Thrombocytosis in Chronic Inflammatory Bowel Disease

Morowitz, David A.; Allen, Lawrence W.; Kirsner, Joseph B.

doi:10.7326/0003-4819-68-5-1013

Cited by 161 publications

(54 citation statements)

References 8 publications

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“…IL-6 levels are commonly increased in inflammatory conditions and have been correlated with reactive thrombocytosis in humans with rheumatoid arthritis (4). Reactive thrombocytosis has also been observed in chronic inflammatory bowel disease (11), chronic pancreatitis (2), and malignant neoplastic diseases (7). Both marmosets in this report had chronic colonic disease, which may have caused an increase in the inflammatory cytokines (e.g., IL-6) leading to reactive thrombocytosis.…”

mentioning

confidence: 82%

Case Report

Logan¹,

Khan²

1996

Toxicol Pathol

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mentioning

confidence: 82%

Case Report

Logan¹,

Khan²

1996

Toxicol Pathol

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“…Patients suffering from exacerbations of Crohn's disease and ulcerative colitis have an increase in circulating platelet numbers (Morowitz et al, 1968). This is often associated with a reduced platelet lifespan and reduction in mean platelet volume (Webberley et al, 1993;Jaremo and SandbergGertzen, 1996).…”

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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“…This study was designed to investigate the basis of the thrombocytosis in patients with Crohn's disease and colitis ulcerosa, which is known to occur in patients with exacerbation of the disease (1,12,13).…”

Section: Discussionmentioning

confidence: 99%

Platelet Count, Platelet Function, Coagulation Activity and Fibrinolysis in the Acute Phase of Inflammatory Bowel Disease

Wersch¹,

Houben²,

Rijken³

1990

Clinical Chemistry and Laboratory Medicine

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Summary:Twenty two patients with exacerbation of inflammatory bowel disease (19 with Crohn's disease, 3 with ulcerative colitis) and thrombocytosis were tested for possible activation of the coagulation and platelet system.Fifteen patients had abnormal platelet function i. e. unphysiologically high sensitivity in vitro towards ADP 2 μηιοΐ/ΐ aggregation induction. In 81.8% of the patients we found enhanced fibrinogen concentrations. In 22.7% of the patients thrombin-antithrombin III values exceeded the upper limit of the reference range, and in 68.2% of the patients the D-Dimer concentration exceeded the upper reference limit as a result of reactive fibrinolysis. The altered platelet count and function, and the increased levels of fibrinogen and thrombinantithrombin III with reactive fibrinolysis activation indicate the presence of prethrombotic factors in patients with exacerbation of inflammatory bowel disease. The presence of enhanced fibrinolysis in these patients might have consequences for the therapeutic treatment.

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Thrombocytosis in Chronic Inflammatory Bowel Disease

Cited by 161 publications

References 8 publications

Case Report

Case Report

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

Platelet Count, Platelet Function, Coagulation Activity and Fibrinolysis in the Acute Phase of Inflammatory Bowel Disease

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