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Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
Inflammatory Bowel Disease IV: Clinical Manifestations01:20

Inflammatory Bowel Disease IV: Clinical Manifestations

Inflammatory bowel disease (IBD) encompasses two major chronic disorders—ulcerative colitis and Crohn’s disease—each characterized by relapsing episodes of gastrointestinal inflammation. Although they share certain clinical features, their patterns of involvement and manifestations differ in ways that aid diagnosis and guide management.Ulcerative ColitisUlcerative colitis is limited to the colon and rectum and involves continuous inflammation of the mucosal layer. The disease course is marked...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...

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Related Experiment Video

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Fluorescence-mediated Tomography for the Detection and Quantification of Macrophage-related Murine Intestinal Inflammation
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Published on: December 15, 2017

Tissue factor exposing microparticles in inflammatory bowel disease.

Julia Palkovits1, Gottfried Novacek, Marietta Kollars

  • 1Department of Internal Medicine III, Division of Gastroenterology and Hepatology; Medical University of Vienna, Vienna, Austria.

Journal of Crohn'S & Colitis
|June 19, 2012
PubMed
Summary
This summary is machine-generated.

Increased numbers of circulating tissue factor-positive microparticles (TF(+)MPs) were found in inflammatory bowel disease (IBD) patients. However, these TF(+)MPs did not correlate with coagulation activation or disease activity in IBD.

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Fluorescence-mediated Tomography for the Detection and Quantification of Macrophage-related Murine Intestinal Inflammation
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Published on: December 15, 2017

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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
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Area of Science:

  • Hematology
  • Gastroenterology
  • Pathophysiology

Background:

  • Circulating procoagulant microparticles (MPs) are implicated in venous thromboembolism (VTE) in inflammatory bowel disease (IBD).
  • The role of tissue factor-positive microparticles (TF(+)MPs), key initiators of coagulation, in IBD pathogenesis remains unstudied.

Purpose of the Study:

  • To investigate the number, origin, and procoagulant activity of TF(+)MPs in IBD patients.
  • To assess the association of TF(+)MPs with hemostasis activation and disease activity in IBD.

Main Methods:

  • A case-control study included 49 IBD patients (Crohn's disease and ulcerative colitis) and 49 healthy controls.
  • Flow cytometry and chromogenic assays quantified TF(+)MPs. D-dimer and C-reactive protein (CRP) measured coagulation and inflammation.
  • Clinical disease activity was assessed using established indices.

Main Results:

  • IBD patients exhibited significantly higher plasma levels of TF(+)MPs compared to controls (P=0.029).
  • Elevated TF(+)MPs were primarily attributed to increased platelet and leukocyte-derived MPs.
  • No correlation was found between TF(+)MP numbers and procoagulant activity, D-dimer levels, or disease activity markers (CRP).

Conclusions:

  • Elevated circulating TF(+)MPs represent a novel hemostatic abnormality in IBD.
  • The lack of correlation with coagulation activation and disease activity challenges the direct pathogenetic role of TF(+)MPs in IBD-related VTE.