View source for Crohn's disease

{{Infobox disease
| Name           = Crohn's disease
| Latin          = morbus Leśniowski-Crohn
| Image          = Patterns of CD.svg
| Caption        = The three most common sites of intestinal involvement in '''Crohn's disease''' are
[[ileum|ileal]], [[ileocolic]] and [[Colon (anatomy)|colonic]].<ref name=Baumgart/>
| DiseasesDB     = 3178
| ICD10          = {{ICD10|K|50||k|50}}
| ICD9           = {{ICD9|555}}
| ICDO           =
| OMIM           = 266600
| MedlinePlus    = 000249
| eMedicineSubj  = med
| eMedicineTopic = 477
| eMedicine_mult = {{eMedicine2|ped|507}} {{eMedicine2|radio|197}}
| MeshID         = D003424
}}

'''Crohn's disease''', also known as ''inflammatory bowel disease,'' ''regional enteritis,'' and ''[[Granuloma]]tous ileocolitis'' disease is an inflammatory disease of the intestines that may affect any part of the [[gastrointestinal tract]] from [[mouth]] to [[anus]], causing a wide variety of [[symptom]]s. It primarily causes [[abdominal pain]], [[diarrhea]]<!-- PLEASE SEE WP:ENGVAR - DO NOT CHANGE THE SPELLING AS IT INTERFERES WITH LINKING AND IS INAPPROPRIATE --> (which may be bloody if inflammation is at its worst), [[vomiting]], or [[weight loss]],<ref name=Baumgart>
{{cite journal
 | author = Baumgart DC, Sandborn WJ
 | date= 12 May 2007
 | title = Inflammatory bowel disease: clinical aspects and established and evolving therapies.
 | journal = The Lancet
 | volume = 369
 | issue = 9573
 | pages = 1641–57
 | month = May
 | pmid = 17499606
 | doi =  10.1016/S0140-6736(07)60751-X
 | accessdate = 2009-11-04
 }}</ref><ref>[http://www.mayoclinic.com/health/crohns-disease/DS00104/DSECTION=symptoms Mayo Clinic: Crohn's Disease]</ref><ref>[http://digestive.niddk.nih.gov/ddiseases/pubs/crohns/ National Digestive Diseases Information Clearinghouse]</ref> but may also cause complications outside of the gastrointestinal tract such as [[skin rashes]], [[arthritis]], [[uveitis|inflammation of the eye]], tiredness, and lack of concentration.<ref name=Baumgart/>

Crohn's disease is thought to be an [[autoimmune disease]], in which the body's [[immune system]] attacks the gastrointestinal tract, causing [[inflammation]]; it is classified as a type of [[inflammatory bowel disease]].  There has been evidence of a [[genetics|genetic]] link to Crohn's disease, putting individuals with siblings afflicted with the disease at higher risk.<ref name="genetic_link">
{{cite journal
 | last = Barrett
 | first = JC et al.
 | year = 2008
 | month = August
 | title = Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease
 | journal = Nature Genetics
 | volume = 40
 | issue = 8
 | pages = 955–962
 | doi = 10.1038/ng.175
 | pmid = 18587394
 | pmc = 2574810
 | accessdate = 2009-11-04
 | last2 = Hansoul
 | first2 = S
 | last3 = Nicolae
 | first3 = DL
 | last4 = Cho
 | first4 = JH
 | last5 = Duerr
 | first5 = RH
 | last6 = Rioux
 | first6 = JD
 | last7 = Brant
 | first7 = SR
 | last8 = Silverberg
 | first8 = MS
 | last9 = Taylor
 | first9 = KD
 }}</ref> It is understood to have a large environmental component as evidenced by the higher number of cases in western industrialized nations. Males and females are equally affected.  Smokers are two times more likely to develop Crohn's disease.<ref name=Cosnes2004>
{{cite journal
 | author = Cosnes J
 | title = Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice
 | journal = Best Pract Res Clin Gastroenterol
 | volume = 18
 | issue = 3
 | pages = 481–96
 | year = 2004
 | month = June
 | pmid = 15157822
 | doi = 10.1016/j.bpg.2003.12.003
 | accessdate = 2009-11-04
}}</ref> Crohn's disease affects between 400,000 and 600,000 people in [[North America]].<ref name=Loftus>{{cite journal | last = Loftus | first = E.V. | coauthors = P. Schoenfeld, W. J. Sandborn | year = 2002 | month = January | title = The epidemiology and natural history of Crohn's disease in population-based patient cohorts from North America: a systematic review | journal = Alimentary Pharmacology & Therapeutics | volume = 16 | issue = 1 | pages = 51–60 | doi =10.1046/j.1365-2036.2002.01140.x | pmid = 11856078 | accessdate = 2009-11-04}}</ref> [[Prevalence]] estimates for Northern Europe have ranged from 27–48 per 100,000.<ref name=Bernstein>
{{cite journal
 | last = Bernstein
 | first = Charles N.
 | title = The epidemiology of inflammatory bowel disease in Canada: a population-based study
 | journal =The American Journal of Gastroenterology
 | year = 2006
 | month = July
 | volume = 101
 | issue = 7
 | pages = 1559–68
 | last2 = Wajda
 | first2 = A
 | last3 = Svenson
 | first3 = LW
 | last4 = Mackenzie
 | first4 = A
 | last5 = Koehoorn
 | first5 = M
 | last6 = Jackson
 | first6 = M
 | last7 = Fedorak
 | first7 = R
 | last8 = Israel
 | first8 = D
 | last9 = Blanchard
 | first9 = JF
 | pmid = 16863561
 | doi =10.1111/j.1572-0241.2006.00603.x
 | accessdate = 2009-11-04
 | author2 = Wajda
 | author3 = Svenson
 | author4 = MacKenzie
 | author5 = Koehoorn
 | author6 = Jackson
 | author7 = Fedorak
 | author8 = Israel
 | author9 = Blanchard
}}</ref> Crohn's disease tends to present initially in the teens and twenties, with another peak incidence in the fifties to seventies, although the disease can occur at any age.<ref name=Baumgart/><ref name = emed/>

There is no known [[medication|pharmaceutical]] or [[surgery|surgical]] cure for Crohn's disease.<ref>
{{cite web
 |first= Tri H
 |last= Le
 |publisher=eMedicine
 |title=Ulcerative colitis
 |url= http://emedicine.medscape.com/article/183084-overview
 | date=March 17, 2010
 | accessdate = 2010-04-15
}}</ref> [[Treatment of Crohn's disease|Treatment options]] are restricted to controlling [[symptom]]s, maintaining [[remission (medicine)|remission]], and preventing [[relapse]].

The disease was named for American [[gastroenterology|gastroenterologist]] [[Burrill Bernard Crohn]], who in 1932, along with two colleagues, described a series of patients with inflammation of the [[terminal ileum]], the area most commonly affected by the illness.<ref name=CrohnBB>{{cite journal |author=Crohn BB, Ginzburg L, Oppenheimer GD |title=Regional ileitis: a pathologic and clinical entity. 1932 |journal=Mt. Sinai J. Med. |volume=67 |issue=3 |pages=263–8 |year=2000 |pmid=10828911 |doi=}}</ref> For this reason, the disease has also been called '''regional ileitis'''<ref name="CrohnBB"/> or regional enteritis.  The condition, however, has been independently identified by others in the literature prior, most notably in 1904 by Polish surgeon [[Antoni Leśniowski]] for whom the condition is additionally named (Leśniowski-Crohn's disease) in the Polish literature.

== Classification ==
[[Image:Distribution of CD.svg|right|thumb|Distribution of gastrointestinal Crohn's disease. Based on data from [[American Gastroenterological Association]].]]
Crohn's disease is one type of [[inflammatory bowel disease]] (IBD). It affects the gastrointestinal tract and can be categorized by the area of the gastrointestinal tract that it affects. ''[[Ileocolic]] Crohn's disease'', which affects both the [[ileum]] (the last part of the [[small intestine]] that connects to the [[large intestine]]) and the large intestine, accounts for fifty percent of cases. ''Crohn's ileitis'', affecting the ileum only, accounts for thirty percent of cases, and ''Crohn's colitis'', affecting 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 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 (MedlinePlus 2010). 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, being affected in other parts of the gastrointestinal tract such as the [[stomach]] and [[esophagus]].<ref name=Baumgart/>

Crohn's disease may also be categorized by the behavior of disease as it progresses. This was formalized in the Vienna classification of Crohn's disease.<ref name=Vienna>{{cite journal | doi = 10.1002/ibd.3780060103 | author = Gasche C, Scholmerich J, Brynskov J, D'Haens G, Hanauer S, Irvine E, Jewell D, Rachmilewitz D, Sachar D, Sandborn W, Sutherland L | title = A simple classification of Crohn's disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998 | journal = Inflamm Bowel Dis | volume = 6 | issue = 1 | pages = 8–15 | year = 2000 | pmid = 10701144}}</ref> There are three categories of disease presentation in Crohn's disease:  stricturing, penetrating, and [[inflammation|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 ([[fistula]]e) between the bowel and other structures such as the skin. ''[[Inflammatory disease]]'' (or non-stricturing, non-penetrating disease) causes inflammation without causing strictures or fistulae.<ref name=Vienna/><ref name=phenotypes>{{cite journal | author = Dubinsky MC, Fleshner PP. | title = Treatment of Crohn's Disease of Inflammatory, Stenotic, and Fistulizing Phenotypes | journal = Curr Treat Options Gastroenterol | volume = 6 | issue = 3 | pages = 183–200 | year = 2003 | pmid = 12744819 | doi = 10.1007/s11938-003-0001-1}}</ref>

=== Gastrointestinal symptoms ===

[[Image:CD serpiginous ulcer.jpg|right|thumb|Endoscopy image of [[colon (anatomy)|colon]] showing [[serpiginous]] ulcer, a classic finding in Crohn's disease]]
Many people with Crohn's disease have symptoms for years prior to the diagnosis.<ref name=Pimentel>{{cite journal | last = Pimentel | first = Mark | coauthors = Michael Chang, Evelyn J. Chow, Siamak Tabibzadeh, Viorelia Kirit-Kiriak, Stephan R. Targan, Henry C. Lin | year = 2000 | title = Identification of a prodromal period in Crohn's disease but not ulcerative colitis | journal = American Journal of Gastroenterology | volume = 95 | issue = 12 | pages = 3458–62 | doi =10.1111/j.1572-0241.2000.03361.x | pmid = 11151877 }}</ref> The usual onset is between 15 and 30 years of age but can occur at any age.<ref>[http://www.emedicinehealth.com/crohn_disease/article_em.htm Crohn's Disease Overview]</ref> Because of the 'patchy' nature of the gastrointestinal disease and the depth of tissue involvement, initial symptoms can be more vague than with ulcerative colitis. People with Crohn's disease will go through periods of flare-ups and remission. <ref name=healthline>
{{cite web
 | first= David
 | last=  Zieve
 | coauthors=George F Longstreth
 | publisher=ADAM Health Illustrated Encyclopedia
 | title=Crohn's Disease
 | url= http://www.healthline.com/adamcontent/crohns-disease
 | date= October 18, 2009
 | accessdate = 2010-08-16
}}</ref>

