Crohn's disease and ulcerative colitis (UC) are the two major chronic inflammatory bowel diseases, together known as IBD. These two diseases, while similar in many ways, can differ in location, symptoms, and the character of the inflammation and ulcerations. Crohn's disease, named after one of the physicians who described it in 1932 and also known as regional enteritis, results in ulcers, or sores in the gastrointestinal tract. It may involve any part of the gastrointestinal system from the mouth to the anus. However, it most often involves the lower part of the small intestine, known as the ileum, and the large intestine (the colon). In contrast, ulcerative colitis causes ulcers only in the large intestine.
The symptoms of Crohn's disease and ulcerative colitis include diarrhea, abdominal pain, blood in the stool, anemia, weight loss, malnutrition, and fever. Patients with ulcerative colitis more often complain of diarrhea and blood in their stools andpatients with Crohn's disease more often complain of diarrhea and abdominal pain. Crohn's disease also may present with delayed growth in adolescence or childhood, intestinal obstruction (severe painful cramping, vomiting, nausea, and abdominal distention), bowel perforation, fistulas (abnormal passages or tunnels from one part of the intestine to another, or to the skin, or less commonly to the abdominal wall, vagina, bladder or other nearby organs), or abscesses. In both UC and Crohn's, patients can experience periods of remission from symptoms and periods of relapse or "flares". About one-quarter of patients for both types of IBD may have extra-intestinal disease manifestations, most commonly arthritis, eye inflammation (uveitis, iritis or episcleritis), and skin inflammation, typically pyoderma gangrenosum and erythema nodosum. Unfortunately, once IBD occurs it tends to be present for life. Ulcerative colitis can be cured by surgical removal of the entire colon including the rectum. Crohn's disease, however, most often returns even after the involved sections of the intestine are surgically removed.
Both diseases appear to be caused by a dysfunctional inflammatory response in the gastrointestinal tract. Inflammation is the body's natural attempt to heal by sending immune cells to the site of an injury or invader. Researchers hypothesize that this immune system response in both ulcerative colitis and Crohn's disease may be triggered by bacteria or viruses, material in the intestinal contents (such as products from food digestion or intestinal bile), or a defective signal from the body's own cells, called an autoimmune response. Inflammation results in pain, heat, redness, and swelling of the tissue, known as edema. Chronic inflammation can impair the proper function of tissues and organs.
Microscopically, ulcerative colitis presents as continuous, shallow ulcers located in the superficial layer of the colon (known as the epithelium). The colon becomes swollen (edematous) and loses the shape of its normal folds. In contrast, Crohn's disease results in discontinuous, "transmural" ulcerations, which typically extend through all layers of the bowel. The formation of large, deep ulcers results in the classic "cobblestone" appearance of the involved intestine. These deep ulcers can form abscesses or scar to cause narrowing of the bowels.It is important to note that, at this time, scientists do not know what triggers Crohn's disease and that there is no cure. The goals of medical therapy for Crohn's disease are to control the active disease and to prevent relapses and complications. Sometimes surgery is recommended for removing inflamed segments of the intestines that do not respond to medical therapy or to treat complications such as abscesses, blockages, perforations, and fistulas. About two-thirds of patients will require surgery to remove a portion of their intestines at some point during the course of their disease. New drugs and research on the genetic and environmental basis of the disorder offer the promise of improved future treatments for Crohn's disease.
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While the cause of Crohn's disease is unknown, it is thought to arise in individuals with a genetically inherited susceptibility that results in an abnormal immune response to an as yet unidentified trigger in the gastrointestinal tract. Scientists hypothesize that infectious bacteria, viruses, or other gut microbes may be involved as triggers. However, there is no evidence that Crohn's disease is caused by an infection, and the disease is not contagious.
Another theory holds that nonpathogenic microbes in food may set off the immune reaction. While diet has been shown to impact the symptoms associated with Crohn's disease and Crohn's disease flares tend to abate in patients placed on elemental diets (diets with pre-digested food), specific dietary products have not been shown to cause the illness.
It is clear that the immune system in patients with Crohn's disease is inappropriately activated. It is believed that this susceptibility to abnormal immune activation is genetically inherited, and research linking Crohn's disease to several genes is ongoing. Over thirty-two regions of the human genome have been identified that increase risk for Crohn's disease. Most important of these are the NOD2 (previously known as the CARD15) gene. Mutations in the NOD2 gene lead in part to the development of about 25% of Crohn's disease in whites. NOD2 Crohn's disease predisposing mutations are uncommon in African Americans and do not appear to be present in Asians. NOD2 normally detects proteins from bacteria and then triggers a response to activate or regulate immune cells. NOD2 gene mutations that increase risk of Crohn's disease severely reduce or eliminate this activity.
