Prothrombin fragment 1+2 and thrombin???antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases

Chamouard, P.; Grunebaum, Lélia; Wiesel, Marie-Louise; Frey, P.; Wittersheim, Christian; Sapin, René; Baumann, René; Cazenave, Jean‐Pierre

doi:10.1097/00042737-199512000-00010

Cited by 71 publications

(44 citation statements)

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“…Several studies have been published describing the markers of activation of coagulation, such as prothrombin fragment 1 ϩ 2 (F1 ϩ 2), the thrombin-antithrombin III complex (TAT), fibrinopeptide A (FPA), and fibrinopeptide B (FPB), indicating subclinical activation of coagulation in IBD. 39,51,52 It is debated whether this evidence of coagulatory cascade activation is secondary to chronic inflammation or represents a primary feature of IBD, independent of disease clinical activity. The potential protective effect of an underlying bleeding predisposition in preventing the development of IBD was investigated by Thompson and colleagues,53 who found a significantly decreased risk of development of either CD or UC among patients with either hemophilia or von Willebrand's disease.…”

Section: Hypercoagulability and Prothrombotic State In Ibdmentioning

confidence: 99%

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

Deban

Correale

Vetrano

et al. 2008

The American Journal of Pathology

124

100

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The etiology of Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease (IBD), is still largely unknown. However, it is now clear that the abnormalities underlying pathogenesis of intestinal inflammation are not restricted to those mediated by classic immune cells but also involve nonimmune cells. In particular, advances in vascular biology have outlined a central and multifaceted pathogenic role for the microcirculation in the initiation and perpetuation of IBD. The microcirculation and its endothelial lining play a crucial role in mucosal immune homeostasis through tight regulation of the nature and magnitude of leukocyte migration from the intravascular to the interstitial space. Chronically inflamed IBD microvessels display significant alterations in microvascular physiology and function compared with vessels from healthy and uninvolved IBD intestine. The investigation into human IBD has demonstrated how endothelial activation present in chronically inflamed IBD microvessels results in a functional phenotype that also includes leakiness, chemokine and cytokine expression, procoagulant activity, and angiogenesis. This review contemplates the newly uncovered contribution of intestinal microcirculation to pathogenesis and maintenance of chronic intestinal inflammation. In particular, we assess the multiple roles of the microvascular endothelium in innate immunity, leukocyte recruitment, coagulation and perfusion, and immune-driven angiogenesis in IBD.

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Section: Hypercoagulability and Prothrombotic State In Ibdmentioning

confidence: 99%

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

Deban

Correale

Vetrano

et al. 2008

The American Journal of Pathology

124

100

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“…Therefore, because myofibroblast-derived PGE 2 is important in regulating epithelial chloride secretion (11), the ability of thrombin to upregulate PGE 2 synthesis in lamina propria myofibroblasts represents a mechanism by which thrombin might further amplify epithelial secretory responses on a longer term basis and contribute to intestinal host defense. An increase in the generation of thrombin from prothrombin has been associated with inflammation in both Crohn's disease (18) and ulcerative colitis (35).…”

mentioning

confidence: 99%

PAR₁-dependent and independent increases in COX-2 and PGE₂ in human colonic myofibroblasts stimulated by thrombin

Seymour

Zaidi

Hollenberg

et al. 2003

American Journal of Physiology-Cell Physiology

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“…To date, however, no consistent relationship with homocysteinemia and development of thromboembolism has been defined in patients with inflammatory bowel disease [12,13] . Finally, changes associated with subclinical activation of the coagulation cascade [14][15][16] along with diminished factor ⅩⅢ have been reported [16,17] .…”

Section: Acquired Risk Factorsmentioning

confidence: 98%

Venous thromboembolism with infl ammatory bowel disease

Freeman

2008

WJG

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Venous thrombosis and thromboembolism appear to be increased in patients with inflammatory bowel disease. Although several acquired and genetic risk factors are known, about half that develop a thromboembolic event have no identifiable risk factor. Control of the inflammatory process is thought to be the key factor in risk reduction for thrombotic events. Prophylactic use of anticoagulants is not universally recommended, but possible use should be reviewed in an individual patient after evaluation of the risks, such as hemorrhage, compared to potential benefits. Particular consideration should be given if there has been a prior thrombotic event, if hospitalization will require surgery, or if an underlying coagulation disorder is present.

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Prothrombin fragment 1+2 and thrombin???antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases

Cited by 71 publications

References 0 publications

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

PAR₁-dependent and independent increases in COX-2 and PGE₂ in human colonic myofibroblasts stimulated by thrombin

Venous thromboembolism with infl ammatory bowel disease

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Prothrombin fragment 1+2 and thrombin???antithrombin III complex as markers of activation of blood coagulation in inflammatory bowel diseases

Cited by 71 publications

References 0 publications

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

Multiple Pathogenic Roles of Microvasculature in Inflammatory Bowel Disease: A Jack of All Trades

PAR1-dependent and independent increases in COX-2 and PGE2 in human colonic myofibroblasts stimulated by thrombin

Venous thromboembolism with infl ammatory bowel disease

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PAR₁-dependent and independent increases in COX-2 and PGE₂ in human colonic myofibroblasts stimulated by thrombin