Abdominal pain may be the initial symptom of Crohn's disease. It is often accompanied by diarrhea, especially in those who have had surgery. The diarrhea may or may not be bloody. People who have had surgery or multiple surgeries often end up with [[short bowel syndrome]] of the gastrointestinal tract. The nature of the diarrhea in Crohn's disease depends on the part of the small intestine or colon that is involved. Ileitis typically results in large-volume watery feces. 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.<ref name=Baumgart/><ref name=emed/><ref name=Podolsky/><ref>{{cite journal | last = Mueller | first = M. H. | coauthors = M. E. Kreis, M. L. Gross, H. D. Becker, T. T. Zittel & E. C. Jehle | year = 2002 | title = Anorectal functional disorders in the absence of anorectal inflammation in patients with Crohn's disease | journal = British Journal of Surgery | volume = 89 | issue = 8 | pages = 1027–31 | doi =10.1046/j.1365-2168.2002.02173.x | pmid = 12153630 }}</ref> Visible bleeding in the feces is less common in Crohn's disease than in ulcerative colitis, but may be seen in the setting of Crohn's colitis.<ref name=Baumgart/> Bloody bowel movements are typically intermittent, and may be bright or dark red in colour. In the setting of severe Crohn's colitis, bleeding may be copious.<ref name=emed/> [[Flatulence]] and bloating may also add to the intestinal discomfort.<ref name=emed/>

Symptoms caused by [[bowel obstruction|intestinal stenosis]] are also common in Crohn's disease. Abdominal pain is often most severe in areas of the bowel with stenoses. In the setting of severe stenosis, vomiting and nausea may indicate the beginnings of small bowel obstruction.<ref name=emed>
{{cite web
 | first= George Y
 | last= Wu
 | coauthors=Marcy L Coash, Senthil Nachimuthu
 | publisher=eMedicine
 | title=Crohn Disease
 | url= http://emedicine.medscape.com/article/172940-overview
 | date= March 17, 2010
 | accessdate = 2010-04-15
}}</ref> 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.<ref>{{cite book|last=Kumar|first=Vinay|coauthors=Abul K. Abbas, Nelson Fausto|title=Robbins and Cotran: Pathologic Basis of Disease|publisher=Elsevier Saunders |location=Philadelphia, Pennsylvania|date=July 30, 2004|edition=7th|pages=847|chapter=Ch 17: The Gastrointestinal Tract|isbn=0-7216-0187-1}}</ref>

Perianal discomfort may also be prominent in Crohn's disease. Itchiness or pain around the [[anus]] may be suggestive of inflammation, [[fistula|fistulization]] or [[abscess]] around the anal area<ref name=Baumgart/> or [[anal fissure]]. Perianal skin [[acrochordon|tags]] are also common in Crohn's disease.<ref>{{cite journal | author = Taylor B, Williams G, Hughes L, Rhodes J | title = The histology of anal skin tags in Crohn's disease: an aid to confirmation of the diagnosis | journal = Int J Colorectal Dis | volume = 4 | issue = 3 | pages = 197–9 | year = 1989 | pmid = 2769004 | doi = 10.1007/BF01649703}}</ref> [[Fecal incontinence]] may accompany peri-anal Crohn's disease. At the opposite end of the gastrointestinal tract, the mouth may be affected by non-healing sores ([[aphthous ulcer]]s). 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.<ref>{{cite journal | last = Fix | first = Oren K. | coauthors = Jorge A. Soto, Charles W. Andrews and Francis A. Farraye | year = 2004 | title = Gastroduodenal Crohn's disease | journal = Gastrointestinel Endoscopy | volume = 60 | issue = 6 | pages = 985 | doi = 10.1016/S0016-5107(04)02200-X | pmid = 15605018 }}</ref>

=== Systemic symptoms ===
Crohn's disease, like many other chronic, inflammatory diseases, can cause a variety of [[B symptoms|systemic symptoms]].<ref name=Baumgart/> Among children, [[growth failure]] is common. Many children are first diagnosed with Crohn's disease based on [[failure to thrive|inability to maintain growth]].<ref name=Beattie/> As Crohn's disease 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.<ref>{{cite journal | last = Büller | first = H.A. | year = 1997 | title = Problems in diagnosis of IBD in children | journal = The Netherlands Journal of Medicine | volume = 50 | issue = 2 | pages = S8–S11 | doi =10.1016/S0300-2977(96)00064-2 | pmid = 9050326 }}</ref> Fever may also be present, though fevers greater than 38.5&nbsp;[[Celsius|˚C]] (101.3&nbsp;[[Fahrenheit|˚F]]) are uncommon unless there is a complication such as an [[abscess]].<ref name=Baumgart/> Among older individuals, Crohn's disease may manifest as weight loss. This is 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.<ref name=Beattie>{{cite journal | last = Beattie | first = R.M. | coauthors = N. M. Croft, J. M. Fell, N. A. Afzal and R. B. Heuschkel | year = 2006 | title = Inflammatory bowel disease | journal = Archives of Disease in Childhood | volume = 91 | issue = 5 | pages = 426–32 | doi =10.1136/adc.2005.080481 | pmid = 16632672 | pmc = 2082730 }}</ref> People with extensive [[small intestine]] disease may also have [[malabsorption]] of [[carbohydrate]]s or [[lipid]]s, which can further exacerbate weight loss.<ref>{{cite journal | last = O'Keefe | first = S. J. | year = 1996 | title = Nutrition and gastrointestinal disease | journal = Scandinavian Journal of Gastroenterology Supplement | issue = 220 | pages = 52–9 | pmid = 8898436 | doi = 10.3109/00365529609094750 | volume = 31 }}</ref>

=== Extraintestinal symptoms ===
[[Image:Crohnie sores 4.JPG|thumb|[[Erythema nodosum]] on the back of a person with Crohn's disease.]]

In addition to systemic and gastrointestinal involvement, Crohn's disease can affect many other organ systems.<ref name=Danese>{{cite journal | last = Danese | first = Silvio | coauthors = Stefano Semeraro, Alfredo Papa, Italia Roberto, Franco Scaldaferri, Giuseppe Fedeli, Giovanni Gasbarrini, Antonio Gasbarrini | year = 2005 | title = Extraintestinal manifestations in inflammatory bowel disease | journal = World Journal of Gastroenterology | volume = 11 | issue = 46 | pages = 7227–36 | pmid = 16437620 | url = http://www.wjgnet.com/1007-9327/11/7227.asp | accessdate = 2009-11-07 }}</ref> Inflammation of the interior portion of the eye, known as [[uveitis]], can cause eye pain, especially when exposed to light ([[photophobia]]). Inflammation may also involve the white part of the eye ([[sclera]]), a condition called [[Scleritis|episcleritis]]. Both episcleritis and uveitis can lead to loss of vision if untreated.

Crohn's disease is associated with a type of [[Rheumatology|rheumatologic disease]] known as [[spondyloarthropathy|seronegative spondyloarthropathy]]. This group of diseases is characterized by inflammation of one or more [[joint]]s ([[arthritis]]) or muscle insertions ([[enthesitis]]). The arthritis can affect larger joints such as the knee or shoulder or may exclusively involve the small joints of the hand and feet. The arthritis may also involve the spine, leading to [[ankylosing spondylitis]] if the entire spine is involved or simply [[sacroiliitis]] if only the lower spine is involved. The symptoms of arthritis include painful, warm, swollen, stiff [[Arthralgia|joints]] and loss of joint mobility or function. <ref name=healthline>
{{cite web
 | publisher=Healthline Networks, Inc.
 | title=Arthritis
 | url= http://www.healthline.com/channel/arthritis.html
 | date= October 10, 2008
 | accessdate = 2010-08-16
}}</ref>

[[Image:Crohnie Pyoderma gangrenosum.jpg|thumb|left|[[Pyoderma gangrenosum]] on the leg of a person with Crohn's disease.]]
Crohn's disease may also involve the skin, blood, and [[endocrine system]]. One type of skin manifestation, [[erythema nodosum]], presents as red nodules usually appearing on the shins. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue and is characterized by septal [[panniculitis]]. Another skin lesion, [[pyoderma gangrenosum]], is typically a painful ulcerating nodule. Crohn's disease also increases the risk of blood clots; painful swelling of the lower legs can be a sign of [[deep venous thrombosis]], while difficulty breathing may be a result of [[pulmonary embolism]]. [[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, pallor, and other symptoms common in [[anemia]]. [[Nail clubbing|Clubbing]], a deformity of the ends of the fingers, may also be a result of Crohn's disease. Finally, Crohn's disease may cause [[osteoporosis]], or thinning of the bones. Individuals with osteoporosis are at increased risk of [[bone fracture]]s.<ref name=Bernstein>{{cite journal | last = Bernstein | first = Michael | coauthors = Sue Irwin and Gordon R. Greenberg | year = 2005 | title = Maintenance infliximab treatment is associated with improved bone mineral density in Crohn's disease | journal = The American Journal of Gastroenterology | volume = 100 | issue = 9 | pages = 2031–5. | doi =10.1111/j.1572-0241.2005.50219.x | pmid = 16128948 }}</ref>

Crohn's disease can also cause neurological complications (reportedly in up to 15% of patients).<ref name="pro">[http://professionals.epilepsy.com/page/inflammatory_crohn.html Crohn's disease]. professionals.epilepsy.com. Retrieved on July 13, 2007.</ref> The most common of these are [[seizures]], [[stroke]], [[myopathy]], [[peripheral neuropathy]], [[headache]] and [[Depression (mood)|depression]].<ref name="pro"/>

Crohn's patients often also have issues with [[small bowel bacterial overgrowth syndrome]], which has similar symptoms.<ref>{{MedlinePlus|000222|Small bowel bacterial overgrowth}}</ref>

=== Complications ===
[[Image:Colorectal cancer endo 2.jpg|right|thumb|[[Colonoscopy|Endoscopic]] image of '''colon cancer''' identified in the sigmoid colon on screening [[colonoscopy]] for Crohn's disease.]]
Crohn's disease can lead to several mechanical complications within the intestines, including [[Bowel obstruction|obstruction]], fistulae, and abscesses. Obstruction typically occurs from [[strictures]] or [[adhesions]] that narrow the lumen, blocking the passage of the intestinal contents. Fistulae 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 collections of [[infection]], which can occur in the [[abdomen]] or in the [[wiktionary:perianal|perianal]] area in Crohn's disease sufferers.

