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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

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Related Experiment Video

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The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
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Thrombin generation in antiphospholipid syndrome.

S Zuily1, K Ait Aissa, A Membre

  • 1Inserm, U961, Vandoeuvre-lès-Nancy, France.

Lupus
|May 29, 2012
PubMed
Summary

Patients with antiphospholipid antibodies (aPL) and systemic lupus erythematosus (SLE) exhibit acquired Activated Protein C (APC) resistance. This resistance indicates a hypercoagulable state, increasing thrombosis risk in these conditions.

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Area of Science:

  • Hematology
  • Immunology
  • Rheumatology

Background:

  • Acquired Activated Protein C (APC) resistance is a condition that can lead to a hypercoagulable state.
  • Antiphospholipid antibodies (aPL) are associated with an increased risk of thrombosis.
  • Systemic lupus erythematosus (SLE) is an autoimmune disease that can be associated with aPL and thrombosis.

Purpose of the Study:

  • To investigate acquired APC resistance in patients with aPL.
  • To compare APC resistance in patients with primary antiphospholipid syndrome (APS) and patients with SLE, with and without APS.

Main Methods:

  • Utilized a thrombin generation assay to measure APC resistance.
  • Quantified APC inhibition of thrombin generation using the IC(50)-APC parameter.
  • Compared patient groups (primary APS, SLE without APS, SLE/APS) with healthy controls.

Main Results:

  • All patient groups showed significantly increased IC(50)-APC values compared to controls (p < 0.001).
  • Patients with SLE/APS had the highest median IC(50)-APC (64.1), followed by SLE without APS (27.3) and primary APS (15.3).
  • Control group median IC(50)-APC was 10.4.

Conclusions:

  • Patients with SLE and primary APS demonstrate acquired APC resistance.
  • This APC resistance contributes to a hypercoagulable state in these patient populations.
  • Findings suggest a potential mechanism for the increased thrombotic risk in patients with aPL and SLE.