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Background

Inflammatory bowel disease (IBD) is an idiopathic disease, probably involving an immune


reaction of the body to its own intestinal tract. The 2 major types of IBD are ulcerative colitis
(UC) and Crohn disease (CD). As the name suggests, ulcerative colitis is limited to the colon.
Crohn disease can involve any segment of the gastrointestinal (GI) tract from the mouth to
the anus (see the images below).
There is a genetic predisposition for IBD. Patients with IBD are more prone to the
development of malignancy. (See Prognosis.) Crohn disease can affect any portion of the GI
tract from the mouth to the anus, involves "skip lesions," and is transmural. (See
Background.)

Inflammatory bowel disease. Severe colitis noted during


colonoscopy. The mucosa is grossly denuded, with active bleeding noted. This patient had her

colon resected very shortly after this view was obtained.


Inflammatory bowel disease. Stricture in the terminal ileum noted during colonoscopy.
Narrowed segment visible upon intubation of the terminal ileum with the colonoscope.
Relatively little active inflammation is present, indicating that this is a cicatrix stricture.
Ulcerative colitis and Crohn disease share many extraintestinal manifestations, although
some of these tend to occur more commonly with either one. Extraintestinal manifestations of
IBD include iritis, episcleritis, arthritis, and skin involvement, as well as pericholangitis and
sclerosing cholangitis. Although both ulcerative colitis and Crohn disease have distinct
pathologic findings, a significant percentage of patients with IBD have indeterminate
findings. Systemic symptoms are common in IBD and include fever, sweats, malaise, and
arthralgias.
The rectum is always involved in ulcerative colitis, and the disease primarily involves
continuous lesions of the mucosa and the submucosa. Both ulcerative colitis and Crohn

disease usually have waxing and waning intensity and severity. When the patient is actively
symptomatic, indicating significant inflammation, the disease is considered to be in an active
stage (the patient is having a flare of the IBD). (See Clinical Presentation.)
The stovepipe sign seen on barium enema is due to chronic ulcerative colitis, in which the
colon becomes a rigid foreshortened tube that lacks its usual haustral markings. In Crohn
disease, the string sign (a narrow band of barium flowing through an inflamed or scarred
area) in the terminal ileum are typically observed on radiographs. (See Workup.)
When the degree of inflammation is less (or absent) and the patient is usually asymptomatic,
then the patient's disease is considered to be in remission. In most cases, symptoms
correspond well to the degree of inflammation present for either disease, although this is not
universally true. In some patients, objective evidence for disease activity should be sought
before administering medications with significant adverse effects (see Medication), because
patients with inflammatory bowel disease can have a coexisting irritable bowel syndrome.
Although ulcerative colitis and Crohn disease have significant differences, many (but not all)
of the treatments available for one condition are also effective for the other. Surgical
intervention for ulcerative colitis is curative for colonic disease and potential colonic
malignancy, but it is not curative for Crohn disease. (See Treatment and Management.)

Next Section: Etiology

Pathophysiology
The pathophysiology of IBD is under active investigation. The common end pathway is
inflammation of the mucosal lining of the intestinal tract, causing ulceration, edema,
bleeding, and fluid and electrolyte loss.
Many inflammatory mediators have been identified in IBD, and considerable evidence
suggests that these mediators play an important role in the pathologic and clinical
characteristic of these disorders. Cytokines, released by macrophages in response to various
antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine
effects. Cytokines differentiate lymphocytes into different types of T cells. Helper T cells,
type 1 (Th-1), are associated principally with Crohn disease, whereas Th-2 cells are
associated principally with ulcerative colitis. The immune response disrupts the intestinal
mucosa and leads to a chronic inflammatory process.[1]

Several animal models are used to study IBD. A local irritant (eg, acetic acid, trinitrobenzene
sulfonic acid) can be inserted via an enema into the colon of rats or rabbits to induce a
chemical colitis. An interleukin-10 (IL-10) knockout mouse has been genetically engineered
to have some characteristics similar to those of a human with IBD. The cotton-top marmoset,
a South American primate, develops a colitis very similar to ulcerative colitis when the
animal is subjected to stress.

