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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...
Clot Retraction and Fibrinolysis01:16

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Formation of the Platelet Plug01:22

Formation of the Platelet Plug

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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...
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Related Experiment Video

Updated: Jun 10, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

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

Published on: February 27, 2026

Thrombin generation in ankylosing spondylitis.

Clément Prati1, Evelyne Racadot, Jean-Pierre Cedoz

  • 1Department of Rheumatology, University Teaching Hospital, Besançon, France.

Clinical Rheumatology
|August 18, 2010
PubMed
Summary
This summary is machine-generated.

Ankylosing spondylitis patients show delayed thrombin generation, not increased, with correlations between thrombin parameters and disease activity markers like ESR and CRP.

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A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
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Last Updated: Jun 10, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

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A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Area of Science:

  • Rheumatology
  • Hematology
  • Cardiovascular Medicine

Background:

  • Ankylosing spondylitis (AS) is a chronic inflammatory disease linked to increased cardiovascular risk.
  • Thrombin generation plays a role in thrombosis risk, with endogenous thrombin potential (ETP) indicating hypercoagulability.

Purpose of the Study:

  • To assess thrombosis risk in AS patients compared to healthy individuals.
  • To identify factors associated with elevated thrombosis risk in AS.

Main Methods:

  • Compared thrombin generation parameters (ETP, lag time, Cmax, Tmax, velocity) in 46 AS patients and 24 healthy controls.
  • Recorded clinical data, disease activity (BASDAI), and laboratory markers (ESR, CRP, D-dimer).
  • Excluded patients with prior thrombosis or anti-thrombotic treatment.

Main Results:

  • AS patients exhibited significantly increased lag time and Tmax, suggesting delayed thrombin generation.
  • No significant differences were found in ETP, Cmax, or velocity between AS patients and controls.
  • Correlations were observed between ETP, Cmax, velocity, and disease activity markers (ESR, CRP, BASDAI), and D-dimers.

Conclusions:

  • This study did not find evidence of increased thrombin generation in AS patients.
  • Delayed thrombin generation, indicated by higher lag time and Tmax, may be characteristic of AS.
  • Thrombin generation parameters correlate with AS disease activity and inflammatory markers.