Inflammatory Bowel Disease

Inflammatory bowel disease consists of two disorders: Crohn's disease and ulcerative colitis. Both conditions result from abnormal activation of the body's immune system, resulting in an inflamed bowel and concurrent systemic symptoms. These are chronic, idiopathic, and relapsing and remitting disorders, more common in the developed world. Crohn's disease is autoimmune and involves widespread inflammation throughout the gastrointestinal tract, while ulcerative colitis is limited to the colon.

The luminal layer of the gastrointestinal tract (called the mucosa) is colonized normally with microflora. This flora is of functional significance. The human body does not consider the flora as an antigenic or pathogenic entity. In inflammatory bowel disease, the tables turn, and the host's immune system gets activated against its own flora, causing an inflammation against the normal mucosa, resulting in defective function. Because the immune response is directed against the body's own tissues, this is an autoimmune disorder, involving abnormal immune responses, genetic predisposition, and environmental triggers.

The development of this disease strongly depends on genetic predisposition. Fifteen percent of inflammatory bowel disease patients have first-degree relatives who also have the disease, and the lifetime risk of either a parent or a sibling being affected is 9 percent. However, the disease is a multigenic trait. This means that several genes will control the eventual clinical presentation of the disease, thus resulting in variable symptoms.

Animal studies have elucidated the importance of gut flora in the development of inflammatory bowel disease. It is thought that defects in the barrier of the gut wall could cause the lymph tissue to be exposed to the microflora resting on the mucosal surface. This causes an immediate immune response against the normal gut flora, causing the inflammation. Environmental triggers, such as irritants in the diet, can also trigger a relapse by acting as a microbe against which an immune response is launched by the body.

The specific nature of the type of immune response is another aspect of inflammatory bowel disease research. T cells of the immune system are involved in autoimmune responses against self-antigenic in the [Page 914]body. These cells are cytotoxic and kill the cells of the body if they exhibit certain apoptotic (suicidal) proteins, or abnormal antigens (such as viral proteins exhibited on the surface of the cell that is infected with the virus). Such cells attack the normal cells in cases of autoimmune disease, and in inflammatory bowel disease, they target the intestinal mucosal cells.

Crohn's disease is a type of delayed hypersensitivity response that is chronic and induced by interferon gamma–producing T helper cells 1. Ulcerative colitis is cause by T helper cells 2. Diagnosis of inflammatory bowel disease is largely dependant on clinical history, radiographic examination, laboratory findings, and pathological examination of tissue. Microscopic histological assessment defines the diseases.

Crohn's disease is also called regional enteritis. The disease consists of patchy areas of affected mucosa alternated by areas of normal mucosa. The region of inflammation could be anywhere throughout the length of the gastrointestinal tract, that is, from the mouth, esophagus, stomach, small intestine, large intestine, rectum to the anus. As a consequence of repeated inflammation, the intestinal wall becomes rubbery and thick due to edema. The tissue undergoes fibrosis and scar formation and the muscular layer of the intestinal wall hypertrophies, causing the lumen itself to reduce. The narrow lumen causes the classic presentation of “stringy sign” in a barium meal's X-ray. Despite the severity of the disease in some areas, other parts of the gastrointestinal tracts may be very much unaffected. Early features of the disease show point sores that progress to ulceration. Ulcerated areas coalesce causing serpentine ulcers along the long axis of the bowel. The normal smoothness of the mucosal surface is lost and fistulas and fissures commonly develop.

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