Chapter 46 - Inflammatory Bowel Disease

Abstract

Inflammatory bowel disease (IBD) traditionally is divided into two related subgroups called Crohn’s disease (CD) and ulcerative colitis (UC) that often differ in location of bowel involved, pathological features, and surgical outcomes. They were thought to be distinct entities. It now appears more likely that both CD and UC are various conditions with somewhat overlapping clinical and pathological features. They are the manifestations of intestinal mucosal immune dysregulation in which the host immunologically overresponds to substances in the natural intestinal stream. IBD presently is not considered a classic autoimmune disease in which host T cells and antibodies inappropriately recognize and attack host tissue. Yet, the microbiota and molecular components of our inner intestinal lumen may be considered a functional “organ” essential for our health. In this sense, IBD could be considered an autoimmune disease in which a poorly regulated mucosal immune response to luminal contents leads to severe collateral damage to the intestinal lining. Advances in genomics have detected gene variants that, to a limited degree, predispose some people to these diseases. However, poorly defined environmental factors were the major cause for the rapid growth of IBD in industrial societies in the latter half of the 20th century and are the primary drive for the precipitous spread of IBD worldwide in the 21st century. Advances in therapy are coming with increasing speed because of exciting new discoveries providing insight into the immune regulatory pathways that drive and limit intestinal inflammation as well as from the enhanced appreciation of the importance of the intestinal microbiota. This also comes with the sobering realization that there is a continual increase in both the prevalence and severity of these diseases, which will increasingly challenge healthcare systems and the quality of life of people everywhere.