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"Crohn" redirects here. It is not to be confused with Croan or Crone.
Crohn's disease
Other names Crohn disease, Crohn syndrome, granulomatous
enteritis, regional enteritis, Leśniowski-Crohn
disease
The three most common sites of intestinal involvement in Crohn's
disease
Specialty Gastroenterology
Symptoms Abdominal pain, diarrhoea (may be
bloody), fever, weight loss[1]
Complications Anemia, skin rashes, arthritis, bowel cancer[1]
Usual onset 20 to 30[2]
Duration Long term[1]
Risk factors Tobacco smoking[3]
Diagnostic method Biopsy, medical imaging[1]

Differential Irritable bowel syndrome, celiac disease, Behçet's
diagnosis disease, nonsteroidal anti-inflammatory
drug enteropathy, intestinal tuberculosis[1][4]
Medication Corticosteroids, methotrexate[1]
Prognosis Slightly increased risk of death[5]
Frequency 3.2 per 1,000 (developed world)[6]
Crohn's disease is a type of inflammatory bowel disease (IBD) that may affect any
segment of the gastrointestinal tract from the mouth to the anus.[2] Symptoms often
include abdominal pain, diarrhea (which may be bloody if inflammation is
severe), fever, abdominal distension, and weight loss.[1][2]
Other complications outside the gastrointestinal tract may include anemia, skin
rashes, arthritis, inflammation of the eye, and fatigue.[1] The skin rashes may be due to
infections as well as pyoderma gangrenosum or erythema nodosum.[1] Bowel
obstruction may occur as a complication of chronic inflammation, and those with the
disease are at greater risk of colon cancer and small bowel cancer.[1]
While the precise causes of Crohn's disease are unknown, it is believed to be caused
by a combination of environmental, immune, and bacterial factors in genetically
susceptible individuals.[2][7][8][9] It results in a chronic inflammatory disorder, in which the
body's immune system defends the gastrointestinal tract, possibly
targeting microbial antigens.[8][10] While Crohn's is an immune-related disease, it does not
appear to be an autoimmune disease (in that the immune system is not being triggered
by the body itself).[11] The exact underlying immune problem is not clear; however, it may
be an immunodeficiency state.[10][12][13] Due to the disease's debated etiology, it has been
described as an autoimmune disease, an autoimmune-related disease, an idiopathic
disease, an immunodeficiency disease, and a disease of unknown etiology.
About half of the overall risk is related to genetics, with more than 70 genes having
been found to be involved.[1][14] Tobacco smokers are twice as likely to develop Crohn's
disease as nonsmokers.[3] It also often begins after gastroenteritis.[1] Diagnosis is based
on a number of findings, including biopsy and appearance of the bowel wall, medical
imaging, and description of the disease.[1] Other conditions that can present similarly
include irritable bowel syndrome and Behçet's disease.[1]
There are no medications or surgical procedures that can cure Crohn's disease.[1]
[2]
Treatment options are intended to help with symptoms, maintain remission, and
prevent relapse.[1] In those newly diagnosed, a corticosteroid may be used for a brief
period of time to rapidly improve symptoms, alongside another medication such as
either methotrexate or a thiopurine used to prevent recurrence.[1] Stopping smoking is
recommended in people with Crohn's disease.[1] One in five people with the disease is
admitted to the hospital each year, and half of those with the disease will require
surgery for the disease at some point over a ten-year period. [1] While surgery should be
used as little as possible, it is necessary to address some abscesses, certain bowel
obstructions, and cancers.[1] Checking for bowel cancer via colonoscopy is
recommended every few years, starting eight years after the disease has begun. [1]
Crohn's disease affects about 3.2 per 1,000 people in Europe and North America,[6] and
around 1.54 in 1000 in the UK.[15] It is less common in Asia and Africa.[16][17] It has
historically been more common in the developed world.[18] Rates have, however, been
increasing, particularly in the developing world, since the 1970s.[17][18] Inflammatory bowel
disease resulted in 47,400 deaths in 2015, [19] and those with Crohn's disease have a
slightly reduced life expectancy.[1] It tends to start in the teens and twenties, though it
can occur at any age.[1][2][20] Males and females are equally affected.[2]
Contents
 1Name
 2Signs and symptoms
o 2.1Gastrointestinal
o 2.2Systemic
o 2.3Extraintestinal
o 2.4Complications
 3Causes
o 3.1Genetics
o 3.2Immune system
o 3.3Microbes
o 3.4Environmental factors
 4Pathophysiology
 5Diagnosis
o 5.1Classification
o 5.2Endoscopy
o 5.3Radiologic tests
o 5.4Blood tests
o 5.5Comparison with ulcerative colitis
o 5.6Differential diagnosis
 6Management
o 6.1Lifestyle changes
o 6.2Medication
o 6.3Surgery
o 6.4Mental health
o 6.5Alternative medicine
 7Prognosis
 8Epidemiology
 9History
 10Research
 11References
 12Further reading
 13External links
Name[edit]
The disease was named after gastroenterologist Burrill Bernard Crohn, who in 1932,
together with two colleagues at Mount Sinai Hospital in New York, described a series of
patients with inflammation of the terminal ileum of the small intestine, the area most
commonly affected by the illness.[21]
Signs and symptoms[edit]

Signs and symptoms
Crohn's disease Ulcerative colitis
Often porridge-like,[22] Often mucus-like