The gastrointestinal tract consists of one continuous passageway beginning with the mouth, then the esophagus, the stomach, the small intestine, the colon (large intestine), and the anus. Crohn's disease can affect any part of the gastrointestinal tract, but most frequently involves the small intestine and the colon.
The small intestine is actually much longer than the large intestine, measuring as much as 19 feet or more, but it is only about one-third the diameter of the large intestine. The small intestine is divided into three parts, the duodenum, which controls the flow of food from the stomach into the intestine and is where bile from the liver and pancreatic juices from the pancreas are released to aid in food digestion, the jejunum, or middle section, and the ileum, the final three fifths of the small intestine. The small intestine absorbs most of the nutrients from digested food. The last stages of protein and carbohydrate digestion occur in the ileum, which leads to the large intestine.
The colon, or large intestine, is a 5- to 6-foot-long muscular tube about 2 1/2 inches in diameter. It extends from the cecum, a pouch that opens to the small intestine, up to just under the rib cage and below the liver and the stomach, and then down into the S-shaped sigmoid colon, to the rectum and anal canal, through which waste passes. The colon is the site of salt and water absorption. Glands in the colon secrete slippery mucus to lubricate the intestines, and aid decomposition of undigested food, cell debris, dead bacteria, and other wastes that must leave the body. The tissue lining the colon absorbs and secretes potassium as needed to maintain proper bodily functions, including heart rate.
In about one third of Crohn's patients, pathological changes are limited to the very end of the small intestine, called the terminal ileum. Some 40 percent of patients have ileocolitis, in which Crohn's disease involves the ileum and part of the colon. About 20 percent of patients have tissue damage only in the colon, or Crohn's colitis. About 5 percent of Crohn's patients suffer from ileojejunitis, in which there is either continuous involvement of the small intestine or multiple areas of disease in the small intestine separated by normal bowel tissue. Less commonly, Crohn's disease may involve the esophagus, stomach and/or duodenum, sometimes at the same time as it involves the lower portions of the digestive tract. Patients who have Crohn's disease may also suffer painful breaks or fissures in the anal canal.
The majority of patients with Crohn's disease are diagnosed in their teens and 20s, with the average age at diagnosis being 27. However, no age group is exempt. About one sixth of patients have the condition before the age of 15, and other patients have been diagnosed in their 70s. Crohn's disease affects a higher proportion of females than males, except in Pacific Asian countries where it tends to affect males more often than females.
Environmental factors have been implicated in Crohn's disease. There is an increased incidence in Western industrialized countries, including North America, Australia, and New Zealand. The disease tends to be more common in more Northern environments such as Scandinavia, Scotland, and Canada. Urban populations suffer more Crohn's disease than do rural residents. Smokers have about twice the risk of Crohn's disease, particularly disease involving the small intestines, as compared to non-smokers. But scientists increasingly believe that genetic factors play a major role in the development of Crohn's disease. About 10 to 20 percent of patients have a family history of the disorder. An additional 5 percent to 7 percent have a family history of ulcerative colitis, a related condition. Identical twins have from 30 to 50 percent concordance. The disease is about 4 times as common in Jews of European ancestry (Ashkenazi Jews) than in their non-Jewish neighbors. Crohn's disease was previously less common in African Americans than in white Americans but the incidence now appears to be similar. In the United States, it appears to be less frequent in Latinos, Native Americans and Asian Americans. Children of two parents with inflammatory bowel disease have a greater than 36 percent risk of developing Crohn's disease. This strong genetic propensity to Crohn's disease suggests a small number of genes involved in development of the disease.
Recent studies of families with Crohn's disease and ulcerative colitis have identified involvement by a number of genes and several chromosomes, with more than 32 unique regions implicated. . Several of the genes involved in Crohn's disease are involved with the body's response to bacteria. Several genes involved with both Crohn's disease and ulcerative colitis affect the inflammatory response in general, particularly the receptor to a mediator of chronic inflammation, known as interleukin (IL) 23. The IL23 gene is also genetically associated with risk of psoriasis, and psoriasis is more common in patients with IBD. Of all the Crohn's disease genes, NOD2 gene mutations, present in about 15% of whites and 3% of African Americans, have the greatest risk. Persons with no normal NOD2 genes have about a 17-fold risk of Crohn's disease compared to persons with no NOD2 mutations. NOD2 by itself usually does not cause Crohn's disease as only about 5% of NOD2 mutation homozygotes will get Crohn's disease.
Last reviewed on 6/4/09
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