Epidemiology of Pediatric Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) comprises of two chronic inflammatory conditions—Crohn’s disease (CD) and Ulcerative colitis (UC) with some overlap. They are thought to occur as an immune dysregulated response to either commensal gut flora or to environm
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Epidemiology of Pediatric Inflammatory Bowel Disease Shehzad Saeed and Subra Kugathasan
Introduction Crohn disease (CD) and ulcerative colitis (UC), collectively known as inflammatory bowel disease (IBD), are chronic inflammatory disorders of the gastrointestinal tract that occur most commonly during the adolescent to young adult ages. IBD is characterized, respectively, by confluent inflammation of the colonic mucosa in UC and discontinuous transmural intestinal inflammation in CD. Approximately 25% of incident cases of IBD occur during childhood and the rest occur throughout adulthood, peaking in the second and third decades of life [1]. Inflammation in IBD is thought to develop as a result of dysregulation of the immune response to “normal” gut flora in a genetically susceptible host. Emerging evidence over the last several years has better characterized these interactions, especially portraying the interplay between genetic predispositions and their relationship with commensal bacteria. Serologic and immune markers have also been implicated in predicting the course of disease progression [2]. The degree of reactivity of certain serological and immune markers may also indicate development of complicating disease characteristics and response to therapy [3]. These developments have enabled us to begin to think about individualized therapy selection, restricting aggressive and more potent therapies (e.g., biologics) for patients that have a high risk profile, and limiting the exposure of toxic medications. Some of the environmental triggers for IBD have been known and implicated as associated with either Crohn disease S. Saeed, MD Department of Pediatrics, University of Cincinnati School of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA S. Kugathasan, MD (*) Department of Pediatric Gastroenterology, Emory University School of Medicine, Atlanta, GA, USA Division of Pediatric Gastroenterology, Emory Children’s Center, 2015, Uppergate Drive, Room 248, Atlanta, GA 30322, USA e-mail: [email protected]
(e.g., smoking) or ulcerative colitis (e.g., appendectomy). Other triggers like breast feeding, diet, drugs, stress, etc. have been associated with IBD but the evidence seems to be conflicting and variable from study to study. Reactivity of commensal bacteria and the role of these in immune dysregulation along with genetic predisposition, are emerging as potential critical factors in the pathogenesis of IBD. A number of studies have identified newer risk polymorphisms for both CD and UC, most of them relating to commensal bacterial sensing, autophagy, and drug metabolism with utilization of these advanced discoveries, the time is not far away when we will be able to select therapy based upon the risk profile of an individual patient along with predictors of response to therapy. In this chapter we will discuss the environmental triggers and descriptive epidemiology of childhood IBD, emerging and exciting areas of growth (“new epidemiology”) includi
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