Defecation
sometimes steatorrhea and with blood[22]
Tenesmus Less common[22] More common[22]
Fever Common[22] Indicates severe disease[22]
Fistulae Common[23] Seldom
Weight
Often More seldom
loss
Gastrointestinal[edit]
An aphthous ulcer on the mucous membrane of the mouth in Crohn's disease.
Many people with Crohn's disease have symptoms for years before the diagnosis. [24] The
usual onset is in the teens and twenties, but can occur at any age. [20][1] Because of the
'patchy' nature of the gastrointestinal disease and the depth of tissue involvement, initial
symptoms can be more subtle than those of ulcerative colitis. People with Crohn's
disease experience chronic recurring periods of flare-ups and remission.[25] The
symptoms expierenced can change over time as inflammation increases and spreads.
Symptoms can also be different depending on which organs are involved. It is generally
thought that the presentation of Crohn's Disease is different for each patient due to the
high variability of symptoms, organ involvement, and initial presentation.
Perianal Perianal discomfort may also be prominent in Crohn's disease. Itchiness or
pain around the anus may be suggestive of inflammation of the anus, or perianal
complications such as anal fissures, fistulae, or abscesses around the anal area.
[1]
Perianal skin tags are also common in Crohn's disease, and may appear with or
without the presence of colorectal polyps.[26] Fecal incontinence may accompany
perianal Crohn's disease.
Intestines The Intestines, especially the Colon and Terminal Ilium are the most
commonly affected areas of the body. Abdominal pain is a common initial symptom of
Crohn's disease,[2] especially in the lower right abdomen.[27] Flatulence, bloating, and
abdominal distension are additional symptoms and may also add to the intestinal
discomfort. Pain is often accompanied by diarrhea, which may or may not be bloody.
Inflammation in different areas of the intestinal tract can affect the quality of
the feces. Ileitis typically results in large-volume, watery feces, while colitis may result in
a smaller volume of feces of higher frequency. Fecal consistency may range from solid
to watery. In severe cases, an individual may have more than 20 bowel movements per
day, and may need to awaken at night to defecate. [1][28][29][30] Visible bleeding in the feces is
less common in Crohn's disease than in ulcerative colitis, but is not unusual. [1] Bloody
bowel movements are usually intermittent, and may be bright red, dark maroon, or even
black in color. The color of bloody stool depends on the location of the beed. In severe
Crohn's colitis, bleeding may be copious.[28]
Stomach and Esophagus The stomach is rarely the sole or predominant site of CD. To
date there are only a few documented case reports of adults with isolated gastric CD
and no reports in the pediatric population. Isolated stomach involvement is very unusual
presentation accounting for less than 0.07% of all gastrointestinal CD. [31] Rarely,
the esophagus and stomach may be involved in Crohn's disease. These can cause
symptoms including difficulty swallowing (dysphagia), upper abdominal pain, and
vomiting.[32]
Oropharynx (Mouth) The mouth may be affected by recurrent sores (aphthous ulcers).
Recurrent aphthous ulcers are common; however, it is not clear whether this is due to
Crohn's disease or simply that they are common in the general population. Other
findings may include diffuse or nodular swelling of the mouth, a cobblestone
appearance inside the mouth, granulomatous ulcers, or pyostomatitis vegetans.
Medications that are commonly prescribed to treat CD, such as anti-inflammatory and
sulfa-containing drugs, may cause lichenoid drug reactions in the mouth. Fungal
infection such as candidiasis is also common due to the immunosuppression required in
the treatment of the disease. Signs of anemia such as pallor and angular cheilitis or
glossitis are also common.
Systemic[edit]
Like many other chronic, inflammatory diseases, Crohn's disease can cause a variety
of systemic symptoms.[1] Among children, growth failure is common. Many children are
first diagnosed with Crohn's disease based on inability to maintain growth.[33] As it may
manifest at the time of the growth spurt in puberty, up to 30% of children with Crohn's
disease may have retardation of growth.[34] Fever may also be present, though fevers
greater than 38.5 °C (101.3 °F) are uncommon unless there is a complication such as
an abscess.[1] Among older individuals, Crohn's disease may manifest as weight loss,
usually related to decreased food intake, since individuals with intestinal symptoms from
Crohn's disease often feel better when they do not eat and might lose their appetite.
[33]
People with extensive small intestine disease may also
have malabsorption of carbohydrates or lipids, which can further exacerbate weight
loss.[35]
Extraintestinal[edit]
Crohn's disease can affect many organ systems beyond the gastrointestinal tract.[36]
Complications
Crohn's Ulcerative
disease colitis
Higher
Nutrient deficiency
risk
Colon cancer risk Slight Considerable
Prevalence of extraintestinal complications[37][38][39]
Female
2.2% 3.2%
s
Iritis/uveitis
Males 1.3% 0.9%
Female
0.3% 1%
s
Primary sclerosing
cholangitis
Males 0.4% 3%
Female
0.7% 0.8%
s
Ankylosing
spondylitis
Males 2.7% 1.5%
Female
1.2% 0.8%
s
Pyoderma
gangrenosum
Males 1.3% 0.7%
Female
1.9% 2%
s
Erythema
nodosum
Males 0.6% 0.7%
Eye Involvement Inflammation of the interior portion of the eye, known as uveitis, can
cause blurred vision and eye pain, especially when exposed to light (photophobia).
[40]
Inflammation may also involve the white part of the eye (sclera) or the overlying
connective tissue (episclera), which causes conditions called scleritis and episcleritis,
respectively.[40] Uveitis can lead to loss of vision if untreated.[36]
Gallbladder Involvement Crohn's disease that affects the ileum may result in an
increased risk of gallstones. This is due to a decrease in bile acid resorption in the
ileum, and the bile gets excreted in the stool. As a result, the cholesterol/bile ratio
increases in the gallbladder, resulting in an increased risk for gallstones.[40] Although the
association is greater in the context of ulcerative colitis, Crohn's disease may also be
associated with primary sclerosing cholangitis, a type of inflammation of the bile ducts.[41]
Joint and Muscle Involvement Crohn's disease is associated with a type
of rheumatologic disease known as seronegative spondyloarthropathy.[40] This group of
diseases is characterized by inflammation of one or more joints (arthritis) or muscle
insertions (enthesitis).[40] The arthritis in Crohn's disease can be divided into two types.
The first type affects larger weight-bearing joints such as the knee (most common),
hips, shoulders, wrists, or elbows.[40] The second type symmetrically involves five or
more of the small joints of the hands and feet. [40] The arthritis may also involve the spine,
leading to ankylosing spondylitis if the entire spine is involved, or simply sacroiliitis if
only the sacroiliac joint is involved.[40] The symptoms of arthritis include painful, warm,
swollen, stiff joints, and loss of joint mobility or function. [42]
Bone Involvement Crohn's disease increases the risk of osteoporosis or thinning of the
bones.[40] Individuals with osteoporosis are at increased risk of bone fractures.[43]
A single lesion of erythema nodosum
Integumentary Involvement Crohn's disease may also involve the skin, blood,

