Overview
Crohn's disease and ulcerative colitis are the two most common
chronic inflammatory bowel diseases
. 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 the physician who first described it in 1932, results in ulcers, or sores, in
any part of the gastrointestinal system
from the mouth to the anus. However, it most often involves the small and large intestines. In contrast, ulcerative colitis causes ulcers only in the large intestine.
While patients with ulcerative colitis often complain of diarrhea, weight loss, blood in their stools, and fever, patients with Crohn's disease can experience a
wide spectrum of symptoms
depending on severity and location of their disease. The typical symptoms of Crohn's disease include diarrhea, crampy abdominal pain, loss of appetite, and weight loss. However, patients may also have symptoms as varied as delayed growth, bloody bowel movements, rectal pain, and symptoms associated with bowel perforation or obstruction (severe painful cramping, vomiting, nausea, and abdominal distention). In both UC and Crohn's, patients can experience periods of remission from symptoms and relapse.
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 an allergen, a bacteria or virus, a genetic reaction, 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. Chronic inflammation, over months or years, impairs the proper function of tissues and organs.
Microscopically, ulcerative colitis presents as continuous, shallow ulcers located in the superficial layer of the colon. In contrast, Crohn's disease results in discontinuous, "transmural" ulcerations, which can 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, scar to cause narrowing of the bowels, or give rise to the formation of abnormalpassages or tunnels between the intestines and adjacent organs, called
fistulas
.
It is important to note that, at this time, scientists do not know what causes 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 or to treat complications such as abscesses, blockages, perforations, and fistulas. Overall, most Crohn's patients are able to live with the 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.
Causes
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, however, it does not appear 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. One of these genes, NOD2/CARD15, plays a role in the body's response to bacteria. Research indicates that people with mutations in this gene are more susceptible to developing Crohn's disease.
Need-to-know anatomy
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, 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 2A? inches in diameter. It extends from the
cecum
, a pouch that opens to the small intestine, up to just under the rib cage, 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. Patients who have Crohn's disease for many years may also suffer painful breaks or fissures in the anal canal.
Risk factors
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 males and females equally.
Environmental factors have been implicated in Crohn's disease. There is an increased incidence in
temperate areas of developed countries
, including North America and Australia. Urban populations suffer more Crohn's disease than do rural residents. But scientists increasingly believe that
genetic factors
play a major role in the development of Crohn's disease. About 10 to 15 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 at least a 53 percent concordance. Children of two Ashkenazi Jewish parents with inflammatory bowel disease have a greater than 50 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, but particularly genes on chromosome 16. One gene, NOD2/CARD15, plays a role in the activation of the body's inflammatory response. Research indicates that three separate mutations of this gene are associated with Crohn's disease. The mutations alone do not cause Crohn's disease, because only about 30 percent of patients have one of these mutations.