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]]. Similarly, people with Crohn's colitis have a [[relative risk]] of 5.6 for developing [[colon cancer]].<ref>{{cite journal |author=Ekbom A, Helmick C, Zack M, Adami H |title=Increased risk of large-bowel cancer in Crohn's disease with colonic involvement |journal=Lancet |volume=336 |issue=8711 |pages=357–9 |year=1990 |pmid=1975343 | doi = 10.1016/0140-6736(90)91889-I}}</ref> Screening for colon cancer with [[colonoscopy]] is recommended for anyone who has had Crohn's colitis for at least eight years.<ref>{{cite journal | author = Collins P, Mpofu C, Watson A, Rhodes J | title = Strategies for detecting colon cancer and/or dysplasia in patients with inflammatory bowel disease | journal = Cochrane Database Syst Rev | volume = | issue = 2| pages = CD000279 | year = 2006| pmid = 16625534 | doi = 10.1002/14651858.CD000279.pub3}}</ref> Some studies suggest that 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.<ref>{{cite journal | author = Lynne V McFarland | title = Colorectal cancer and dysplasia in inflammatory bowel disease | journal = World Journal of Gastroenterology | volume = | issue = | pages = 2665 | year = 2008| pmid = | doi = }}</ref>

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.<ref>{{cite journal | author = Evans J, Steinhart A, Cohen Z, McLeod R | title = Home total parenteral nutrition: an alternative to early surgery for complicated inflammatory bowel disease | journal = J Gastrointest Surg | volume = 7 | issue = 4 | pages = 562–6 | year = 2003 | pmid = 12763417 | doi = 10.1016/S1091-255X(02)00132-4}}</ref>

Crohn's disease can cause significant complications including [[bowel obstruction]], abscesses, free [[Bowel perforation|perforation]] and [[hemorrhage]].<ref>{{cite web|url=https://www.livingwithcrohnsdisease.com/livingwithcrohnsdisease/crohns_disease/complications_of_crohns.html |title=Complications of Crohn's Disease| publisher= [[Centocor Ortho Biotech]] |accessdate = 2009-11-07 }}</ref>

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 allows preventative measures to be taken. In some cases, remission can occur during pregnancy. Certain medications can also impact [[sperm count]] or may otherwise adversely affect a man's ability to [[Fertilisation|conceive]].<ref>{{cite web | url = http://www.ccfa.org/about/news/pregnancy | publisher = [[Crohn's and Colitis Foundation of America]] | date = 2005-10-21 | title = IBD and Pregnancy: What You Need to Know | last = Kaplan | first = C | accessdate = 2009-11-07 }}</ref>

== Cause ==
Although the exact cause of Crohn's disease is still unknown, a combination of environmental factors and genetic predisposition seems to cause the disease.<ref>
{{cite journal
| author = Braat H, Peppelenbosch MP, Hommes DW
| title = Immunology of Crohn's disease
| journal = Ann. N. Y. Acad. Sci.
| volume = 1072
| issue =
| pages = 135–54
| year = 2006
| month = August
| accessdate = 2009-11-04
| doi = 10.1196/annals.1326.039
| pmid = 17057196
}}</ref> The genetic risk factors have now more or less been comprehensively elucidated, making Crohn's disease the first genetically complex disease of which the genetic background has been resolved.<ref>{{cite journal
| author = Henckaerts L, Figueroa C, Vermeire S, Sans M
| title = The role of genetics in inflammatory bowel disease
| journal = Curr Drug Targets
| volume = 9
| issue = 5
| pages = 361–8
| year = 2008
| month = May
| accessdate = 2009-11-04
| doi = 10.2174/138945008784221161
| pmid = 18473763
}}</ref> The relative risks of contracting the disease when one has a mutation in one of the risk genes, however, are actually very low (approximately 1:200). Broadly speaking, the genetic data indicate that innate immune systems in patients with Crohn's disease malfunction, and direct assessment of patient immunity confirms this notion.<ref name=Marks2006>
{{cite journal
 |author= Marks DJ, Harbord MW, MacAllister R, Rahman FZ, Young J, Al-Lazikani B, Lees W, Novelli M, Bloom S, Segal AW
 |title= Defective acute inflammation in Crohn's disease: a clinical investigation
 |journal= Lancet
 |volume= 367
 |issue= 9511
 |pages= 668–78
 |year= 2006
 |pmid= 16503465
 |doi= 10.1016/S0140-6736(06)68265-2
 |pmc= 2092405
}}</ref> This had led to the notion that Crohn's disease should be viewed as innate immune deficiency, chronic inflammation being caused by adaptive immunity trying to compensate for the reduced function of the innate immune system.<ref>
{{cite journal
| author = Comalada M, Peppelenbosch MP
| title = Impaired innate immunity in Crohn's disease
| journal = Trends Mol Med
| volume = 12
| issue = 9
| pages = 397–9
| year = 2006
| month = September
| accessdate = 2009-11-04
| doi = 10.1016/j.molmed.2006.07.005
| pmid = 16890491
}}</ref>

=== Genetics ===
[[Image:NOD2 CARD15.svg|right|thumb|Schematic of NOD2 CARD15 gene, which is associated with certain disease patterns in Crohn's disease.]]
Some research has indicated that Crohn's disease may have a genetic link.<ref>{{cite web | url = http://www.ccfa.org/reuters/geneticlink | title = Crohn's disease has strong genetic link: study | publisher = [[Crohn's and Colitis Foundation of America]] | date = 2007-04-16 | accessdate = 2009-11-07 }}</ref> The disease runs in families and those with a sibling with the disease are 30 times more likely to develop it than the general population.

[[Mutation]]s in the [[CARD15]] gene (also known as the NOD2 [[gene]]) are associated with Crohn's disease<!-- --><ref>{{cite journal |author=Ogura Y, Bonen DK, Inohara N, ''et al.'' |title=A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease |journal=Nature |volume=411 |issue=6837 |pages=603–6 |year=2001 |pmid=11385577 |doi=10.1038/35079114 |url= |last12=Brant |first12=SR |last13=Bayless |first13=TM |last14=Kirschner |first14=BS |last15=Hanauer |first15=SB |last16=Nuñez |first16=G |last17=Cho |first17=JH}}</ref> and with susceptibility to certain phenotypes of disease location and activity.<ref><!--
-->{{cite journal | author = Cuthbert A, Fisher S, Mirza M, ''et al.'' | title = The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease | journal = Gastroenterology | volume = 122 | issue = 4 | pages = 867–74 | year = 2002 | pmid = 11910337 | doi = 10.1053/gast.2002.32415 | last12 = Lewis | first12 = CM | last13 = Mathew | first13 = CG}}</ref> In earlier studies, only two genes were linked to Crohn's, but scientists now believe there are over thirty genes that show genetics play a role in the disease, either directly through causation or indirectly as with a [[mediator variable]]. Anomalies in the [[XBP1]] gene have recently been identified as a factor, pointing towards a role for the [[unfolded protein response]] pathway of the [[endoplasmatic reticulum]] in inflammatory bowel diseases.<ref>{{cite journal |title=XBP1 Links ER Stress to Intestinal Inflammation and Confers Genetic Risk for Human Inflammatory Bowel Disease|journal=Cell|volume=134|pages=743–756|publisher=Cell Press|author=Kaser et al.|date=5 September 2008|doi=10.1016/j.cell.2008.07.021|pmid=18775308|last1=Kaser|first1=A|last2=Lee|first2=AH|last3=Franke|first3=A|last4=Glickman|first4=JN|last5=Zeissig|first5=S|last6=Tilg|first6=H|last7=Nieuwenhuis|first7=EE|last8=Higgins|first8=DE|last9=Schreiber|first9=S|issue=5|author2=Lee|author3=Franke|author4=Glickman|author5=Zeissig|author6=Tilg|author7=Nieuwenhuis|author8=Higgins|author9=Schreiber|first10=LH|pmc=2586148}}</ref><ref>{{cite journal |author=Clevers H |title=Inflammatory Bowel Disease, Stress, and the Endoplasmic Reticulum |journal=N Engl J Med |volume=360 |issue=7 |pages=726–727 |year=2009|doi= 10.1056/NEJMcibr0809591 |pmid=19213688 |last1=Clevers |first1=H}}</ref>

=== Environmental factors ===
Diet is believed to be linked to its higher prevalence in industrialized parts of the world. A positive correlation has been found between the incidence of the disease and an increased intake of animal [[protein]], milk protein and an increased ratio of [[Omega-6 fatty acid|n-6]] to [[Omega-3 fatty acid|n-3]] [[Polyunsaturated fat|polyunsaturated fatty acids]].<ref name="Shoda">
{{cite journal 
|  author= R Shoda, K Matsueda, S Yamato and N Umeda 
|  title = Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan
|  journal = American Journal of Clinical Nutrition
|  volume = 64
|  pages = 741–745
|  year = 1996
|  publisher =  The American Society for Clinical Nutrition
}}</ref> 
Negative correlation of the disease incidence was found to the increased consumption of vegetable protein, and no correlation to fish protein.<ref name="Shoda"/>
[[Tobacco smoking|Smoking]] has been shown to increase the risk of the return of active disease, or "flares".<ref name=Cosnes2004/> The introduction of [[hormonal contraception]] in the United States in the 1960s is linked with a dramatic increase in the incidence rate of Crohn's disease. Although a causal linkage has not been effectively shown, there remain fears that these drugs work on the digestive system in ways similar to smoking.<ref>
{{cite journal 
| author = Lesko S, Kaufman D, Rosenberg L, ''et al.'' 
| title = Evidence for an increased risk of Crohn's disease in oral contraceptive users 
| journal = Gastroenterology 
| volume = 89 
| issue = 5 
| pages = 1046–9 
| year = 1985 
| pmid = 4043662
}}</ref>

=== Immune system ===
Abnormalities in the [[immune]] system have often been invoked as being causes of Crohn's disease. Crohn's disease is thought to be an autoimmune disease, with inflammation stimulated by an over-active [[T helper cell#Th1/Th2 Model for helper T cells|T<sub>h</sub>1]] [[cytokine]] response.<ref>{{cite journal |author=Cobrin GM, Abreu MT |title=Defects in mucosal immunity leading to Crohn's disease |journal=Immunol. Rev. |volume=206 |issue= |pages=277–95 |year=2005 |pmid=16048555 |doi=10.1111/j.0105-2896.2005.00293.x |url=}}</ref>  However, more recent evidence has shown that [[Th17|T<sub>h</sub>17]] is of greater importance in the disease.<ref name=Elson2007>{{Cite journal
 | last = Elson | first =  C.
 | year = 2007
 | title = Monoclonal Anti–Interleukin 23 Reverses Active Colitis in a T Cell–Mediated Model in Mice
 | journal = Gastroenterology
 | volume = 132
 | pages = 2359
 | doi = 10.1053/j.gastro.2007.03.104
 | pmid = 17570211
 | last1 = Elson
 | first1 = CO
 | last2 = Cong
 | first2 = Y
 | last3 = Weaver
 | first3 = CT
 | last4 = Schoeb
 | first4 = TR
 | last5 = Mcclanahan
 | first5 = TK
 | last6 = Fick
 | first6 = RB
 | last7 = Kastelein
 | first7 = RA
 | issue = 7
 | author2 = Cong
 | author3 = Weaver
 | author4 = Schoeb
 | author5 = McClanahan
 | author6 = Fick
 | author7 = Kastelein
}}</ref> The most recent gene to be implicated in Crohn's disease is [[ATG16L1]], which may induce [[Autophagy (cellular)|autophagy]] and hinder the body's ability to attack invasive bacteria.<ref>{{cite journal |author=Prescott NJ, Fisher SA, Franke A, ''et al.'' |title=A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn's disease and is independent of CARD15 and IBD5 |journal=Gastroenterology |volume=132 |issue=5 |pages=1665–71 |year=2007 |pmid=17484864 |doi=10.1053/j.gastro.2007.03.034 |url= |last12=Lewis |first12=CM |last13=Schreiber |first13=S |last14=Mathew |first14=CG}}</ref>