and endocrine system. Erythema nodosum is the most common type of skin problem,
occurring in around 8% of people with Crohn's disease, producing raised, tender
red nodules usually appearing on the shins.[40][44][45] Erythema nodosum is due to
inflammation of the underlying subcutaneous tissue, and is characterized
by septal panniculitis.[44]
Pyoderma gangrenosum is a less common skin problem, occurring in under 2%, [45] and
is typically a painful ulcerating nodule.[44][36]
Clubbing, a deformity of the ends of the fingers, may also be a result of Crohn's
disease.
Circulatory Involvement Crohn's disease also increases the risk of blood clots;
[40]
painful swelling of the lower legs can be a sign of deep venous thrombosis, while
difficulty breathing may be a result of pulmonary embolism.
Neurological Involvement Crohn's disease can also cause neurological complications
(reportedly in up to 15%).[46] The most common of these
are seizures, stroke, myopathy, peripheral neuropathy, headache, and depression.[46]
Psychological Involvement Crohn's Disease is linked to many psychological
disorders, including depression and anxiety, denial of your disease, the need for
dependence or dependent behaviors, feeling overwhelmed, and having a poor self-
image.[47]
Endocrinological Involvement Autoimmune hemolytic anemia, a condition in which
the immune system attacks the red blood cells, is also more common in Crohn's
disease and may cause fatigue, a pale appearance, and other symptoms common
in anemia.
Secondary amyloidosis (AA) is another rare but serious complication of inflammatory
bowel disease (IBD), generally seen in Crohn's disease. At least 1% of patients with
Crohn's disease develop amyloidosis. In the literature, the time lapse between the onset
of Crohn's disease and the diagnosis of amyloidosis has been reported to range from
one to 21 years.
Respiratory Involvement Laryngeal involvement in inflammatory bowel disease is
extremely rare. Only 12 cases of laryngeal involvement in Crohn disease have been
reported until now. Moreover, only one case of laryngeal manifestations in ulcerative
colitis has been reported so far.[48] 9 patients complained of difficulty in breathing due
to edema and ulceration from the larynx to the hypopharynx[49] Hoarseness, sore throat,
and odynophagia are other symptoms of laryngeal involvement of Crohn's Disease. [50]
Considering extraintestinal manifestations of CD, those involving the lung are relatively
rare. However, there is a wide array of lung manifestations, ranging from subclinical
alterations, airway diseases and lung parenchymal diseases to pleural diseases and
drug-related diseases. The most frequent manifestation is bronchial inflammation
and suppuration with or without bronchiectasis. There are a number of mechanisms by
which the lungs may become involved in CD. These include the same embryological
origin of the lung and gastrointestinal tract by ancestral intestine, similar immune
systems in the pulmonary and intestinal mucosa, the presence of circulating immune
complexes and auto-antibodies, and the adverse pulmonary effects of some drugs. [51]
Malnutrition Symptoms People with Crohn's disease may develop anemia due to vitamin
B12, folate, iron deficiency, or due to anemia of chronic disease. The most common
[52][53]
is iron deficiency anemia from chronic blood loss, reduced dietary intake, and
[52]
persistent inflammation leading to increased hepcidin levels, restricting iron absorption

in the duodenum.[53] As Crohn's disease most commonly affects the terminal ileum where
the vitamin B12/intrinsic factor complex is absorbed, B12 deficiency may be seen. [53] This
is particularly common after surgery to remove the ileum. [52] Involvement of the
duodenum and jejunum can impair the absorption of many other nutrients
including folate. People with Crohn's often also have issues with small bowel bacterial
overgrowth syndrome, which can produce micronutrient deficiencies. [54][55]
Complications[edit]
Intestinal Damage Crohn's disease can lead to several mechanical complications
within the intestines, including obstruction,[56] fistulae,[57] and abscesses.[58] Obstruction
typically occurs from strictures or adhesions that narrow the lumen, blocking the
passage of the intestinal contents. A fistula can develop between two loops of bowel,
between the bowel and bladder, between the bowel and vagina, and between the bowel
and skin. Abscesses are walled-off concentrations of infection, which can occur in
the abdomen or in the perianal area. Crohn's is responsible for 10% of vesicoenteric
fistulae, and is the most common cause of ileovesical fistulae. [59]
Symptoms caused by intestinal stenosis, or the tightening and narrowing of the bowel,
are also common in Crohn's disease. Abdominal pain is often most severe in areas of
the bowel with stenosis. Persistent vomiting and nausea may indicate stenosis
from small bowel obstruction or disease involving the stomach, pylorus, or duodenum.[28]
Intestinal granulomas are a walled-off portions of the intestine by macrophages in order
to isolate infections. Granuloma formation is more often seen in younger patients, and
mainly in the severe, active penetrating disease.[60] Granuloma is considered the
hallmark of microscopic diagnosis in Crohn’s disease (CD), but granulomas can be
detected in only 21-60% of CD patients. [60]
Cancer Crohn's disease also increases the risk of cancer in the area of inflammation.
For example, individuals with Crohn's disease involving the small bowel are at higher
risk for small intestinal cancer.[61] Similarly, people with Crohn's colitis have a relative
risk of 5.6 for developing colon cancer.[62] Screening for colon cancer with colonoscopy is
recommended for anyone who has had Crohn's colitis for at least eight years. [63]
Some studies suggest there is a role for chemoprotection in the prevention of colorectal
cancer in Crohn's involving the colon; two agents have been
suggested, folate and mesalamine preparations.[64] Also, immunomodulators and biologic
agents used to treat this disease may promote developing extra-intestinal cancers. [65]
Endoscopic image of colon cancer identified in the sigmoid colon on screening colonoscopy for Crohn's

disease
Major Complications The major complications of Crohn's disease include bowel
obstruction, abscesses, free perforation, and hemorrhage, which in rare cases may be
fatal.[66][67]
Other Complications Individuals with Crohn's disease are at risk of malnutrition for
many reasons, including decreased food intake and malabsorption. The risk increases
following resection of the small bowel. Such individuals may require oral supplements to
increase their caloric intake, or in severe cases, total parenteral nutrition (TPN). Most
people with moderate or severe Crohn's disease are referred to a dietitian for
assistance in nutrition.[68]
Small intestinal bacterial overgrowth (SIBO) is characterized by excessive proliferation
of colonic bacterial species in the small bowel. Potential causes of SIBO include
fistulae, strictures or motility disturbances. Hence, patients with Crohn's Disease (CD)
are especially predisposed to develop SIBO. As result, CD patients may experience
malabsorption and report symptoms such as weight loss, watery diarrhea, meteorism,
flatulence and abdominal pain, mimicking acute flare in these patients. [55]
Pregnancy Crohn's disease can be problematic during pregnancy, and some
medications can cause adverse outcomes for the fetus or mother. Consultation with
an obstetrician and gastroenterologist about Crohn's disease and all medications
facilitates preventive measures. In some cases, remission occurs during pregnancy.
Certain medications can also lower sperm count or otherwise adversely affect a
man's fertility.[69]
Ostomy-related Complications Common complications of an ostomy (a common
surgery in crohn's disease) are: Mucosal edema, Peristomal dermatitis, Retraction,
Ostomy prolapse, Mucosal/skin detachment, Hematoma, Necrosis, Parastomal hernia,
and Stenosis.[70]
Causes[edit]
Risk factors
Smokin Higher risk for

