Platelet factor 4 and β‐thromboglobulin in inflammatory bowel disease and giant cell arteritis

Vrij, A.A.; Rijken, J.; Wersch, J. W. J. Van; Stockbrügger, Reinhold W.

doi:10.1046/j.1365-2362.2000.00616.x

Cited by 48 publications

(38 citation statements)

References 33 publications

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“…7,8 Furthermore, strong activation of the platelets in IBD patients is supported by the expression of platelet activation markers such as P-selectin (CD62P) and by serum measurements of β-thromboglobulin (β-TG). 9,10 Enhanced platelet activation in IBD is also supported by reports showing an elevation in various products such as platelet factor 4 (PF4) and CD40 ligand (CD40L). 9,11,12 Platelets respond to a number of stimuli by changing their shape from discoid cells to spherical spiny cells, and by aggregating into large clumps.…”

Section: Introductionmentioning

confidence: 85%

Increased aggregation response of platelets in patients with inflammatory bowel disease

et al. 2006

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Section: Introductionmentioning

confidence: 85%

Increased aggregation response of platelets in patients with inflammatory bowel disease

et al. 2006

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“…This is often associated with a reduced platelet lifespan and reduction in mean platelet volume (Webberley et al, 1993;Jaremo and SandbergGertzen, 1996). Furthermore, platelets from inflammatory bowel disease (IBD) patients are more sensitive to platelet agonists in vitro (van Wersch et al, 1990), while the plateletspecific chemokines PF-4 and b-TG are detected in plasma, revealing activation in vivo (Collins et al, 1994;Vrij et al, 2000). A role for platelets in mediating leukocyte recruitment to the inflamed colon is likely since platelet P-selectin and RANTES are also detected (Fagerstam et al, 2000), and this is localized to the intestinal microcirculation (Collins et al, 1997).…”

Section: Platelet Activation In Inflammatory Bowel Diseasementioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…For statistical purposes, the classification was quantitatively modified [31]. The score in severe disease was between 15 and 18, in moderate disease between 9 and 14, in mild disease between 4 and 8 and in inactive disease it was 3 or less.…”

Section: Patientsmentioning

confidence: 99%

Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis

Vrij¹,

Rijken²,

Wersch³

et al. 2003

Pathophysiol Haemos Thromb

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Background: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. Materials and Methods: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-α₂-antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn’s disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. Results: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. Conclusions: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis.

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Platelet factor 4 and β‐thromboglobulin in inflammatory bowel disease and giant cell arteritis

Abstract: Platelet factors were correlated with inflammatory bowel disease activity. Levels of platelet factor 4 and beta-thromboglobulin, however, were markedly raised for a long time in clinically inactive inflammatory bowel disease, which might point to a pre-thrombotic state of disease.

Cited by 48 publications

References 33 publications

Increased aggregation response of platelets in patients with inflammatory bowel disease

Increased aggregation response of platelets in patients with inflammatory bowel disease

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Coagulation and Fibrinolysis in Inflammatory Bowel Disease and in Giant Cell Arteritis

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