Contrary to the prevailing view that Crohn's disease is a primary T cell autoimmune disorder, there is an increasing body of evidence in favor of the hypothesis that Crohn's disease results from an impaired innate immunity.<ref>{{cite journal| author= Marks DJ, Segal AW. |title=Innate immunity in inflammatory bowel disease: a disease hypothesis|journal=  J Pathol. |volume =214 |issue= 2 |pages=260–6 |year=2008 | month = January | doi= 10.1002/path.2291| pmc= 2635948 | accessdate = 2009-11-04| pmid= 18161747}}</ref> The immunodeficiency, which has been shown to be due to (at least in part) impaired cytokine secretion by macrophages, is thought to lead to a sustained microbial-induced inflammatory response, particularly in the colon where the bacterial load is especially high.<ref name=Marks2006/><ref>
{{cite journal| author= Dessein R, Chamaillard M, Danese S |title=Innate immunity in Crohn's disease: the reverse side of the medal |journal=  J Clin Gastroenterol |volume =42 |issue= Suppl 3 Pt 1 |pages=S144–7 |year=2008 |month= September |pmid= 18806708 | doi= 10.1097/MCG.0b013e3181662c90| accessdate = 2009-11-04}}</ref>

=== Microbes ===
A variety of pathogenic bacteria were initially suspected of being causative agents of Crohn's disease.<ref>{{cite web |url=http://www.crohns.org/research/index.htm |title=OVERVIEW: MAP and Crohn's Disease Research |publisher=Paratuberculosis Awareness & Research Association | accessdate = 2009-11-07 }}</ref> However, most healthcare professionals now believe that a variety of microorganisms are taking advantage of their host's weakened mucosal layer and inability to clear bacteria from the intestinal walls, both symptoms of the disease.<ref><!--
-->{{cite journal | author = Sartor, R. | title = Mechanisms of Disease: pathogenesis of Crohn's disease and ulcerative colitis | journal = Nature Clinical Practice Gastroenterology & Hepatology | year = 2006 | month = July | volume = 3 | issue = 7 | pmid = 16819502 | pages = 390–407 | url= http://www.nature.com/nrgastro/journal/v3/n7/full/ncpgasthep0528.html | doi = 10.1038/ncpgasthep0528 }} PMID 16819502</ref> Some studies have suggested that ''[[Mycobacterium avium subspecies paratuberculosis]]'' (MAP) plays a role in Crohn's disease, in part because it causes a very similar disease, [[Johne's disease]], in cattle.<ref>{{cite journal |author=Naser SA, Collins MT |title=Debate on the lack of evidence of Mycobacterium avium subsp. paratuberculosis in Crohn's disease |journal=Inflamm. Bowel Dis. |volume=11 |issue=12 |pages=1123 |year=2005 |pmid=16306778 |doi= 10.1097/01.MIB.0000191609.20713.ea|url=}}</ref>  The [[mannose]] bearing antigens (mannins) from yeast may also elicit an [[antibody]] response.<ref name="pmid1398231">{{cite journal | author = Giaffer MH, Clark A, Holdsworth CD | title = Antibodies to Saccharomyces cerevisiae in patients with Crohn's disease and their possible pathogenic importance | journal = Gut | volume = 33 | issue = 8 | pages = 1071–5 | year = 1992 | pmid = 1398231 | doi = 10.1136/gut.33.8.1071 | pmc = 1379444}}</ref> Other studies have linked specific strains of enteroadherent ''[[E. coli]]'' to the disease.<ref>{{cite journal | author = Baumgart M ''et al.'' | title = Culture independent analysis of ileal mucosa reveals a selective increase in invasive Escherichia coli of novel phylogeny relative to depletion of Clostridiales in Crohn's disease involving the ileum  | pmid = 18043660 | journal = The ISME Journal | year = 2007 | url = http://www.nature.com/ismej/journal/v1/n5/full/ismej200752a.html | doi = 10.1038/ismej.2007.52 | volume = 1 | pages = 403 | last12 = Schukken | first12 = Y | last13 = Scherl | first13 = E | last14 = Simpson | first14 = KW | issue = 5 }}</ref>  Still, this relationship between specific types of bacteria and Crohn's disease remains unclear.<ref name=scah_out38>{{cite web |url=http://ec.europa.eu/food/fs/sc/scah/out38_en.pdf |title=Possible links between Crohn’s disease and Paratuberculosis |format=PDF |work=EUROPEAN COMMISSION DIRECTORATE-GENERAL HEALTH & CONSUMER PROTECTION | accessdate = 2009-11-07}}</ref><ref>{{cite journal |author=Gui GP, Thomas PR, Tizard ML, Lake J, Sanderson JD, Hermon-Taylor J |title=Two-year-outcomes analysis of Crohn's disease treated with rifabutin and macrolide antibiotics |journal=J. Antimicrob. Chemother. |volume=39 |issue=3 |pages=393–400 |year=1997 |month=March |pmid=9096189 |doi= 10.1093/jac/39.3.393|url=http://jac.oxfordjournals.org/cgi/reprint/39/3/393 | format = PDF }}</ref>

Some studies have suggested that 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.<ref>{{cite journal |author=Cenac N, Andrews CN, Holzhausen M, ''et al.'' |title=Role for protease activity in visceral pain in irritable bowel syndrome |journal=J. Clin. Invest. |volume=117 |issue=3 |pages=636–47 |year=2007 |month=March |pmid=17304351 |doi=10.1172/JCI29255 |url= |last12=Ferraz |first12=JG |last13=Shaffer |first13=E |last14=Vergnolle |first14=N |pmc=1794118}}</ref>  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.<ref>{{cite journal |author=Cenac N, Coelho AM, Nguyen C, ''et al.'' |title=Induction of intestinal inflammation in mouse by activation of proteinase-activated receptor-2 |journal=Am. J. Pathol. |volume=161 |issue=5 |pages=1903–15 |year=2002 |month=November |pmid=12414536 |doi= |url=http://ajp.amjpathol.org/cgi/pmidlookup?view=long&pmid=12414536 |last12=Vergnolle |first12=N |pmc=1850779}}</ref>  The authors of that study were unable to identify the source of the protease, but a separate review noted that regional and temporal variations in those illnesses follow those associated with infection with a poorly understood protozoan, [[Blastocystis]].<ref>{{cite journal |author=Boorom KF, Smith H, Nimri L, ''et al.'' |title=Oh my aching gut: irritable bowel syndrome, Blastocystis, and asymptomatic infection |journal=Parasit Vectors |volume=1 |issue=1 |pages=40 |year=2008 |month=October |pmid=18937874 |doi=10.1186/1756-3305-1-40 |url= |pmc=2627840}}</ref>

A study in 2003 put forth the "cold-chain" hypothesis, that [[psychrotrophic bacteria]] such as Yersinia spp and Listeria spp 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.<ref>{{Cite journal
  | last1 = Hugot
  | first1 = Jean-Pierre
  | last2 = Alberti
  | first2 = Corinne
  | last3 = Berrebi
  | first3 = Dominique
  | last4 = Bingen
  | first4 = Edouard
  | last5 = Cezard
  | first5 = Jean-Pierre
  | title = Crohn's disease: the cold chain hypothesis
  | journal = The Lancet
  | volume = 362
  | issue = 9400
  | pages = 2012–2015
  | date = 2003-12-13
  | url = http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(03)15024-6
  | doi = 10.1016/S0140-6736(03)15024-6 }}</ref><ref>{{Cite news
  | title = Fridges blamed for Crohn's disease rise
  | newspaper = Medical News TODAY
  | date = 2003-12-12
  | url = http://www.medicalnewstoday.com/articles/4849.php}}</ref> Later studies have provided support for this hypothesis.<ref>{{Cite journal
  | last1 = Forbes
  | first1 = Alastair
  | last2 = Kalantzis
  | first2 = Tommy
  | title = Crohn's disease : the cold chain hypothesis
  | journal = International Journal of Colorectal Disease
  | volume = 21
  | issue = 5
  | pages = 399–401
  | publisher = Springer Berlin / Heidelberg
  | issn = 0179-1958
  | year = 2006
  | month = July
  | url = http://www.springerlink.com/content/p6q21tp76x013u51/
  | doi = 10.1007/s00384-005-0003-7
  | pmid = 16059694
  | accessdate = 2009-11-04
  | author2 = Kalantzis
}}</ref>

Studies done at the University of Liverpool have offered ideas that would explain the apparent connection between Crohn's disease, Mycobacterium, other pathogenic bacteria, and genetic markers.<ref>{{Cite journal
  | last1 = Subramanian | first1 = Sreedhar | last2 = Carol | first2 = L. Roberts | last3 = Hart | first3 = C. Anthony | last4 = Martin | first4 = Helen M. | first5 = Steve W. | last6 = Rhodes | first6 = Jonathan M. | last7 = Campbell | first7 = Barry J. | title = Replication of Colonic Crohn's Disease Mucosal Escherichia coli Isolates within Macrophages and Their Susceptibility to Antibiotics | journal = Antimicrobial Agents and Chemotherapy | volume = 52 | pages = 427–434 | year = 2008 | url = http://aac.asm.org/cgi/content/abstract/52/2/427 | doi = 10.1128/AAC.00375-07
  | pmid = 18070962
  | last5 = Edwards
  | issue = 2
  | author2 = Roberts
  | author3 = Hart
  | author4 = Martin
  | author5 = Edwards
  | author6 = Rhodes
  | author7 = Campbell
  | pmc = 2224732 }}</ref><ref>{{Cite journal | last1 = Mpofu | first1 = Chiedzo M. | last2 = Cambell | first2 = Barry J. | last3 = Subramanin | first3 = Sreedhar | last4 = Marshall-Clarke | first4 = Stuart | last5 = Hart | first5 = Anthony C. | last6 = Cross | first6 = Andy | last7 = Roberts | first7 = Carol L. | last8 = McGoldrick | first8 = Adrian | last9 = Edwards | first9 = Steven W. | title = Microbial Mannan Inhibits Bacterial Killing by Macrophages: A Possible Pathogenic Mechanism for Crohn’s Disease | journal = Gastroenterology, the official journal of the AGA Institute | volume = 133 | issue = 5 | pages = 1487–1498 | year = 2007 | url = http://www.gastrojournal.org/article/S0016-5085(07)01450-3/abstract | doi = 10.1053/j.gastro.2007.08.004 | pmid = 17919633 | author2 = Campbell | author3 = Subramanian | author4 = Marshall-clarke | author5 = Hart | author6 = Cross | author7 = Roberts | author8 = McGoldrick | author9 = Edwards | first10 = JM }}</ref> In many individuals genetic factors predispose individuals to Mycobacterium avium subsp. paratuberculosis infection.  This bacteria then produce mannins, which protect both itself and various bacteria from phagocytosis, which causes a variety of secondary infections.<ref>{{Cite web | url = http://www.liv.ac.uk/researchintelligence/issue33/crohns.htm |title=New insights into Crohn's Disease}}</ref> Other mycobacterial diseases, such as [[leprosy]] and [[Tuberculosis]] could be considered similar in that they have strong genetic components, but are not genetic per se.