Lower risk for smokers[71]
g smokers
Usual onset between Peak incidence between

Age
15 and 30 years[72] 15 and 25 years
While the exact cause or causes are unknown, Crohn's disease seems to be due to a
combination of environmental factors and genetic predisposition.[73] Crohn's is the first
genetically complex disease in which the relationship between genetic risk factors and
the immune system is understood in considerable detail. [74] Each individual
risk mutation makes a small contribution to the overall risk of Crohn's (approximately
1:200). The genetic data, and direct assessment of immunity, indicates a malfunction in
the innate immune system.[75] In this view, the chronic inflammation of Crohn's is caused
when the adaptive immune system tries to compensate for a deficient innate immune
system.[76]
Genetics[edit]
NOD2 protein model with schematic diagram. Two N-terminal CARD domains (red) connected via helical linker
(blue) with central NBD domain (green). At C-terminus LRR domain (cyan) is located. Additionally, some
mutations which are associated with certain disease patterns in Crohn's disease are marked in red wire
representation.[77]
Crohn's has a genetic component.[78] Because of this, siblings of known people with

Crohn's are 30 times more likely to develop Crohn's than the general population. [79]
The first mutation found to be associated with Crohn's was a frameshift in
the NOD2 gene (also known as the CARD15 gene),[80] followed by the discovery of point
mutations.[81] Over 30 genes have been associated with Crohn's; a biological function is
known for most of them. For example, one association is with mutations in
the XBP1 gene, which is involved in the unfolded protein response pathway of
the endoplasmic reticulum.[82][83] The gene variants of NOD2/CARD15 seem to be related
with small-bowel involvement.[84] Other well documented genes which increase the risk of
developing Crohn's disease are ATG16L1,[85] IL23R,[86] IRGM,[87] and SLC11A1.[88] There is
considerable overlap between susceptibility loci for IBD and mycobacterial infections.
[89]
Genome-wide association studies have shown that Crohn's disease is genetically
linked to coeliac disease.[90]
Crohn's has been linked to the gene LRRK2 with one variant potentially increasing the
risk of developing the disease by 70%, while another lowers it by 25%. The gene is
responsible for making a protein, which collects and eliminates waste product in cells,
and is also associated with Parkinson's disease.[91]
Immune system[edit]
There was a prevailing view that Crohn's disease is a primary T cell autoimmune
disorder; however, a newer theory hypothesizes that Crohn's results from an impaired
innate immunity.[92] The later hypothesis describes impaired cytokine secretion
by macrophages, which contributes to impaired innate immunity and leads to a
sustained microbial-induced inflammatory response in the colon, where the bacterial
load is high.[8][75] Another theory is that the inflammation of Crohn's was caused by an
overactive Th1 and Th17 cytokine response.[93][94]
In 2007, the ATG16L1 gene was implicated in Crohn's disease, which may
induce autophagy and hinder the body's ability to attack invasive bacteria. [85] Another
study theorized that the human immune system traditionally evolved with the presence
of parasites inside the body and that the lack thereof due to modern hygiene standards
has weakened the immune system. Test subjects were reintroduced to harmless
parasites, with positive response.[95]
Microbes[edit]
It is hypothesized that maintenance of commensal microorganism growth in the GI
tract is dysregulated, either as a result or cause of immune dysregulation.[96][97]
There is an apparent connection between Crohn's disease, Mycobacterium, other
pathogenic bacteria, and genetic markers.[98][99] A number of studies have suggested a
causal role for Mycobacterium avium subspecies paratuberculosis (MAP), which
causes a similar disease, Johne's disease, in cattle.[100][101] In many individuals, genetic
factors predispose individuals to Mycobacterium
avium subsp. paratuberculosis infection. This bacterium may produce certain
compounds containing mannose, which may protect both itself and various other
bacteria from phagocytosis, thereby possibly causing a variety of secondary infections.
[102]
NOD2 is a gene involved in Crohn's genetic susceptibility. It is associated

with macrophages' diminished ability to phagocytize MAP. This same gene may reduce
innate and adaptive immunity in gastrointestinal tissue and impair the ability to resist
infection by the MAP bacterium.[103] Macrophages that ingest the MAP bacterium are
associated with high production of TNF-α.[104][105]
Other studies have linked specific strains of enteroadherent E. coli to the disease.
[106]
Adherent-invasive Escherichia coli (AIEC), are more common in people with CD,[107][108]
[106]
have the ability to make strong biofilms compared to non-AIEC strains correlating
with high adhesion and invasion indices[109][110] of neutrophils and the ability to
block autophagy at the autolysosomal step, which allows for intracellular survival of the
bacteria and induction of inflammation.[111] Inflammation drives the proliferation of AIEC
and dysbiosis in the ileum, irrespective of genotype.[112] AIEC strains replicate extensively
inside macrophages inducing the secretion of very large amounts of TNF-α. [113]
Mouse studies have suggested some symptoms of Crohn's disease, ulcerative colitis,
and irritable bowel syndrome have the same underlying cause. Biopsy samples taken
from the colons of all three patient groups were found to produce elevated levels of
a serine protease.[114] Experimental introduction of the serine protease into mice has
been found to produce widespread pain associated with irritable bowel syndrome, as
well as colitis, which is associated with all three diseases. [115] Regional and temporal
variations in those illnesses follow those associated with infection with the
protozoan Blastocystis.[116]
The "cold-chain" hypothesis is that psychrotrophic bacteria such
as Yersinia and Listeria species contribute to the disease. A statistical correlation was
found between the advent of the use of refrigeration in the United States and various
parts of Europe and the rise of the disease.[117][118][119]
There is also a tentative association between Candida colonization and Crohn's
disease.[120]
Still, these relationships between specific pathogens and Crohn's disease remain
unclear.[121][122]
Environmental factors[edit]
The increased incidence of Crohn's in the industrialized world indicates an
environmental component. Crohn's is associated with an increased intake of
animal protein, milk protein, and an increased ratio of omega-6 to omega-
3 polyunsaturated fatty acids.[123] Those who consume vegetable proteins appear to have
a lower incidence of Crohn's disease. Consumption of fish protein has no association.
[123]
Smoking increases the risk of the return of active disease (flares). [3] The introduction
of hormonal contraception in the United States in the 1960s is associated with a
dramatic increase in incidence, and one hypothesis is that these drugs work on the
digestive system in ways similar to smoking.[124] Isotretinoin is associated with Crohn's.[125]
[126][127]
Although stress is sometimes claimed to exacerbate Crohn's disease, there is no

concrete evidence to support such claim.[2] Dietary microparticles, such as those found
in toothpaste, have been studied as they produce effects on immunity, but they were not
consumed in greater amounts in patients with Crohn's. [128][129] The use of doxycycline has
also been associated with increased risk of developing inflammatory bowel diseases. [130]
[131][132]
In one large retrospective study, patients who were prescribed doxycycline for
their acne had a 2.25-fold greater risk of developing Crohn's disease. [131]
Pathophysiology[edit]
Pathophysiology

