DOI: 10.1097/MCG.0b013e31825003cc
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PMID: 22565604
Issn Print: 0192-0790
Publication Date: 2012/07/01
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Excerpt
The human coagulation system has been recognized as a contributor in the multifaceted process of chronic intestinal inflammation.1 Crohn’s disease and ulcerative colitis, the 2 major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions characterized by local and systemic inflammation. In both the forms of IBD, a hypercoaguable and prothrombotic state exists and activation of the coagulation cascade occurs during inflammation.2 The existence of these coagulation abnormalities offers a potential target for the treatment of IBD.
The purpose of our study was to assess the effect of antiplatelet therapy on patients with preexisting IBD who received treatment with clopidogrel (Plavix Bristol-Myers Squibb, New York City) and/or aspirin therapy during the course of their illness. We hypothesized a reduction in disease activity or flare-ups due to the anti-inflammatory properties of these drugs.
A retrospective chart review was performed to assess disease progression of patients identified with IBD who were started on aspirin and/or Plavix during a 5-year interval. We identified 43 patients (34 from the division of cardiology and 9 from private gastroenterologists) with IBD who took Plavix and aspirin for at least 6 months after having a percutaneous coronary intervention for coronary artery disease. A control group of 97 patients with IBD who never used antiplatelet therapy (Plavix or aspirin) since the diagnosis of IBD were matched for sex, age, type, and duration of IBD. A questionnaire was then mailed out to each patient in the case and control group (n=140) asking questions pertaining to type of IBD and disease activity. Episodes of rectal bleeding, necessary changes in medication due to disease exacerbations, recent hospitalization for flare-ups, and overall patient well being were evaluated during the 5-year interval using yes or no responses. Patients were also specifically asked to report on whether or not they experienced increased rectal bleeding since the initiation of antiplatelet therapy.
There were no statistically significant differences between case and control subjects in terms of age, sex, type of IBD, and duration of disease. There were no significant differences between case and control patients in terms of the need to change IBD medications to control disease exacerbation over a 5-year duration (P-value=1.00) or required hospitalization secondary to disease exacerbation (P-value=0.169). There was also no statistically significant difference between case and control groups with increased rectal bleeding since the initiation of antiplatelet therapy; however the P-value of 0.093 was close to significance.
There are several possible causative factors that have been implicated at the onset of IBD with genetic and environmental causes at the forefront with strong evidence that dysregulation of the normally controlled immune response to commensal bacteria in a genetically susceptible individual drives IBD.3 A persistent challenge for investigators is defining the mechanisms of communication between components of the innate and adaptive immune systems in light of the multiple established genetic variants associated with IBD. Nevertheless, the paramount approach to IBD involves treatment of active inflammation. Keeping this in mind, we investigated a novel approach to subdue active inflammation with the use of medications (aspirin, Plavix) generally reserved for management of cardiovascular disease.
Platelets are thought to propagate the inflammatory process of atherosclerosis by interaction with leukocytes. It has been suggested that decreased platelet activation may limit interaction with endothelial and inflammatory cells, thus resulting in fewer proinflammatory mediators and subsequently less inflammation.1 In fact, in vitro studies have demonstrated that platelets spontaneously aggregate in >30% of IBD patients compared with controls.4 Reactive thrombocytosis frequently occurs during the active phase of IBD, which correlates well with disease severity and can be used as a marker for inflammation.