Ulcerative colitis
In ulcerative colitis, inflammation begins in the rectum and extends proximally in an
uninterrupted fashion to the proximal colon, eventually involving the entire length of the
large intestine. The rectum is always involved in ulcerative colitis, and no "skip areas" (ie,
normal areas of the bowel interspersed with diseased areas) are present, unlike Crohn disease.
The disease remains confined to the rectum in approximately 25% of cases, and in the
remainder of cases, ulcerative colitis spreads proximally and contiguously. Pancolitis occurs
in 10% of patients. The small intestine is never involved, except when the distal terminal
ileum is inflamed in a superficial manner, referred to as backwash ileitis. Even with less than
total colonic involvement, the disease is strikingly and uniformly continuous. As ulcerative
colitis becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual
haustral markings, leading to the lead pipe appearance observed on barium enema.

Crohn disease
Crohn disease can affect any portion of the GI tract from the mouth to the anus and causes 3
patterns of involvement: inflammatory disease, strictures, and fistulas. This disease consists
of segmental involvement by a nonspecific granulomatous inflammatory process. The most
important pathologic feature of Crohn disease is that it is transmural, involving all layers of
the bowel, not just the mucosa and the submucosa, which is characteristic of ulcerative
colitis. Furthermore, Crohn disease is discontinuous, with skip areas interspersed between
one or more involved areas. See the image below.

Inflammatory bowel disease. Inflammation in the terminal


ileum noted during colonoscopy. Areas of inflammation, friability, and ulceration in the
terminal ileum are consistent with mild-to-moderate Crohn disease.
Late in the disease, the mucosa develops a cobblestone appearance, which results from deep,
longitudinal ulcerations interlaced with intervening normal mucosa. The 3 major patterns of
involvement in Crohn disease are disease in the ileum and cecum (40% of patients); disease
confined to the small intestine (30% of patients); and disease confined to the colon (25% of
patients). Rectal sparing is a typical but not constant feature of Crohn disease. However,

anorectal complications (eg, fistulas, abscesses) are common. Much less commonly, Crohn
disease involves the more proximal parts of the GI tract, including the mouth, tongue,
esophagus, stomach, and duodenum.
The incidence of gallstones and kidney stones is increased in Crohn disease because of
malabsorption of fat and bile salts. Gallstones are formed because of increased cholesterol
concentration in the bile, caused by a reduced bile salt pool.
Patients who have Crohn disease with ileal disease or resection are also likely to form
calcium oxalate kidney stones. With the fat malabsorption, unabsorbed long-chain fatty acids
bind calcium in the lumen. Oxalate in the lumen is normally bound to calcium. Calcium
oxalate is poorly soluble and poorly absorbed; however, if calcium is bound to malabsorbed
fatty acids, oxalate combines with sodium to form sodium oxalate, which is soluble and is
absorbed in the colon (enteric hyperoxaluria). The development of calcium oxalate stones in
Crohn disease requires an intact colon to absorb oxalate. Patients with ileostomies generally
do not develop calcium oxalate stones.

Next Section: Epidemiology

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Next Section: Epidemiology

Etiology
The triggering event for the activation of the immune response in IBD has yet to be
identified. Possible factors related to this event include a pathogenic organism (as yet
unidentified), an immune response to an intraluminal antigen (eg, protein from cow milk), or
an autoimmune process whereby an appropriate immune response to an intraluminal antigen

and an inappropriate response to a similar antigen is present on intestinal epithelial cells (ie,
alteration in barrier function).
No mechanism has been implicated as the primary cause, but many are postulated as potential
causes. The lymphocyte population in persons with IBD is polyclonal, making the search for
a single precipitating cause difficult. In any case, activation of the immune system leads to
inflammation of the intestinal tract, both acute (neutrophilic) and chronic (lymphocytic,
histiocytic).
The E3N prospective study found that high animal protein intake (meat or fish) was
associated with a higher risk of inflammatory bowel disease.[2]

Genetics
Persons with IBD have a genetic predisposition (or, perhaps, susceptibility) for the disease[3]
and a great deal of research has been performed to discover potential genes linked to IBD. An
early discovery was on chromosome 16 (IBD1 gene), which led to the identification of the
NOD2 gene (now called CARD15) as the first gene clearly associated with IBD (as a
susceptibility gene for Crohn disease). Studies have also provided strong support for IBD
susceptibility genes on chromosomes 5 (5q31) and 6 (6p21 and 19p). NOD2/CARD15 is a
polymorphic gene involved in the innate immune system. The gene has more than 60
variations, of which 3 play a role in 27% of patients with Crohn disease, primarily in patients
with ileal disease. With all of these potential genes, it is important to note that they appear to
be permissive (ie, allow IBD to occur) but not causative (ie, just because the gene is present
does not necessarily mean the disease will develop).
First-degree relatives have a 5- to 20-fold increased risk of developing IBD compared with
persons from unaffected families. The child of a parent with IBD has a 5% risk of developing
IBD. Twin studies show a concordance of approximately 70% in identical twins versus 510% in nonidentical twins. Of patients with IBD, 10-25% is estimated to have a first-degree
relative with the disease. Monozygous twin studies show a high concordance for Crohn
disease but less so for ulcerative colitis.