Cytokine respons
Associated with Th17[133] Vaguely associated with Th2
e
During a colonoscopy, biopsies of the colon are often taken to confirm the diagnosis.
Certain characteristic features of the pathology seen point toward Crohn's disease; it
shows a transmural pattern of inflammation, meaning the inflammation may span the
entire depth of the intestinal wall.[1] Ulceration is an outcome seen in highly active
disease. There is usually an abrupt transition between unaffected tissue and the ulcer—
a characteristic sign known as skip lesions. Under a microscope, biopsies of the
affected colon may show mucosal inflammation, characterized by focal infiltration
of neutrophils, a type of inflammatory cell, into the epithelium. This typically occurs in
the area overlying lymphoid aggregates. These neutrophils, along with mononuclear
cells, may infiltrate the crypts, leading to inflammation (crypititis) or abscess (crypt
abscess).
Granulomas, aggregates of macrophage derivatives known as giant cells, are found in
50% of cases and are most specific for Crohn's disease. The granulomas of Crohn's
disease do not show "caseation", a cheese-like appearance on microscopic
examination characteristic of granulomas associated with infections, such
as tuberculosis. Biopsies may also show chronic mucosal damage, as evidenced by
blunting of the intestinal villi, atypical branching of the crypts, and a change in the tissue
type (metaplasia). One example of such metaplasia, Paneth cell metaplasia, involves
the development of Paneth cells (typically found in the small intestine and a key
regulator of intestinal microbiota) in other parts of the gastrointestinal system. [134][135]
Diagnosis[edit]
The diagnosis of Crohn's disease can sometimes be challenging, [24] and many tests are
often required to assist the physician in making the diagnosis. [28] Even with a full battery
of tests, it may not be possible to diagnose Crohn's with complete certainty; a
colonoscopy is approximately 70% effective in diagnosing the disease, with further tests
being less effective. Disease in the small bowel is particularly difficult to diagnose, as a
traditional colonoscopy allows access to only the colon and lower portions of the small
intestines; introduction of the capsule endoscopy[136] aids in endoscopic diagnosis. Giant
(multinucleate) cells, a common finding in the lesions of Crohn's disease, are less
common in the lesions of lichen nitidus.[137]
Endoscopic image of Crohn's colitis showing deep ulceration


CT scan showing Crohn's disease in the fundus of the stomach

Endoscopic biopsy showing granulomatous inflammation of the colon in

a case of Crohn's disease.

Section of colectomy showing transmural inflammation

Resected ileum from a person with Crohn's disease
Classification[edit]
Distribution of gastrointestinal Crohn's disease.
Crohn's disease is one type of inflammatory bowel disease (IBD). It typically manifests

in the gastrointestinal tract and can be categorized by the specific tract region affected.
A disease of both the ileum (the last part of the small intestine that connects to the large
intestine), and the large intestine, Ileocolic Crohn's accounts for fifty percent of cases.
Crohn's ileitis, manifest in the ileum only, accounts for thirty percent of cases, while
Crohn's colitis, of the large intestine, accounts for the remaining twenty percent of cases
and may be particularly difficult to distinguish from ulcerative colitis.
Gastroduodenal Crohn's disease causes inflammation in the stomach and the first part
of the small intestine called the duodenum. Jejunoileitis causes spotty patches of
inflammation in the top half of the small intestine, called the jejunum. [138] The disease can
attack any part of the digestive tract, from mouth to anus. However, individuals affected
by the disease rarely fall outside these three classifications, with presentations in other
areas.[1]
Crohn's disease may also be categorized by the behavior of disease as it progresses.
These categorizations formalized in the Vienna classification of the disease. [139] There
are three categories of disease presentation in Crohn's disease: stricturing, penetrating,
and inflammatory. Stricturing disease causes narrowing of the bowel that may lead to
bowel obstruction or changes in the caliber of the feces. Penetrating disease creates
abnormal passageways (fistulae) between the bowel and other structures, such as the
skin. Inflammatory disease (or nonstricturing, nonpenetrating disease) causes
inflammation without causing strictures or fistulae. [139][140]
Endoscopy[edit]
A colonoscopy is the best test for making the diagnosis of Crohn's disease, as it allows
direct visualization of the colon and the terminal ileum, identifying the pattern of disease
involvement. On occasion, the colonoscope can travel past the terminal ileum, but it
varies from person to person. During the procedure, the gastroenterologist can also
perform a biopsy, taking small samples of tissue for laboratory analysis, which may help
confirm a diagnosis. As 30% of Crohn's disease involves only the ileum, [1] cannulation of
the terminal ileum is required in making the diagnosis. Finding a patchy distribution of
disease, with involvement of the colon or ileum, but not the rectum, is suggestive of
Crohn's disease, as are other endoscopic stigmata. [141] The utility of capsule endoscopy
for this, however, is still uncertain.[142] A "cobblestone"-like appearance is seen in
approximately 40% of cases of Crohn's disease upon colonoscopy, representing areas
of ulceration separated by narrow areas of healthy tissue.
Radiologic tests[edit]
A small bowel follow-through may suggest the diagnosis of Crohn's disease and is
useful when the disease involves only the small intestine. Because colonoscopy
and gastroscopy allow direct visualization of only the terminal ileum and beginning of
the duodenum, they cannot be used to evaluate the remainder of the small intestine. As
a result, a barium follow-through X-ray, wherein barium sulfate suspension is ingested
and fluoroscopic images of the bowel are taken over time, is useful for looking for
inflammation and narrowing of the small bowel. [141][143] Barium enemas, in which barium is
inserted into the rectum and fluoroscopy is used to image the bowel, are rarely used in
the work-up of Crohn's disease due to the advent of colonoscopy. They remain useful
for identifying anatomical abnormalities when strictures of the colon are too small for a
colonoscope to pass through, or in the detection of colonic fistulae (in this case contrast
should be performed with iodate substances).[144]
CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.
[145]
They are also useful for looking for intra-abdominal complications of Crohn's disease,
such as abscesses, small bowel obstructions, or fistulae. [146] Magnetic resonance
imaging (MRI) is another option for imaging the small bowel as well as looking for
complications, though it is more expensive and less readily available. [147] MRI techniques
such as diffusion-weighted imaging and high-resolution imaging are more sensitive in
detecting ulceration and inflammation compared to CT. [148][149]
Blood tests[edit]
A complete blood count may reveal anemia, which commonly is caused by blood loss
leading to iron deficiency or by vitamin B deficiency, usually caused by ileal disease
12
impairing vitamin B absorption. Rarely autoimmune hemolysis may occur.

