...) . Hypercoagulable features include elevated fibrinogen levels and a hypofibrinolytic state, whereas hypocoagulable features include decreased thrombin generating capacity and platelet dysfunction. Our results may contribute to a more rational approach to hemostatic management in these patients.

2019 PLoS ONE

278. VWF/ADAMTS13 imbalance, but not global coagulation or fibrinolysis, is associated with outcome and bleeding in acute liver failure. Full Text available with Trip Pro

VWF levels and lower ADAMTS13 activity compared to those without bleeding. Thrombin generation and CLT did not differ significantly between bleeding and non-bleeding patients.Rebalanced hemostatic status was confirmed in a large cohort of patients with ALI/ALF demonstrating that VWF/ADAMTS13 imbalance is associated with poor outcome and bleeding. The association between VWF/ADAMTS13 imbalance and bleeding suggest that bleeding in ALF relates more to systemic inflammation than a primary (...) of well-characterized ALF patients from the Acute Liver Failure Study Group (ALFSG).Citrated plasma samples taken on admission from 676 patients with ALF or acute liver injury (ALI; INR ≥ 2.0 without hepatic encephalopathy) were used to determine levels of VWF, ADAMTS13 activity, thrombomodulin-modified thrombin generation, and clot lysis time (CLT) and compared with levels in 40 healthy controls.Patients had 3-fold increased VWF levels, 4-fold decreased ADAMTS13 activity, similar thrombin generating

2020 Hepatology

279. Fibrin lysability is associated with central obesity and inflammation in women with polycystic ovary syndrome. (Abstract)

with PCOS and 35 controls of comparable age and body mass index were included. Hemostatic markers (fibrin lysability, fibrinogen, coagulation factor XIII, plasminogen, plasminogen activator inhibitor 1 [PAI-1], plasmin inhibitor, thrombin activatable fibrinolysis inhibitor (TAFI), D-dimer), C-reactive protein (CRP), body mass index, waist-to-hip ratio, CFM determined by Dual-energy X-ray absorptiometry scan, and sex hormones (testosterone estradiol, and sex hormone binding globulin) were determined.TAFI (...) Fibrin lysability is associated with central obesity and inflammation in women with polycystic ovary syndrome. Polycystic ovary syndrome (PCOS) is characterized by increased central fat mass (CFM), hyper-inflammation, and hemostatic alterations; the risk of cardiovascular disease may also be increased. Reduced fibrin lysability is a risk factor for cardiovascular disease. The present study assessed fibrin lysability in women with PCOS and controls of similar age and body mass index.Ninety women

2020 Acta Obstetricia et Gynecologica Scandinavica

280. Global Coagulation Assays in Transgender Women on Oral and Transdermal Estradiol Therapy. (Abstract)

study.General community.Transgender women, cisgender male and cisgender female controls.Citrated blood samples were analyzed for (i) whole blood thromboelastography (TEG®5000), (ii) platelet-poor plasma thrombin generation (calibrated automated thrombogram); and (iii) platelet-poor plasma fibrin generation (overall hemostatic potential assay). Mean difference (95% confidence intervals) between groups are presented.Twenty-six transgender women (16 oral estradiol, 10 transdermal estradiol) were compared (...) Global Coagulation Assays in Transgender Women on Oral and Transdermal Estradiol Therapy. The thrombotic effects of estradiol therapy in transgender women are unclear. Global coagulation assays (GCA) may be better measures of hemostatic function compared with standard coagulation tests.To assess the GCA profiles of transgender women in comparison to cisgender controls and to compare how GCA differ between routes of estradiol therapy in transgender women.Cross-sectional case-control

2020 Journal of Clinical Endocrinology and Metabolism

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