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result(s) for
"Xi"
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Abelacimab for Prevention of Venous Thromboembolism
2021
In patients undergoing total knee replacement, a single injection of abelacimab (an antibody to factor XI) administered postoperatively was superior to standard care with enoxaparin for the prevention of venous thromboembolism. Bleeding events were rare.
Journal Article
Abelacimab versus Rivaroxaban in Patients with Atrial Fibrillation
by
Murphy, Sabina A.
,
Bloomfield, Daniel
,
Giugliano, Robert P.
in
Administration, Oral
,
Aged
,
Aged, 80 and over
2025
Abelacimab is a fully human monoclonal antibody that binds to the inactive form of factor XI and blocks its activation. The safety of abelacimab as compared with a direct oral anticoagulant in patients with atrial fibrillation is unknown.
Patients with atrial fibrillation and a moderate-to-high risk of stroke were randomly assigned, in a 1:1:1 ratio, to receive subcutaneous injection of abelacimab (150 mg or 90 mg once monthly) administered in a blinded fashion or oral rivaroxaban (20 mg once daily) administered in an open-label fashion. The primary end point was major or clinically relevant nonmajor bleeding.
A total of 1287 patients underwent randomization; the median age was 74 years, and 44% were women. At 3 months, the median reduction in free factor XI levels with abelacimab at a dose of 150 mg was 99% (interquartile range, 98 to 99) and with abelacimab at a dose of 90 mg was 97% (interquartile range, 51 to 99). The trial was stopped early on the recommendation of the independent data monitoring committee because of a greater-than-anticipated reduction in bleeding events with abelacimab. The incidence rate of major or clinically relevant nonmajor bleeding was 3.2 events per 100 person-years with 150-mg abelacimab and 2.6 events per 100 person-years with 90-mg abelacimab, as compared with 8.4 events per 100 person-years with rivaroxaban (hazard ratio for 150-mg abelacimab vs. rivaroxaban, 0.38 [95% confidence interval {CI}, 0.24 to 0.60]; hazard ratio for 90-mg abelacimab vs. rivaroxaban, 0.31 [95% CI, 0.19 to 0.51]; P<0.001 for both comparisons). The incidence and severity of adverse events appeared to be similar in the three groups.
Among patients with atrial fibrillation who were at moderate-to-high risk for stroke, treatment with abelacimab resulted in markedly lower levels of free factor XI and fewer bleeding events than treatment with rivaroxaban. (Funded by Anthos Therapeutics; AZALEA-TIMI 71 ClinicalTrials.gov number, NCT04755283.).
Journal Article
The Sultan of Byzantium
A sweeping novel weaving ancient Byzantine history and legend with a searing modern day romantic adventure.
Factor XI Antisense Oligonucleotide for Prevention of Venous Thrombosis
by
Monia, Brett P
,
Büller, Harry R
,
Bhanot, Sanjay
in
Adult
,
Aged
,
Anticoagulants - administration & dosage
2015
Enoxaparin is used to prevent deep-vein thrombosis in patients undergoing total knee arthroplasty. In this study, an antisense oligonucleotide against factor XI was more effective than enoxaparin in preventing deep-vein thrombosis and caused less bleeding.
Patients undergoing total knee arthroplasty are at risk for postoperative venous thromboembolism. Conventional therapies for the prevention of this complication involve inhibitors of factor Xa or thrombin, such as enoxaparin. These drugs are effective but are associated with a risk of bleeding.
1
The pathogenesis of venous thromboembolism after surgery is incompletely understood, but tissue factor exposed at the surgical site is thought to be the major driver through the extrinsic pathway of coagulation (Figure 1).
2
The role of the intrinsic pathway in this process is uncertain.
Experimental data suggest that targeting factor XI, a key component of the intrinsic pathway, . . .
Journal Article
Disseminated intravascular coagulation
by
Toh, Cheng-Hock
,
Gando, Satoshi
,
Levi, Marcel
in
631/250/2500
,
692/420/256/1980
,
692/699/1585/2159
2016
Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by widespread intravascular activation of coagulation that can be caused by infectious insults (such as sepsis) and non-infectious insults (such as trauma). The main pathophysiological mechanisms of DIC are inflammatory cytokine-initiated activation of tissue factor-dependent coagulation, insufficient control of anticoagulant pathways and plasminogen activator inhibitor 1-mediated suppression of fibrinolysis. Together, these changes give rise to endothelial dysfunction and microvascular thrombosis, which can cause organ dysfunction and seriously affect patient prognosis. Recent observations have pointed to an important role for extracellular DNA and DNA-binding proteins, such as histones, in the pathogenesis of DIC. The International Society on Thrombosis and Haemostasis (ISTH) established a DIC diagnostic scoring system consisting of global haemostatic test parameters. This scoring system has now been well validated in diverse clinical settings. The theoretical cornerstone of DIC management is the specific and vigorous treatment of the underlying conditions, and DIC should be simultaneously managed to improve patient outcomes. The ISTH guidance for the treatment of DIC recommends treatment strategies that are based on current evidence. In this Primer, we provide an updated overview of the pathophysiology, diagnosis and management of DIC and discuss the future directions of basic and clinical research in this field.
Disseminated intravascular coagulation can be caused by various infectious and non-infectious insults, such as sepsis and trauma, respectively. It is characterized by the widespread activation of coagulation and, depending on the underlying condition, can manifest as bleeding and/or thrombosis.
Journal Article