12
[150]
Ferritin levels help assess if iron deficiency is contributing to the anemia. Erythrocyte
sedimentation rate (ESR) and C-reactive protein help assess the degree of
inflammation, which is important as ferritin can also be raised in inflammation. [151] Serum
iron, total iron binding capacity and transferrin saturation may be more easily interpreted
in inflammation. Anemia of chronic disease results in a normocytic anemia.
Other causes of anemia include medication used in treatment of inflammatory bowel
disease, like azathioprine, which can lead to cytopenia, and sulfasalazine, which can
also result in folate deficiency. Testing for Saccharomyces cerevisiae antibodies
(ASCA) and antineutrophil cytoplasmic antibodies (ANCA) has been evaluated to
identify inflammatory diseases of the intestine [152] and to differentiate Crohn's disease
from ulcerative colitis.[153] Furthermore, increasing amounts and levels of serological
antibodies such as ASCA, antilaminaribioside [Glc(β1,3)Glb(β); ALCA], antichitobioside
[GlcNAc(β1,4)GlcNAc(β); ACCA], antimannobioside [Man(α1,3)Man(α)AMCA],
antiLaminarin [(Glc(β1,3))3n(Glc(β1,6))n; anti-L] and antichitin [GlcNAc(β1,4)n; anti-C]
associate with disease behavior and surgery, and may aid in the prognosis of Crohn's
disease.[154][155][156][157]
Low serum levels of vitamin D are associated with Crohn's disease. [158] Further studies
are required to determine the significance of this association. [158]
Comparison with ulcerative colitis[edit]
The most common disease that mimics the symptoms of Crohn's disease is ulcerative
colitis, as both are inflammatory bowel diseases that can affect the colon with similar
symptoms. It is important to differentiate these diseases, since the course of the
diseases and treatments may be different. In some cases, however, it may not be
possible to tell the difference, in which case the disease is classified as indeterminate
colitis.[1][28][29]
Diagnostic findings
Terminal
Commonly Seldom
ileum involvement
Colon involvement Usually Always
Rectum involvement Seldom Usually (95%)[71]
Involvement around
Common[23] Seldom
the anus
No increase in rate of primary sclerosing

Bile duct involvement Higher rate[159]
cholangitis
Continuous area of
Distribution of disease Patchy areas of inflammation (skip lesions)
inflammation[71]
Deep geographic and serpiginous (snake-

Endoscopy Continuous ulcer
like) ulcers
Depth of inflammation May be transmural, deep into tissues[23][160] Shallow, mucosal

Stenosis Common Seldom
May have non-necrotizing non-peri-intestinal Non-peri-intestinal

Granulomas on biopsy
crypt granulomas[23][161][162] crypt granulomas not seen[163]
Differential diagnosis[edit]
Other conditions with similar symptoms as Crohn's disease includes
intestinal tuberculosis, Behçet's disease, ulcerative colitis, nonsteroidal anti-
inflammatory drug enteropathy, irritable bowel syndrome and celiac disease.[4] Irritable
bowel syndrome is excluded when there are inflammatory changes. [4] Celiac disease
cannot be excluded if specific antibodies (anti-transglutaminase antibodies) are
negative,[164][165] nor in absence of intestinal villi atrophy.[166][167]
Management[edit]
Main article: Management of Crohn's disease
Management
Mesalazine Less useful[168] More useful[168]
Antibiotics Effective in long-term[169] Generally not useful[170]
Often returns following Usually cured by removal

Surgery
removal of affected part of colon
There is no cure for Crohn's disease and remission may not be possible or prolonged if