== Pathophysiology ==
[[Image:Crohn's transmural path.jpg|thumb|80px|left|Section of [[colectomy]] showing transmural inflammation]]
During a [[colonoscopy]], [[Biopsy|biopsies]] of the colon are often taken in order to confirm the diagnosis. There are certain characteristic features of the [[pathology]] seen that point toward Crohn's disease. Crohn's disease shows a transmural pattern of [[inflammation]], meaning that the inflammation may span the entire depth of the intestinal wall.<ref name=Baumgart/> Grossly, [[Peptic ulcer|ulceration]] is an outcome seen in highly active disease. There is usually an abrupt transition between unaffected tissue and the ulcer. Under a microscope, biopsies of the affected colon may show [[mucosa]]l inflammation. This inflammation is characterized by focal infiltration of [[neutrophils]], a type of inflammatory cell, into the [[epithelium]]. This typically occurs in the area overlying [[lymphoid tissue|lymphoid]] aggregates. These neutrophils, along with [[lymphocyte|mononuclear cells]], may infiltrate into the [[Crypts of Lieberkuhn|crypts]] leading to inflammation (crypititis) or abscess (crypt abscess). [[Granuloma]]s, 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 that is characteristic of granulomas associated with infections such as [[tuberculosis]]. Biopsies may also show chronic mucosal damage as evidenced by blunting of the intestinal [[Intestinal villus|villi]], atypical branching of the crypts, and change in the tissue type ([[metaplasia]]). One example of such metaplasia, ''Paneth cell metaplasia'', involves development of Paneth cells (typically found in the small intestine) in other parts of the gastrointestinal system.<ref name=Robbins>Crawford JM. "The Gastrointestinal tract, Chapter 17". In Cotran RS, Kumar V, Robbins SL. ''Robbins Pathologic Basis of Disease: 5th Edition''. W.B. Saunders and Company, Philadelphia, 1994.</ref>

== Diagnosis ==
[[Image:CD colitis.jpg|thumb|right|[[Colonoscopy|Endoscopic]] image of Crohn's colitis showing deep ulceration]]
[[Image:CT scan gastric CD.jpg|thumb|right|[[CT scan]] showing Crohn's disease in the fundus of the [[stomach]]]]
[[Image:CD colitis 2.jpg|thumb|Crohn's disease can mimic ulcerative colitis on endoscopy. This [[Colonoscopy|endoscopic]] image is of Crohn's colitis showing diffuse loss of [[mucosa]]l architecture, [[friable|friability]] of mucosa in sigmoid colon and exudate on wall, all of which can be found with ulcerative colitis.]]

The diagnosis of Crohn's disease can sometimes be challenging,<ref name=Pimentel/> and a number of tests are often required to assist the physician in making the diagnosis.<ref name=emed/> 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 only allows access to the colon and lower portions of the small intestines; introduction of the [[capsule endoscopy]]<ref>[http://www.givenimaging.com/en-us/HealthcareProfessionals/Pages/pageHCP.aspx HCP: Pill Cam, Capsule Endoscopy, Esophageal Endoscopy<!-- Bot generated title -->]</ref> aids in endoscopic diagnosis. Multinucleated giant cells, a common finding in the lesions of Crohn's disease, are less common in the lesions of lichen nitidus.<ref>Scheinfeld NS, Teplitz E, McClain SA. Crohn’s disease & lichen nitidus. Inflammatory Bowel Dis. 2001;7:314-8. [PMID: 11720321]</ref>

=== Endoscopy ===
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 patient to patient. 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,<ref name=Baumgart/> [[cannula]]tion 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.<!-- is passed in the patient's faeces. It has been used in the search for Crohn's disease in the small bowel, which cannot be reached with colonoscopy or gastroscopy. --><ref name="Hara2006"/>
The utility of capsule endoscopy for this, however, is still uncertain.
<ref>{{cite journal | last = Triester | first = Stuart L. | coauthors = Jonathan A. Leighton, Grigoris I. Leontiadis, Suryakanth R. Gurudu, David E. Fleischer, Amy K. Hara, Russell I. Heigh, Arthur D. Shiff, and Virender K. Sharma | year = 2006 | title = A meta-analysis of the yield of capsule endoscopy compared to other diagnostic modalities in patients with non-stricturing small bowel Crohn's disease | journal = The American Journal of Gastroenterology | volume = 101 | issue = 5 | pages = 954–64 | doi =10.1111/j.1572-0241.2006.00506.x | pmid = 16696781 | accessdate = 2009-11-04}}</ref>

=== Radiologic tests ===
A [[barium follow-through|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 [[Esophagogastroduodenoscopy|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 [[fluoroscopy|fluoroscopic]] images of the bowel are taken over time, is useful for looking for inflammation and narrowing of the small bowel.<!--
 --><ref name="Hara2006">{{cite journal | last = Hara | first = Amy K. | coauthors = Jonathan A. Leighton, Russell I. Heigh, Virender K. Sharma, Alvin C. Silva, Giovanni De Petris, Joseph G. Hentz and David E. Fleischer | year = 2006 | month = January | title = Crohn disease of the small bowel: preliminary comparison among CT enterography, capsule endoscopy, small-bowel follow-through, and ileoscopy | journal = Radiology | volume = 238 | issue = 1 | pages = 128–34 | doi =10.1148/radiol.2381050296 | pmid = 16373764 | accessdate = 2009-11-04}}</ref><!--
 --><ref>{{cite journal | last = Dixon | first = P.M. | coauthors = M.E. Roulston and D.J. Nolan | year = 1993 | title = The small bowel enema: a ten year review | journal = Clinical Radiology | volume = 47 | issue = 1 | pages = 46–8 | doi =10.1016/S0009-9260(05)81213-9 | pmid = 8428417 }}</ref> Barium enemas, in which barium is inserted into the rectum and fluoroscopy 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.<!--
 --><ref>{{cite journal | last = Carucci | first = L. R. | coauthors = M. S. Levine | year = 2002 | title = Radiographic imaging of inflammatory bowel disease | journal = Gastroenterology Clinics of North America | volume = 31 | issue = 1 | pages = 93–117 | pmid = 12122746 | doi = 10.1016/S0889-8553(01)00007-3 }}</ref>

[[Computed tomography|CT]] and [[MRI]] scans are useful for evaluating the small bowel with [[enteroclysis]] protocols.<!--
 --><ref>{{cite journal | last = Rajesh | first = A. | coauthors = D.D.T. Maglinte | year = 2006 | title = Multislice CT enteroclysis: technique and clinical applications | journal = Clinical Radiology | volume = 61 | issue = 1 | pages = 31–9 | doi =10.1016/j.crad.2005.08.006 | pmid = 16356814 }}</ref><!--
-->They are also useful for looking for intra-abdominal complications of Crohn's disease such as [[abscess]]es, small bowel obstruction, or fistulae.<!--
 --><ref>{{cite journal | last = Zissin | first = Rivka | coauthors = Marjorie Hertz, Alexandra Osadchy, Ben Novis and Gabriela Gayer | year = 2005 | title = Computed Tomographic Findings of Abdominal Complications of Crohn’s Disease—Pictorial Essay | journal = Canadian Association of Radiologists Journal | volume = 56 | issue = 1 | pages = 25–35 | pmid = 15835588 | url =http://www.carj.ca/issues/2005-Feb/25/pg25.pdf | format = PDF | accessdate = 2009-11-07 |archiveurl = http://web.archive.org/web/20080406030552/http://www.carj.ca/issues/2005-Feb/25/pg25.pdf |archivedate = April 6, 2008|deadurl=yes}}</ref> [[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<!--
 --><ref>{{cite journal | last = MacKalski | first = B. A. | coauthors = C. N. Bernstein | year = 2005 | title = New diagnostic imaging tools for inflammatory bowel disease | journal = Gut | volume = 55 | issue = 5 | pages = 733–41 | doi =10.1136/gut.2005.076612 | pmid = 16609136 | pmc = 1856109 }}</ref>