Smoking
The risk of developing ulcerative colitis is higher in nonsmokers and former smokers than in
current smokers. The onset of ulcerative colitis occasionally appears to coincide with
smoking cessation. This does not imply that smoking would improve the symptoms of
ulcerative colitis; interestingly, some success in the use of nicotine patches has been reported.
Instead, patients with Crohn disease have a higher incidence of smoking than the general
population, and those patients with Crohn disease who continue to smoke appear to be less
likely to respond to medical therapy.

Next Section: Prognosis

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Epidemiology
United States statistics
Before 1960, the incidence of ulcerative colitis was several times higher than that of Crohn
disease. The latest data suggest that the current incidence of Crohn disease is approaching
that of ulcerative colitis, although this change may reflect improved recognition and
diagnosis of Crohn disease.
An estimated 1-2 million people in the United States have ulcerative colitis or Crohn disease,
with an incidence rate of 70-150 cases per 100,000 individuals. Among persons of European
descent in Olmstead County, Minnesota, the incidence of ulcerative colitis was 7.3 cases per
100,000 people per year with a prevalence of 116 cases per 100,000 people, and the incidence
of Crohn disease was 5.8 cases per 100,000 people per year, with a prevalence of 133 cases
per 100,000 people.[4, 5]
The prevalence of IBD among Americans of African descent is estimated to be the same as
the prevalence among Americans of European descent, but the prevalence is lower among
Americans of Asian and Hispanic descent. The incidence of IBD among white individuals is
approximately 4 times that of other races, with the highest rates reported to be in Jewish
populations, followed by non-Jewish white populations. The prevalence rates of IBD among
the American Jewish population are approximately 4-5 times that of the general population.

In fact, however, data suggest that the incidence rates in non-Jewish, black, and Hispanic
populations are increasing.
The male-to-female ratio is approximately equal for ulcerative colitis and Crohn disease, with
females having a slightly greater incidence. Both diseases are most commonly diagnosed in
young adults (ie, late adolescence to the third decade of life).
The age distribution of newly diagnosed IBD cases is bell-shaped; the peak incidence occurs
in people in the early part of their second decade of life, with the vast majority of new
diagnoses made in people aged 15-40 years. A second, smaller peak in incidence occurs in
patients aged 55-65 years. However, children younger than 5 years and elderly persons are
occasionally diagnosed. Of patients with IBD, 10% are younger than 18 years.

International statistics
The incidence of IBD varies within different geographic areas, with the highest rates assumed
to be in developed countries and lowest in developing regions; colder climate regions and
urban areas have a greater rate of IBD than those of warmer climates and rural areas.
Internationally, the incidence of IBD is approximately 2.2-14.3 cases per 100,000 personyears for ulcerative colitis and 3.1-14.6 cases per 100,000 person-years for Crohn disease.
Overall, the combined incidence for IBD is 10 cases per 100,000 annually.[4, 5]

Next Section: Patient Education

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Prognosis
Multiple studies on mortality in patients with IBD have been conducted from regions
throughout the world. The standardized mortality ratio for IBD generally ranges from
approximately 1.4 times the general population (Sweden) to 5 times the general population
(Spain). In general, the 95% confidence intervals suggest that the increase in relative risk is
real.
Ulcerative colitis and Crohn disease have approximately equal mortality rates. Although the
mortality from ulcerative colitis has decreased over the past 40-50 years, with one study
reporting a standardized mortality ratio of 0.6 in Florence, Italy, the vast majority of studies
indicate a small but significant increase in mortality associated with IBD. The most frequent
cause of death in persons with IBD is the primary disease, followed by malignancy,
thromboembolic disease, peritonitis with sepsis, and complications of surgery.
Patients with IBD are more prone to the development of malignancy. Persons with Crohn
disease have a higher rate of small bowel malignancy. Patients with pancolitis, particularly
ulcerative colitis, are at a higher risk of developing colonic malignancy after 8-10 years of
disease. The current standard of practice is to screen these patients with colonoscopy at 2year intervals once they have had the disease for that duration. If a patient refuses appropriate
screening, document it in the medical record.
Long-term morbidity can also result from complications of medical therapy, especially longterm steroids.