achieved. In cases where remission is possible, relapse can be prevented
and symptoms controlled with medication, lifestyle and dietary changes, changes to
eating habits (eating smaller amounts more often), reduction of stress, moderate
activity, and exercise. Surgery is generally contraindicated and has not been shown to
prevent remission. Adequately controlled, Crohn's disease may not significantly restrict
daily living.[171] Treatment for Crohn's disease is only when symptoms are active and
involve first treating the acute problem, then maintaining remission.
Lifestyle changes[edit]
Certain lifestyle changes can reduce symptoms,
including dietary adjustments, elemental diet, proper hydration, and smoking cessation.
Diets that include higher levels of fiber and fruit are associated with reduced risk, while
diets rich in total fats, polyunsaturated fatty acids, meat, and omega-6 fatty acids may
increase the risk of Crohn's.[172] Maintaining a balanced diet with proper portion control
can help manage symptoms of the disease. Eating small meals frequently instead of big
meals may also help with a low appetite. A food diary may help with identifying foods
that trigger symptoms. Some people should follow a low fiber diet to control acute
symptoms especially if fibrous foods cause symptoms.[171] Some find relief in
eliminating casein (a protein found in cow's milk) and gluten (a protein found in wheat,
rye and barley) from their diets. They may have specific dietary intolerances (not
allergies).[173] Fatigue can be helped with regular exercise, a healthy diet, and enough
sleep. Smoking may worsen symptoms, and stopping is recommended. [171]
Medication[edit]
Acute treatment uses medications to treat any infection (normally antibiotics) and to
reduce inflammation (normally aminosalicylate anti-inflammatory drugs
and corticosteroids). When symptoms are in remission, treatment enters maintenance,
with a goal of avoiding the recurrence of symptoms. Prolonged use of corticosteroids
has significant side-effects; as a result, they are, in general, not used for long-term
treatment. Alternatives include aminosalicylates alone, though only a minority are able
to maintain the treatment, and many require immunosuppressive drugs. [23] It has been
also suggested that antibiotics change the enteric flora, and their continuous use may
pose the risk of overgrowth with pathogens such as Clostridium difficile.[174]
Medications used to treat the symptoms of Crohn's disease include 5-aminosalicylic
acid (5-ASA) formulations, prednisone, immunomodulators such as azathioprine (given
as the prodrug for 6-mercaptopurine), methotrexate,[175] infliximab, adalimumab,
[29]
certolizumab,[176] vedolizumab, ustekinumab,[177] and natalizumab.[178][179] Hydrocortisone s
hould be used in severe attacks of Crohn's disease. [180] Biological therapies are
medications used to avoid long-term steroid use, decrease inflammation, and treat
people who have fistulas with abscesses.[27] The monoclonal antibody ustekinumab
appears to be a safe treatment option, and may help people with moderate to severe
active Crohn's disease.[181] The long term safety and effectiveness of monoclonal
antibody treatment is not known.[181] The monoclonal antibody briakinumab is not
effective for people with active Crohn's disease and it is no longer being manufactured.
[181]
The gradual loss of blood from the gastrointestinal tract, as well as chronic
inflammation, often leads to anemia, and professional guidelines suggest routinely
monitoring for this.[182][183][184] Adequate disease control usually improves anemia of chronic
disease, but iron deficiency may require treatment with iron supplements. Guidelines
vary as to how iron should be administered. Besides, other problems include a limitation
in possible daily resorption and an increased growth of intestinal bacteria.
Some[184] advise parenteral iron as first line as it works faster, has fewer gastrointestinal
side effects, and is unaffected by inflammation reducing enteral absorption.
Other guidelines[183] advise oral iron as first-line with parenteral iron reserved for those
that fail to adequately respond as oral iron is considerably cheaper. All agree that
severe anemia (hemoglobin under 10g/dL) should be treated with parenteral iron. Blood
transfusion should be reserved for those who are cardiovascularly unstable, due to its
relatively poor safety profile, lack of long-term efficacy, and cost. [183]
Surgery[edit]
Crohn's cannot be cured by surgery, as the disease eventually recurs, though it is used
in the case of partial or full blockage of the intestine. [185] Surgery may also be required for
complications such as obstructions, fistulas, or abscesses, or if the disease does not
respond to drugs. After the first surgery, Crohn's usually comes back at the site where
the diseased intestine was removed and the healthy ends were rejoined; it can also
come back in other locations. After a resection, scar tissue builds up, which can
cause strictures, which form when the intestines become too small to allow excrement
to pass through easily, which can lead to a blockage. After the first resection, another
resection may be necessary within five years.[186] For patients with an obstruction due to
a stricture, two options for treatment are strictureplasty and resection of that portion of
bowel. There is no statistical significance between strictureplasty alone versus
strictureplasty and resection in cases of duodenal involvement. In these cases, re-
operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe
and effective treatment for selected people with duodenal involvement. [187]
Postsurgical recurrence of Crohn's disease is relatively common. Crohn's lesions are
nearly always found at the site of the resected bowel. The join (or anastomosis) after
surgery may be inspected, usually during a colonoscopy, and disease activity graded.
The "Rutgeert's score" is an endoscopic scoring system for postoperative disease
recurrence in Crohn's disease. Mild postsurgical recurrences of Crohn's disease are
graded i1 and i2, moderate to severe recurrences are graded i3 and i4. [188] Fewer lesions
result in a lower grade. Based on the score, treatment plans can be designed to give the
patient the best chance of managing the recurrence of the disease. [189]
Short bowel syndrome (SBS, also short gut syndrome or simply short gut) is caused by
the surgical removal of part of the small intestine. It usually develops in those patients
who have had half or more of their small intestines removed. [190] Diarrhea is the main
symptom, but others may include weight loss, cramping, bloating, and heartburn. Short
bowel syndrome is treated with changes in diet, intravenous feeding, vitamin and
mineral supplements, and treatment with medications. In some cases of SBS, intestinal
transplant surgery may be considered; though the number of transplant centres offering
this procedure is quite small and it comes with a high risk due to the chance of infection
and rejection of the transplanted intestine. [191]
Bile acid diarrhea is another complication following surgery for Crohn's disease in which
the terminal ileum has been removed. This leads to the development of excessive
watery diarrhea. It is usually thought to be due to an inability of the ileum to reabsorb
bile acids after resection of the terminal ileum and was the first type of bile acid
malabsorption recognized.[192]
Mental health[edit]
Crohn's may result in anxiety or mood disorders, especially in young people who may
have stunted growth or embarrassment from fecal incontinence.[193] Counselling as well
as antidepressant or anxiolytic medication may help some people manage.[193]
As of 2017 there is a small amount of research looking at mindfulness-based therapies,
hypnotherapy, and cognitive behavioural therapy.[194]
Alternative medicine[edit]
It is common for people with Crohn's disease to try complementary or alternative
therapy.[195] These include diets, probiotics, fish oil, cannabidiol[196] and other herbal and
nutritional supplements.
 Acupuncture is used to treat inflammatory bowel disease