=== Blood tests ===
A [[complete blood count]] may reveal [[anemia]], which may be caused either by blood loss or by [[Cyanocobalamin|vitamin B{{ssub|12}}]] deficiency. The latter may be seen with ileitis because vitamin B{{ssub|12}} is absorbed in the [[ileum]].<!--
 --><ref name=Goh>{{cite journal | last = Goh | first = Jason | coauthors = C. A. O'Morain | year = 2003 | title = Review article: nutrition and adult inflammatory bowel disease | journal = Alimentary Pharmacology & Therapeutics | volume = 17 | issue = 3 | pages = 307–20 | doi =10.1046/j.1365-2036.2003.01482.x | pmid = 12562443 }}</ref><!--
--> [[Erythrocyte sedimentation rate]], or ESR, and [[C-reactive protein]] measurements can also be useful to gauge the degree of inflammation.<!--
 --><ref>{{cite journal | last = Chamouard | first = Patrick | coauthors = Zoe Richert, Nicolas Meyer, Gabriel Rahmi, René Baumann | year = 2006 | title = Diagnostic Value of C-Reactive Protein for Predicting Activity Level of Crohn's Disease | journal = Clinical Gastroenterology and Hepatology | doi =10.1016/j.cgh.2006.02.003 | pmid = 16630759  | volume = 4 | pages = 882 | issue = 7}} Epub ahead of print</ref> It is also true in patients with ilectomy done in response to the complication. Another cause of anaemia is anaemia of chronic disease, characterized by its microcytic and hypochromic anaemia. There can be various reasons for anaemia, including medication used in treatment of inflammatory bowel disease like azathioprine, which can lead to cytopenia, and sulfasalazine, which can also result in folate malabsorption, etc. Testing for anti-''[[Saccharomyces cerevisiae]]'' antibodies (ASCA) and [[anti-neutrophil cytoplasmic antibody|anti-neutrophil cytoplasmic antibodies]] (ANCA) has been evaluated to identify inflammatory diseases of the intestine<ref>{{cite journal | last = Kaila | first = B | coauthors = K Orr and C N Bernstein | year = 2005 | title = The anti-Saccharomyces cerevisiae antibody assay in a province-wide practice: accurate in identifying cases of Crohn's disease and predicting inflammatory disease | journal = The Canadian Journal of Gastroenterology | volume = 19 | issue = 12 | pages = 717–21 | pmid = 16341311 | url =http://www.pulsus.com/journals/abstract.jsp?sCurrPg=journal&jnlKy=2&atlKy=743&isuKy=263&isArt=t | accessdate = 2006-07-02 }}</ref><!--
--> and to differentiate Crohn's disease from ulcerative colitis.<!----><ref>{{cite journal | last = Israeli | first = E. | coauthors = I. Grotto, B. Gilburd, R. D. Balicer, E. Goldin, A. Wiik and Y. Shoenfeld | year = 2005 | title = Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease | journal = Gut | volume = 54 | issue = 9 | pages = 1232–6 | doi =10.1136/gut.2004.060228 | pmid = 16099791 | pmc = 1774672 }}</ref> Furthermore, increasing amounts and levels of serological antibodies such as ASCA, anti-laminaribioside [Glc(β1,3)Glb(β); ALCA], anti-chitobioside (GlcNAc(β1,4)GlcNAc(β); ACCA], anti-mannobioside [Man(α1,3)Man(α)AMCA], anti-Laminarin [Glc(β1,3))3n(Glc(β1,6))n; anti-L] and anti-Chitin [(GlcNAc(β1,4)n; anti-C] associate with disease behavior and surgery, and may aid in the prognosis of Crohn's disease.<!----><ref>{{cite journal | last = Ferrante | first = M. | coauthors = L. Henckaerts, M. Joossens, M. Pierik, S. Joossens, N. Dotan, G.L. Norman , R.T. Altstock , K. Van Steen , P. Rutgeerts , G. Van Assche and S.Vermeire | year = 2007 | title = New serological markers in inflammatory bowel disease are associated with complicated disease behaviour | journal = Gut | volume = 56 | issue = 10 | pages = 1394–403 | doi =10.1136/gut.2006.108043 | pmid = 17456509 | last12 = Vermeire | first12 = S }}</ref><ref>{{cite journal | last = Papp | first = M. | coauthors = I. Altorjay, N. Dotan, K. Palatka, I. Foldi, J. Tumpek, S. Sipka, M. Udvardy, T. Dinya, L. Lakatos, A. Kovacs, T. Molnar, Z. Tulassay, P. Mihelle, G.L. Norman, T. Szamosi , J. Papp; Hungarian IBD Study Group and  P.L. Lakatos | year = 2008 | title = New serological markers for inflammatory bowel disease are associated with earlier age at onset, complicated disease behavior, risk for surgery, and NOD2/CARD15 genotype in a Hungarian IBD cohort | journal = Am J Gastroenterol | volume = 104 | issue = 6 | pages = 1426–34 | doi =10.1111/j.1572-0241.2007.01652.x | pmid = 18047543 | last12 = Molnar | first12 = T | last13 = Tulassay | first13 = Z | last14 = Miheller | first14 = P | last15 = Norman | first15 = GL | last16 = Szamosi | first16 = T | last17 = Papp | first17 = J | last18 = Hungarian Ibd Study | first18 = Group | last19 = Lakatos | first19 = PL }}</ref><ref>{{cite journal | last = Seow | first = C.H. | coauthors = J.M. Stempak, W. Xu, H. Lan, A.M. Griffiths, G.R. Greenberg, A.H. Steinhart, N. Dotan and M.S. Silverberg  | year = 2009 | title = Novel anti-glycan antibodies related to inflammatory bowel disease diagnosis and phenotype | journal = Am J Gastroenterol | volume = 104 | issue = 6 | pages = 1426–34 | doi =10.1038/ajg.2009.79 | pmid = 19491856 }}</ref><ref>{{cite journal | last = Dotan | first = I. | year = 2007 | title = Serologic markers in inflammatory bowel disease: tools for better diagnosis and disease stratification | journal = Expert Rev Gastroenterol Hepatol | volume = 1| issue = 2 | pages = 265–74 | doi =10.1586/17474124.1.2.265 | pmid = 19072419}}</ref>

=== Comparison with ulcerative colitis ===
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 (anatomy)|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'''.<ref name=Baumgart/><ref name=emed/><ref name=Podolsky/>

{| class="wikitable" cellpadding=1 style="text-align:left"
|+ '''Comparisons of various factors in Crohn's disease and ulcerative colitis'''
|-
! !! Crohn's disease !! Ulcerative colitis
|-
| [[Terminal ileum]] involvement || Commonly || Seldom
|-
| Colon involvement || Usually || Always
|-
| Rectum involvement || Seldom || Usually<ref name="Kornbluth-Sachar2004">{{cite journal | last = Kornbluth | first = Asher | coauthors = David B. Sachar | year = 2004 | month = July | title = Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee | journal = American Journal of Gastroenterology | volume = 99 | issue = 7 | pages = 1371–85 | doi = 10.1111/j.1572-0241.2004.40036.x | pmid = 15233681 | url = http://www.acg.gi.org/physicians/guidelines/UlcerativeColitisUpdate.pdf | format = PDF | accessdate = 2009-11-07|archiveurl = http://web.archive.org/web/20080406030552/http://www.acg.gi.org/physicians/guidelines/UlcerativeColitisUpdate.pdf |archivedate = April 6, 2008|deadurl=yes}}</ref>
|-
| Involvement around the [[anus]] || Common<ref name="HanauerCrohns">{{cite journal | last = Hanauer | first = Stephen B. | coauthors = William Sandborn | month = March | date=2001-03-01 | title = Management of Crohn's disease in adults | journal=American Journal of Gastroenterology | volume = 96 | issue = 3 | pages = 635–43 | doi = 10.1111/j.1572-0241.2001.03671.x | pmid = 11280528 | url = http://www.acg.gi.org/physicians/guidelines/CrohnsDiseaseinAdults.pdf | format = PDF | accessdate = 2009-11-07}}</ref>
 || Seldom
|-
| Bile duct involvement || No increase in rate of [[primary sclerosing cholangitis]] || Higher rate<ref>{{cite journal | last = Broomé | first = Ulrika | coauthors = Annika Bergquist | year = 2006 | month = February | title = Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer | journal = Seminars in Liver Disease | volume = 26 | issue = 1 | pages = 31–41 | doi =10.1055/s-2006-933561 | pmid = 16496231 }}</ref>
|-
| Distribution of Disease || Patchy areas of inflammation (Skip lesions) || Continuous area of inflammation<ref name="Kornbluth-Sachar2004"/>
|-
| Endoscopy || Deep geographic and serpiginous (snake-like) [[Peptic ulcer|ulcers]]
 || Continuous ulcer
|-
| Depth of inflammation || May be transmural, deep into tissues<ref name=Baumgart/><ref name="HanauerCrohns"/>
 || Shallow, mucosal
|-
| [[Fistula]]e || Common<ref name="HanauerCrohns"/>
 || Seldom
|-
| [[Stenosis]] || Common || Seldom
|-
| [[Autoimmunity|Autoimmune disease]] || Widely regarded as an autoimmune disease || No consensus
|-
| [[Cytokine]] response || Associated with [[Th17|T<sub>h</sub>17]] <ref name=Elson2007/> || Vaguely associated with T<sub>h</sub>2
|-
| [[Granuloma]]s on biopsy || May have non-[[necrosis|necrotizing]] non-peri-[[intestinal crypt]] granulomas<ref name="HanauerCrohns"/><ref name=pmid12147095>{{Cite journal  | last1 = Shepherd | first1 = NA. | title = Granulomas in the diagnosis of intestinal Crohn's disease: a myth exploded? | journal = Histopathology | volume = 41 | issue = 2 | pages = 166–8 | month = August | year = 2002 | doi =  10.1046/j.1365-2559.2002.01441.x| pmid = 12147095 }}</ref><ref name=pmid12121237 >{{Cite journal  | last1 = Mahadeva | first1 = U. | last2 = Martin | first2 = JP. | last3 = Patel | first3 = NK. | last4 = Price | first4 = AB. | title = Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis. | journal = Histopathology | volume = 41 | issue = 1 | pages = 50–5 | month = July | year = 2002 | doi =  10.1046/j.1365-2559.2002.01416.x| pmid = 12121237 }}</ref>
 || Non-peri-[[intestinal crypt]] granulomas not seen<ref name="Kornbluth-Sachar2004"/>
|-
| Surgical cure || Often returns following removal of affected part || Usually cured by removal of colon
|-
| [[Tobacco smoking|Smoking]] || Higher risk for smokers || Lower risk for smokers<ref name="Kornbluth-Sachar2004"/>
|}

== Treatment ==
{{Main|Treatment of Crohn's disease|Biological therapy for inflammatory bowel disease}}
Currently there is no cure for Crohn's disease and [[remission (medicine)|remission]] may not be possible or prolonged if achieved.<ref>{{cite web | url = http://www.ccfa.org/ccfaprof/research-grant-opps/documents/May-2007-Newsletter.pdf | format = PDF | title = Clinical Research Alliance Update | publisher = [[Crohn's and Colitis Foundation of America]] | date = 2007-05-01 | accessdate = 2008-02-14 }}</ref> In cases where remission is possible, [[relapse]] can be prevented and [[symptom]]s controlled with medication, lifestyle changes and in some cases, surgery. Adequately controlled, Crohn's disease may not significantly restrict daily living.<ref name = WebMD>{{cite web | url = http://www.webmd.com/digestive-disorders/features/crohns-disease-54-tips-to-help-you-manage |title=Crohn's Disease: 54 Tips to Help You Manage | publisher = [[WebMD]] | last1 = Fries | first1 = WS | last2 = Nazario|first2= B | date = 2007-05-16 | accessdate = 2008-02-14 }}</ref> Treatment for Crohn's disease is only when symptoms are active and involve first treating the [[acute (medical)|acute]] problem, then maintaining [[remission (medicine)|remission]].

