Upon completion of the chapter, the reader will be able to:
Characterize the pathophysiologic mechanisms underlying inflammatory bowel disease (IBD).
Recognize the signs and symptoms of IBD, including major differences between ulcerative colitis (UC) and Crohn disease (CD).
Identify appropriate therapeutic outcomes for patients with IBD.
Describe pharmacologic treatment options for patients with acute or chronic symptoms of UC and CD.
Create a patient-specific drug treatment plan based on symptoms, severity, and location of UC or CD.
Recommend appropriate monitoring parameters and patient education for drug treatments for IBD.
The term inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn disease (CD). Both disorders are associated with acute and chronic inflammation of the gastrointestinal (GI) tract. Differences exist between UC and CD with regard to regions of the GI tract that may be affected and the distribution and depth of intestinal inflammation. Patients with IBD may also develop inflammation involving organs other than the GI tract, known as extraintestinal manifestations. Symptoms of IBD are associated with significant morbidity, reduction in quality of life, and costs to the health-care system.1–6
EPIDEMIOLOGY AND ETIOLOGY
IBD is most common in Western countries such as the United States and Northern Europe. The age of initial presentation is bimodal, with patients typically diagnosed between the ages of 20 to 40 or 60 to 80 years. Approximately 1.5 million Americans have UC or CD.2 Up to 70,000 new cases of IBD are diagnosed in the United States each year.3
Men and women are approximately equally affected by IBD in Western countries.6 In general, White patients are affected more often than African American and Asian patients, and persons of Jewish descent are also at higher risk.1,5,6 A positive family history of IBD is found in 8% to 14% of patients, and genetic risk may be more of a contributing factor in some ethic groups.1,2,6
The cause of IBD is not fully understood. Dysregulation of the inflammatory response within the GI tract in response to environmental or microbiologic factors is thought to be the prevailing mechanism.3–5 The fact that a positive family history is a strong predictor of IBD supports the theory that genetic predisposition is involved in many cases. Many potential candidate genes have been identified.1,2,4–6
An alteration in the inflammatory response regulated by intestinal epithelial cells may also contribute to development of IBD. This may involve inappropriate processing of antigens presented to the GI epithelial cells.3–5,7,8 The inflammatory response in IBD may be directed at bacteria that normally colonize the GI tract. Products derived from these bacteria may translocate across the mucosal layer of the GI tract and interact with ...