Ulcerative colitis
The average patient with ulcerative colitis has a 50% probability of having another flare
during the next 2 years. However, the range of experiences is very broad; some patients may
only have one flare over 25 years (as many as 10%), and others may have almost constant
flares (much less common). A small percentage of patients with ulcerative colitis have a
single attack and no recurrence. Typically, however, remissions and exacerbations are
characteristic of this disease, with acute attacks lasting weeks to months.
Patients with ulcerative colitis limited to the rectum and sigmoid at the time of diagnosis have
a greater than 50% chance of progressing to more extensive disease and a 12% rate of
colectomy over 25 years. More than 70% of patients presenting with proctitis alone continue
to have disease limited to the rectum over 20 years, and most patients who develop more
extensive disease do so within 5 years of diagnosis. Of patients with ulcerative colitis
involving the entire colon, 60% eventually require colectomy, whereas very few of those with
proctitis require colectomy. Of interest, most surgical interventions are required in the first
year of disease, and the annual colectomy rate after the first year is 1% for all patients.
Surgical resection for ulcerative colitis is considered curative for this disease, although
postoperative pouchitis may occur in some patients. Of note, pouchitis is far more common in
patients who have had a colectomy for ulcerative colitis than in those who have had a
colectomy for other reasons (eg, familial adenomatous polyposis).
A generally accepted postulation is that the risk of colorectal cancer is not significantly higher
in persons with ulcerative colitis than in the general population until several years after
diagnosis. Beyond 8-10 years after diagnosis, the risk of colorectal cancer increases by 0.5-

1.0% per year. Data suggest that surveillance colonoscopies with random biopsies reduce
mortality from colorectal cancer in patients with ulcerative colitis, primarily by allowing the
detection of carcinoma at an earlier Duke stage.

Crohn disease
The clinical course of Crohn disease is much more variable than that of ulcerative colitis, and
it is independent of the anatomic location and extent of disease. Periodic remissions and
exacerbations are the rule in Crohn disease. A patient in remission has a 42% likelihood of
being free of relapse for 2 years and only a 12% likelihood of being free of relapse for 10
years. Over a 4-year period, approximately 25% of patients remain in remission, 25% have
frequent flares, and 50% have a course that fluctuates between periods of flares and
remissions.
Approximately 50% of patients with Crohn disease require surgical intervention. Of patients
who undergo surgery, 50% require a second operation, and half of the patients who undergo a
second operation will undergo a third. The rate of disease recurrence is 25-50% within 1 year
for patients whose condition has responded to medical management; this rate is higher for
patients who require surgery.
Surgery for Crohn disease is generally performed for complications (eg, stricture, stenosis,
obstruction, fistula, bleeding) rather than for the inflammatory disease itself. However,
although surgery is an important treatment option for Crohn disease, patients should be aware
that it is not curative and that disease recurrence after surgery is the rule. Postsurgery, the
frequency of recurrence of Crohn disease is high, generally in a pattern mimicking the
original disease pattern, often on one or both sides of the surgical anastomosis. Endoscopic
evidence of recurrent inflammation is present in 93% of patients 1 year after surgery for
Crohn disease.
Overall, the patient's quality of life with Crohn disease generally is lower than that of
individuals with ulcerative colitis. Data suggest that persons with Crohn colitis involving the
entire colon have a risk of developing malignancy equal to that of persons with ulcerative
colitis; however, the risk for most patients with Crohn disease is much smaller (albeit poorly
quantified). Death usually occurs as a consequence of surgery, pulmonary embolus, or sepsis.
Intestinal cancer may become a more important long-term complication in patients with
Crohn disease because of longer survival.

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Patient Education
Patients with inflammatory bowel disease (IBD) benefit tremendously from education about
their disease. As a chronic, often lifelong, disease that is frequently diagnosed in young
adulthood, increasing patient knowledge improves medical compliance and assists in the
management of symptoms.
The Crohn's & Colitis Foundation of America is the most prominent organization in the
United States that can directly provide educational materials for patients. This organization
also supplies physicians with educational brochures at no cost upon request.
Encourage the patient to join an IBD support group, such as the Crohn's and Colitis
Foundation of America (386 Park Avenue South, 17th Floor; New York, NY 10016; 1-800932-2423).
For excellent patient education resources, visit eMedicine's Crohn Disease Center and
Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education articles
Inflammatory Bowel Disease, Crohn Disease, Crohn Disease FAQs, and Irritable Bowel
Syndrome.

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