=== Medication ===
Acute treatment uses medications to treat any infection (normally [[antibiotic]]s) and to reduce inflammation (normally [[Aminosalicylic acid|aminosalicylate]] anti-inflammatory drugs and [[corticosteroid]]s). When symptoms are in remission, treatment enters maintenance with a goal of avoiding the recurrence of symptoms. Prolonged use of corticosteroids has significant [[Adverse effect (medicine)|side-effects]]; as a result they are generally 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.<ref name="HanauerCrohns"/> 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]]''.<ref name="Shanahan">
{{cite journal
| first= Fergus
| last= Shanahan
| title = Crohn's disease
| journal = The Lancet
| pages = 67
| volume = 359
| issue = 9300
| year = 2002
| publisher = Elsevier Science
}}</ref>

Medications used to treat the symptoms of Crohn's disease include [[mesalazine|5-aminosalicylic acid]] (5-ASA) formulations, [[prednisone]], immunomodulators such as [[azathioprine]], [[mercaptopurine]], [[methotrexate]], [[infliximab]], [[adalimumab]],<ref name=Podolsky>{{Cite journal|last=Podolsky|first= Daniel K.|title=Inflammatory bowel disease|journal=New England Journal of Medicine|year=2002|volume=346|issue=6|pages=417–29
|url=http://content.nejm.org/cgi/content/extract/347/6/417|accessdate=2006-07-02|pmid=12167685|doi=10.1056/NEJMra020831}}</ref> [[certolizumab]]<ref>
{{cite press release
 | url=http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116882.htm
 | title=FDA Approves Cimzia to Treat Crohn's Disease
 | publisher=[[Food and Drug Administration (United States)|Food and Drug Administration]]
 | date=April 22, 2008
| accessdate = 2009-11-04
}}</ref> and [[natalizumab]].<ref name=Sandborn2005>{{cite journal | author = Sandborn, W.J. | coauthors = Colombel, J.F.; Enns, R.; Feagan, B.G.; Hanauer, S.B.; Lawrance, I.C.; Panaccione, R.; Sanders, M.; Schreiber, S.; Targan, S.; Others, | year = 2005 | title = Natalizumab Induction and Maintenance Therapy for Crohn's Disease | journal = New England Journal of Medicine | volume = 353 | issue = 18 | pages = 1912 | doi = 10.1056/NEJMoa043335 | pmid = 16267322 | last12 = Goldblum | first12 = R | last13 = Despain | first13 = D | last14 = Hogge | first14 = GS | last15 = Rutgeerts | first15 = P | last16 = International Efficacy Of Natalizumab As Active Crohn's Therapy (Enact-1) Trial | first16 = Group | last17 = Evaluation Of Natalizumab As Continuous Therapy (Enact-2) Trial | first17 = Group }}</ref><ref name=MacDonald2006>{{cite journal | author = MacDonald, J.K. | coauthors = McDonald, J.W.D. | year = 2006 | title = Natalizumab for induction of remission in Crohn's disease (Cochrane Review) | journal = The Cochrane Database of Systematic Reviews | pages = 1465–858 | url = http://dellboy.update-software.com/abstracts/AB006097.htm | accessdate = 2008-02-15 | doi = 10.1002/14651858.CD006097 | pmid = 16856112 | last1 = Macdonald | first1 = JK | last2 = Mcdonald | first2 = JW | volume = 3 | issue = }} {{Dead link|date=June 2010| bot=DASHBot}}</ref> [[Hydrocortisone]] should be used in severe attacks of Crohn's disease.<ref name="OHCM">{{cite book | last=Longmore | first=Murray | coauthors=Ian Wilkinson, Tom Turmezei, Chee Kay Cheung | title=Oxford Handbook of Clinicial Medicine, 7th edition | publisher=Oxford University Press | year=2007 | pages=266–7 | isbn=0-19-856837-1 }}</ref>

Low doses of the opiate receptor antagonist [[Naltrexone]] (also [[Low dose naltrexone]]) have been found to be effective in inducing remission in 67% of patients with Crohn's disease in a small study conducted at Pennsylvania State University. Dr. Jill Smith, Professor of Gastroenterology at Pennsylvania State University's College of Medicine concluded that "LDN therapy appears effective and safe in subjects with active Crohn’s disease."<ref>*{{cite journal | author =  Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS  | title = Low-dose naltrexone therapy improves active Crohn's disease.  | journal = Am J Gastroenterol  | pages = 820–8 | volume = 102 | issue = 4 | month = April | year = 2007 | pmid = 17222320  | doi = 10.1111/j.1572-0241.2007.01045.x}}</ref> Smith and her colleagues have since received a NIH grant and are proceeding with a definitive Phase II placebo-controlled [[clinical trial]].

Since late 1990s, biological medications are available (see [[Infliximab]]).

=== Lifestyle changes ===
Certain lifestyle changes can reduce symptoms, including [[Diet (nutrition)|dietary]] adjustments, proper [[Drinking water|hydration]], and [[smoking cessation]]. Smoking may increase Crohn's disease; stopping is recommended.  Eating small meals frequently instead of big meals may also help with a low appetite.  To manage symptoms have a balanced diet with proper portion control. [[Fatigue (medical)|Fatigue]] can be helped with regular exercise, a healthy diet, and enough sleep.  A [[food diary]] may help with identifying foods that trigger symptoms.  Some patients should follow a low [[dietary fiber]] diet to control symptoms especially if fibrous foods cause symptoms.<ref name = WebMD/>

=== Surgery ===
Crohn's cannot be cured by [[surgery]], though it is used when partial or a full blockage of the intestine occurs. Surgery may also be required for complications such as obstructions, fistulas and/or abscesses, or if the disease does not respond to drugs. After the first surgery, Crohn's usually shows up at the site of the resection though it can appear in other locations. After a resection, scar tissue builds up, which can cause [[stenosis|strictures]]. A stricture is 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.<ref>{{cite web | url = http://ibdcrohns.about.com/od/surgeryprocedures/a/resectioncrohns.htm | title = Resection Surgery for Crohn's Disease | publisher = [[About.com]] | accessdate = 2008-02-14 | date = 2007-01-12 | last = Tresca | first = AJ }}</ref> 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 [[Duodenum|duodenal]] involvement. In these cases, re-operation rates were 31% and 27%, respectively, indicating that strictureplasty is a safe and effective treatment for selected patients with duodenal involvement.<ref name="pmid8918424">{{cite journal | author = Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA | title = Reoperative rates for Crohn's disease following strictureplasty. Long-term analysis | journal = Dis. Colon Rectum | volume = 39 | issue = 11 | pages = 1199–203 | year = 1996 | pmid = 8918424| doi = 10.1007/BF02055108}}</ref>

[[Short bowel syndrome]] (SBS, also short gut syndrome or simply short gut) can be caused by the surgical removal of the small intestines.  It usually develops if a person has had half or more of their small intestines removed.<ref>[http://digestive.niddk.nih.gov/ddiseases/pubs/shortbowel/ Short Bowel Syndrome] as defined by the [[National Institute of Diabetes and Digestive and Kidney Diseases]]</ref> Diarrhea is the main symptom of short bowel syndrome though other symptoms may include cramping, bloating and heartburn.  Short bowel syndrome is treated with changes in diet, intravenous feeding, vitamin and mineral supplements and treatment with medications. Another complication following surgery for Crohn's disease where the terminal ileum has been removed is the development of excessive watery diarrhea. This is due to an inability to reabsorb bile acids after resection of the terminal ileum. {{Citation needed|date=March 2009}}

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.<ref>{{cite web | url = http://www.revolutionhealth.com/conditions/digestive/crohns-disease/surgery/intestinal-transplant | title = Intestinal transplant for Crohn's disease | publisher =Everyday Health | accessdate = 2009-03-22 | date = 2006-10-24 | last = Rhodes | first = M }}</ref>

=== Prospective treatments ===
Researchers at [[University College London]] have questioned the wisdom of suppressing the immune system in Crohn's, as the problem may be an under-active rather than an over-active immune system: their study found that Crohn's patients showed an abnormally low response to an introduced infection, marked by a poor flow of blood to the wound, and the response improved when the patients were given [[sildenafil|sildenafil citrate]].<ref name=Marks2006/>

Recent studies using [[helminthic therapy]] or [[hookworms]] to treat Crohn's Disease and other (non-viral) auto-immune diseases seem to yield promising results.<ref>{{cite journal |author=Croese J, O'neil J, Masson J, ''et al.'' |title=A proof of concept study establishing ''[[Necator americanus]]'' in Crohn's patients and reservoir donors |journal=Gut |volume=55 |issue=1 |pages=136–7 |year=2006 |pmid=16344586 |doi=10.1136/gut.2005.079129 |pmc=1856386}}</ref>

=== Complementary and alternative medicine ===
More than half of Crohn's disease sufferers have tried complementary or alternative therapy.<ref>{{cite journal | author = Caprilli R, Gassull M, Escher J ''et al.'' | title = European evidence based consensus on the diagnosis and management of Crohn's disease: special situations | journal = Gut | volume = 55 Suppl 1 | issue = | pages = i36–58 | year = 2006| pmid = 16481630 | last12 = Hildebrand | first12 = H | last13 = Kolacek | first13 = S | last14 = Riis | first14 = L | last15 = Lukas | first15 = M | last16 = De Franchis | first16 = R | last17 = Hamilton | first17 = M | last18 = Jantschek | first18 = G | last19 = Michetti | first19 = P | last20 = O'morain | first20 = C | last21 = Anwar | first21 = MM | last22 = Freitas | first22 = JL | last23 = Mouzas | first23 = IA | last24 = Baert | first24 = F | last25 = Mitchell | first25 = R | last26 = Hawkey | first26 = CJ | last27 = European Crohn's And Colitis | first27 = Organisation | doi = 10.1136/gut.2005.081950c | pmc = 1859996}}</ref> These include diets, [[probiotics]], fish oil and other [[Herbalism|herbal]] and nutritional supplements. The benefit of these medications is uncertain.