in China, and is being used more frequently in Western
society.[197] At this time, evidence is insufficient to
recommend the use of acupuncture.[195]
 A 2006 survey in Germany found that about half of people
with IBD used some form of alternative medicine, with the
most common being homeopathy, and a study in France
found that about 30% used alternative medicine.
[198]
Homeopathic preparations are not proven with this or
any other condition,[199][200][201] with large-scale studies finding
them to be no more effective than a placebo.[202][203][204]
 There are contradicting studies regarding the effect
of medical cannabis on inflammatory bowel disease,[205] and
its effects on management are uncertain.[206]
Prognosis[edit]
Crohn's disease is a chronic condition for which there is no known cure. It is
characterised by periods of improvement followed by episodes when symptoms flare
up. With treatment, most people achieve a healthy weight, and the mortality rate for the
disease is relatively low. It can vary from being benign to very severe, and people with
CD could experience just one episode or have continuous symptoms. It usually
reoccurs, although some people can remain disease-free for years or decades. Up to
80% of people with Crohn's disease are hospitalized at some point during the course of
their disease, with the highest rate occurring in the first year after diagnosis. [5] Most
people with Crohn's live a normal lifespan. [207] However, Crohn's disease is associated
with a small increase in risk of small bowel and colorectal carcinoma (bowel cancer). [208]
Epidemiology[edit]
The percentage of people with Crohn's disease has been determined in Norway and
the United States and is similar at 6 to 7.1:100,000. The Crohn's and Colitis Foundation
of America cites this number as approx 149:100,000; NIH cites 28 to 199 per 100,000. [209]
[210]
Crohn's disease is more common in northern countries, and with higher rates still in
the northern areas of these countries.[211] The incidence of Crohn's disease is thought to
be similar in Europe but lower in Asia and Africa.[209] It also has a higher incidence
in Ashkenazi Jews[1][212] and smokers.[213]
Crohn's disease begins most commonly in people in their teens and 20s, and people in
their 50s through to their 70s.[1][28][20] It is rarely diagnosed in early childhood. It usually
affects female children more severely than males. [214] However, only slightly more women
than men have Crohn's disease.[215] Parents, siblings or children of people with Crohn's
disease are 3 to 20 times more likely to develop the disease. [216] Twin studies find that if
one has the disease there is a 55% chance the other will too. [217]
The incidence of Crohn's disease is increasing in Europe [218] and in newly industrialised
countries.[219] For example, in Brazil, there has been an annual increase of 11% in the
incidence of Crohn's disease since 1990.[219]
History[edit]
Main article: List of people diagnosed with Crohn's disease
Inflammatory bowel diseases were described by Giovanni Battista Morgagni (1682–
1771) and by Scottish physician T Kennedy Dalziel in 1913.[220]
Ileitis terminalis was first described by Polish surgeon Antoni Leśniowski in 1904,
although it was not conclusively distinguished from intestinal tuberculosis. [221] In Poland, it
is still called Leśniowski-Crohn's disease (Polish: choroba Leśniowskiego-
Crohna). Burrill Bernard Crohn, an American gastroenterologist at New York
City's Mount Sinai Hospital, described fourteen cases in 1932, and submitted them to
the American Medical Association under the rubric of "Terminal ileitis: A new clinical
entity". Later that year, he, along with colleagues Leon Ginzburg and Gordon
Oppenheimer, published the case series "Regional ileitis: a pathologic and clinical
entity". However, due to the precedence of Crohn's name in the alphabet, it later
became known in the worldwide literature as Crohn's disease. [21]
Research[edit]
Some evidence supports the hypothesis that the bacterium Mycobacterium
avium subspecies paratuberculosis (MAP) is a cause of Crohn's disease (see
also Johne's disease). As a result, researchers are looking at the eradication of MAP as
a therapeutic option.[222] The Crohns MAP Vaccine is an experimental vaccine based on
this hypothesis.[223] Treating MAP using specific antibiotics that MAP may be susceptible
to has been examined and the results are unclear but tentatively beneficial. [224][225]
Crohn's is common in parts of the world where helminthic colonisation is rare and
uncommon in those areas where most people carry worms. Infections with helminths
may alter the autoimmune response that causes the disease. Trials of extracts from the
worm Trichuris suis showed promising results when used in people with IBD. [226][227]
[228]
However, these trials (TRUST -I & TRUST -II) failed in Phase 2 clinical trials and
were then discontinued after consistent failure in both North America and Europe. [229][230]
There is no good evidence that thalidomide or lenalidomide is useful to bring about or
maintain remission.[231][232]
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Further reading[edit]
 Lichtenstein GR, Loftus EV, Isaacs KL, Regueiro MD,
Gerson LB, Sands BE (April 2018). "ACG Clinical
Guideline: Management of Crohn's Disease in Adults". Am.
J. Gastroenterol. 113 (4): 481–
517. doi:10.1038/ajg.2018.27. PMID 29610508.
External links[edit]
 "Crohn's disease". MedlinePlus. U.S. National Library of
Medicine.
Classification D
ICD-10: K50
ICD-9-CM: 555
OMIM: 266600
MeSH: D003424
DiseasesDB: 3178
External resources MedlinePlus: 000249

eMedicine: med/477 ped/507 radio/197
Patient UK: Crohn's disease
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Crohn's disease

From Wikipedia, the free encyclopedia

Other names Crohn disease, Crohn syndrome, granulomatous

enteritis, regional enteritis, Leśniowski-Crohn

The three most common sites of intestinal involvement in Crohn's

Symptoms Abdominal pain, diarrhoea (may be

Complications Anemia, skin rashes, arthritis, bowel cancer[1]

Usual onset 20 to 30[2]

Duration Long term[1]

Risk factors Tobacco smoking[3]

Diagnostic method Biopsy, medical imaging[1]

diagnosis disease, nonsteroidal anti-inflammatory

Prognosis Slightly increased risk of death[5]

Frequency 3.2 per 1,000 (developed world)[6]

Signs and symptoms[edit]

Crohn's disease Ulcerative colitis

Often porridge-like,[22] Often mucus-like

Tenesmus Less common[22] More common[22]

Fever Common[22] Indicates severe disease[22]

Fistulae Common[23] Seldom

Prevalence of extraintestinal complications[37][38][39]

Males 1.3% 0.9%

A single lesion of erythema nodosum

Integumentary Involvement Crohn's disease may also involve the skin, blood,

persistent inflammation leading to increased hepcidin levels, restricting iron absorption

Endoscopic image of colon cancer identified in the sigmoid colon on screening colonoscopy for Crohn's

Crohn's disease Ulcerative colitis

Smokin Higher risk for

Usual onset between Peak incidence between

Crohn's has a genetic component.[78] Because of this, siblings of known people with

NOD2 is a gene involved in Crohn's genetic susceptibility. It is associated

Although stress is sometimes claimed to exacerbate Crohn's disease, there is no

Crohn's disease Ulcerative colitis

Endoscopic image of Crohn's colitis showing deep ulceration

CT scan showing Crohn's disease in the fundus of the stomach

Endoscopic biopsy showing granulomatous inflammation of the colon in

Section of colectomy showing transmural inflammation

Resected ileum from a person with Crohn's disease

Crohn's disease is one type of inflammatory bowel disease (IBD). It typically manifests

impairing vitamin B absorption. Rarely autoimmune hemolysis may occur.

Crohn's disease Ulcerative colitis

Colon involvement Usually Always

Rectum involvement Seldom Usually (95%)[71]

No increase in rate of primary sclerosing

Deep geographic and serpiginous (snake-

Depth of inflammation May be transmural, deep into tissues[23][160] Shallow, mucosal

May have non-necrotizing non-peri-intestinal Non-peri-intestinal

Crohn's disease Ulcerative colitis

Mesalazine Less useful[168] More useful[168]

Antibiotics Effective in long-term[169] Generally not useful[170]

Often returns following Usually cured by removal

There is no cure for Crohn's disease and remission may not be possible or prolonged if

 Acupuncture is used to treat inflammatory bowel disease

Sandborn WJ (August 2012). "Crohn's disease". Lancet. 380 (9853):

disease". The New England Journal of Medicine (Submitted

considerations for inflammatory bowel disease". The Proceedings of

Richard A.; Reinshagen, Max; von Tirpitz C, Christian (July 30,

Ferenc; Lonovics, János (May 28, 2005). "Clinical significance of

External resources MedlinePlus: 000249

Patient UK: Crohn's disease

Wikimedia Commons has

Inflammatory bowel disease: Crohn's disease and ulcerative colitis

Diseases of the digestive system