* [[Acupuncture]] is used to treat inflammatory bowel disease in [[China]], and is being used more frequently in [[Western world|Western society]].<ref name=Joos>{{cite journal |author=Joos S, Brinkhaus B, Maluche C, ''et al.'' |title=Acupuncture and moxibustion in the treatment of active Crohn's disease: a randomized controlled study |journal=Digestion |volume=69 |issue=3 |pages=131–9 |year=2004 |pmid=15114043 |doi=10.1159/000078151}}</ref>  However, there is no evidence that acupuncture has benefits beyond the [[placebo effect]].<ref name = Joos/>
* [[Homeopathy]] treatment may also be beneficial for treatment of Crohn's disease without any side effects. Since Homeopathy focusses more on symptoms rather than the disease, so the medicine prescribed will vary from person to person depending upon  symptoms shown. It is best to consult a homeopathy physician for treatment. The doctor would want to know your constitution, behaviour, feelings, background and symptoms before customising treatment for you.
* [[Methotrexate]] is a [[folate]] anti-metabolite drug that is also used for [[chemotherapy]].  It is useful in maintenance of remission for those no longer taking corticosteroids.<ref>{{cite journal |author=Feagan BG, Fedorak RN, Irvine EJ, ''et al.'' |title=A comparison of methotrexate with placebo for the maintenance of remission in Crohn's disease. North American Crohn's Study Group Investigators |journal=N. Engl. J. Med. |volume=342 |issue=22 |pages=1627–32 |year=2000 |pmid=10833208 |doi=10.1056/NEJM200006013422202 |last12=Mcdonald |first12=JW}}</ref>
* [[Metronidazole]] and [[ciprofloxacin]] are antibiotics used to treat Crohn's that have colonic or perianal involvement, although, in the United States, this use has not been approved by the [[Food and Drug Administration]].<ref>{{cite journal |author=Ursing B, Alm T, Bárány F, ''et al.'' |title=A comparative study of metronidazole and sulfasalazine for active Crohn's disease: the cooperative Crohn's disease study in Sweden. II. Result |journal=Gastroenterology |volume=83 |issue=3 |pages=550–62 |year=1982 |pmid=6124474 |doi= |last12=Nordle |first12=O |last13=Rosén |first13=A}}</ref>  They are also used for treatment of complications, including abscesses and other infections accompanying Crohn's disease.<ref name=emed/>
* [[Thalidomide]] has shown response in reversing [[endoscopy|endoscopic]] evidence of disease.<ref>{{cite journal |author=Cohen LB |title=Re: Disappearance of Crohn's ulcers in the terminal ileum after thalidomide therapy. Can J Gastroenterol 2004; 18(2): 101-104 |journal=Can. J. Gastroenterol. |volume=18 |issue=6 |pages=419; author reply 419 |year=2004 |pmid=15230268 |doi=}}</ref>
* [[Medical Cannabis|Cannabis]]-derived drugs may be used to treat Crohn's Disease with their anti-inflammatory properties.  Cannabis-derived drugs may also help to heal the gut lining.<ref>[http://www.medicalnewstoday.com/articles/28584.php Cannabis-based drugs could offer new hope for inflammatory bowel disease patients]</ref>
* [[Soluble Fiber]] has been used by some to treat symptoms.^ a b c Tungland BC, Meyer D, Nondigestible oligo- and polysaccharides (dietary fiber): their physiology and role in human health and food, Comp Rev Food Sci Food Safety, 3:73-92, 2002 (Table 3)[1]
* [[Probiotics]] include [[Sacchromyces boulardii]]<ref>Saccharomyces boulardii in maintenance treatment of Crohn's disease. Guslandi M, Mezzi G, Sorghi M, Testoni PA. Dig Dis Sci 2000;45:1462-1464.</ref> and E. coli Nissle 1917.<ref>
{{cite journal
| author = Malchow HA
| title = Crohn's disease and Escherichia coli. A new approach in therapy to maintain remission of colonic Crohn's disease?
| journal = Journal of Clinical Gastroenterology
| volume = 25
| issue = 4
| pages = 653–8
| year = 1997
| month = December
| pmid = 9451682
| doi =
10.1097/00004836-199712000-00021| issn =
| accessdate = 2010-04-16
}}</ref>
* [[Boswellia]] is an ayurvedic (Indian traditional medicine) herb, used as a natural drug. One study has found that the effectiveness of "Boswellia serrata extract H 15" is not inferior to [[mesalazine]], and concludes that the Boswellia extract's safety and efficacy make it superior to [[mesalazine]] in benefit-risk evaluations.<ref>
{{cite journal
| author = Gerhardt H, Seifert F, Buvari P, Vogelsang H, Repges R
| title = Therapie des aktiven Morbus Crohn mit dem Boswellia-serrata-Extrakt H 15
| trans_title = Therapy of active Crohn disease with Boswellia serrata extract H 15
| language = German
| journal = Zeitschrift Für Gastroenterologie
| volume = 39
| issue = 1
| pages = 11–7
| year = 2001
| month = January
| pmid = 11215357
| doi = 10.1055/s-2001-10708
| issn =
| accessdate = 2010-04-16
}}</ref>

== Prognosis ==
{{Expand section|date=October 2009}}
Crohn's disease is a [[Chronic (medicine)|chronic]] condition for which there is currently no cure. It is characterised by periods of improvement followed by episodes when symptoms flare up. With treatment, most people achieve a healthy height and weight, and the mortality rate for the disease is relatively low. However, Crohn's disease is associated with an increased risk of small bowel and colorectal carcinoma, including bowel cancer.<ref name=Canavan>{{cite journal | last = Canavan | first = C. | coauthors = K. R. Abrams, J. Mayberry | year = 2006 | title = Meta-analysis : colorectal and small bowel cancer risk in patients with Crohn's disease | journal = Alimentary pharmacology & therapeutics | volume = 23 | issue = 8 | pages = 1097–104 | id = ISSN 0269-2813 | url = http://cat.inist.fr/?aModele=afficheN&cpsidt=17660183 | accessdate = 2007-05-23 | doi = 10.1111/j.1365-2036.2006.02854.x | pmid = 16611269 | last1 = Canavan | first1 = C | last2 = Abrams | first2 = KR | last3 = Mayberry | first3 = J }}</ref>

== Epidemiology ==
The incidence of Crohn's disease has been ascertained from population studies in [[Norway]] and the [[United States]] and is similar at 6 to 7.1:100,000.<ref name=Hiatt>{{cite journal | last = Hiatt | first = Robert A. | coauthors = Leon Kaufman | year = 1988 | title = Epidemiology of inflammatory bowel disease in a defined northern California population | journal = Western Journal of Medicine | volume = 149 | issue = 5 | pages = 541–6 | pmid = 3250100 | url = | accessdate = 2006-07-02 | pmc = 1026530 }}</ref><ref>{{cite journal | last = Moum | first = B. | coauthors =M. H. Vatn, A. Ekbom, E. Aadland, O. Fausa, I. Lygren, N. Stray, J. Sauar, T. Schulz | year = 1996 | title = Incidence of Crohn's disease in four counties in southeastern Norway, 1990-93. A prospective population-based study. The Inflammatory Bowel South-Eastern Norway (IBSEN) Study Group of Gastroenterologists | journal = Scandinavian Journal of Gastroenterology | volume = 31 | issue = 4 | pages = 355–61 | pmid = 8726303 | doi = 10.3109/00365529609006410 }}</ref> Crohn's disease is more common in northern countries, and shows a higher preponderance in northern areas of the same country.<ref>{{cite journal | last = Shivananda | first = S. | coauthors = J. Lennard-Jones, R. Logan, N. Fear, A. Price, L. Carpenter and M. van Blankenstein | year = 1996 | title = Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD) | journal = Gut | volume = 39 | issue = 5 | pages = 690–7 | pmid = 9014768 | doi = 10.1136/gut.39.5.690 | pmc = 1383393 }}</ref> The incidence of Crohn's disease is thought to be similar in [[Europe]] but lower in [[Asia]] and [[Africa]].<ref name=Hiatt/> It also has a higher incidence in [[Ashkenazi Jews]].<ref name=Podolsky/>

Crohn's disease has a [[bimodal distribution]] in [[incidence (epidemiology)|incidence]] as a function of age: the disease tends to strike people in their teens and 20s, and people in their 50s through to their 70s, and ages in between due to not being diagnosed with Crohn's and being diagnosed instead with [[irritable bowel syndrome]] (IBS).<ref name=Baumgart/><ref name=emed/> It is rarely diagnosed in early childhood. It usually strikes females who are pediatric patients more severely than males.<ref>{{cite web |url=http://www.ccfa.org/reuters/ibdboysgirls |title=Crohn's disease manifests differently in boys and girls |format= |publisher = [[Crohn's and Colitis Foundation of America]] |accessdate=}}</ref> However, only slightly more women than men have Crohn's disease.<ref>{{cite web |url=http://www.webmd.com/hw-popup/who-is-affected-by-crohns-disease |title=Who is affected by Crohn's disease |format= |publisher = Healthwise |accessdate=}}</ref> Parents, siblings or children of people with Crohn's disease are 3 to 20 times more likely to develop the disease.<ref>{{cite journal |author=Satsangi J, Jewell DP, Bell JI |title=The genetics of inflammatory bowel disease |journal=Gut |volume=40 |issue=5 |pages=572–4 |year=1997 |pmid=9203931 |pmc=1027155 |doi= }}</ref> Twin studies show a concordance of greater than 55% for Crohn's disease.<ref>{{cite journal |author=Tysk C, Lindberg E, Järnerot G, Flodérus-Myrhed B |title=Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking |journal=Gut |volume=29 |issue=7 |pages=990–6 |year=1988 |pmid=3396969 |pmc=1433769 |doi= 10.1136/gut.29.7.990 }}</ref>

== History ==
{{Expand section|date=October 2009}}
Inflammatory bowel diseases were described by [[Giovanni Battista Morgagni]] (1682–1771) and by [[Scotland|Scottish]] physician T. Kennedy Dalziel in 1913.<ref>{{cite journal |author=Kirsner JB |title=Historical aspects of inflammatory bowel disease |journal=J. Clin. Gastroenterol. |volume=10 |issue=3 |pages=286–97 |year=1988 |pmid=2980764 |doi= 10.1097/00004836-198806000-00012|url=}}</ref>

''Ileitis terminalis'' was first described by Polish surgeon [[Antoni Leśniowski]] in 1904, however, due to the precedence of Crohn's name in the alphabet, it became later to be known in the worldwide literature as Crohn’s disease.{{Citation needed|date=August 2010}} Only in [[Poland]] it continues to be named '''Leśniowski-Crohn’s disease'''. [[Burrill Bernard Crohn]], an American gastroenterologist at [[New York City]]'s [[Mount Sinai Hospital, New York|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 as "Regional ileitis: a pathologic and clinical entity".<ref name=CrohnBB/>

== See also ==

* [[Crohn's Disease Activity Index]]

== References ==
{{Reflist|2}}

== External links ==
* {{DMOZ|/Health/Conditions_and_Diseases/Digestive_Disorders/Intestinal/Inflammatory_Bowel_Disease/Crohn%27s_Disease/}}
* [http://www.ccfa.org/ Crohn's & Colitis Foundation of America]
* [http://www.myibd.org/ The Foundation for Clinical Research in Inflammatory Bowel Disease]

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[[Category:Autoimmune diseases]]
[[Category:Noninfective enteritis and colitis]]
[[Category:Genetic disorders]]
[[Category:Inflammations]]
[[Category:Abdominal pain]]

[[ar:داء كرون]]
[[bs:Crohnova bolest]]
[[ca:Malaltia de Crohn]]
[[cs:Crohnova choroba]]
[[da:Crohns sygdom]]
[[de:Morbus Crohn]]
[[et:Crohni tõbi]]
[[es:Enfermedad de Crohn]]
[[eo:Crohn-malsano]]
[[eu:Crohn gaitza]]
[[fa:کرون (بیماری)]]
[[fr:Maladie de Crohn]]
[[fy:Sykte fan Crohn]]
[[gl:Mal de Crohn]]
[[ko:크론씨병]]
[[hr:Crohnova bolest]]
[[it:Malattia di Crohn]]
[[he:מחלת קרוהן]]
[[kn:ಕ್ರೋನ್ಸ್ ಕಾಯಿಲೆ]]
[[hu:Crohn-betegség]]
[[mk:Кронова болест]]
[[nl:Ziekte van Crohn]]
[[ja:クローン病]]
[[no:Crohns sykdom]]
[[pl:Choroba Leśniowskiego-Crohna]]
[[pt:Doença de Crohn]]
[[ru:Болезнь Крона]]
[[sq:Morbus Crohn]]
[[simple:Crohn's disease]]
[[sk:Crohnova choroba]]
[[sl:Crohnova bolezen]]
[[sr:Кронова болест]]
[[fi:Crohnin tauti]]
[[sv:Crohns sjukdom]]
[[ta:கிரோன் நோய்]]
[[te:క్రోన్'స్ వ్యాధి]]
[[tr:Crohn hastalığı]]
[[zh:克隆氏症]]
[[Category:2Fix]]