Crohn's disease

{{Short description|Type of inflammatory bowel disease}} {{Use mdy dates|date=May 2025}} {{cs1 config|name-list-style=vanc|display-authors=6}} {{Infobox medical condition (new) | name = Crohn's disease | image = Macro Iléon terminal, caecum et côlon ascendant - Maladie de Crohn 55-o.apatho-1691p-ilcaco.jpg | caption = A preserved section of the terminal ileum, the cecum, and the ascending colon, all of which display signs of severe Crohn's disease | image2 = Crohn's Disease vs Colitis ulcerosa.svg | caption2 = The three most common sites of intestinal involvement in Crohn's disease (left) compared to the areas affected by ''ulcerative colitis'' (''colitis ulcerosa'', right) | field = Gastroenterology | synonyms = Crohn disease, Crohn syndrome, granulomatous enteritis, regional enteritis, Leśniowski-Crohn disease | symptoms = Abdominal pain, diarrhea (may be bloody), fever, weight loss,<ref name="Baumgart2012" /> fatigue, mouth sores, reduced appetite<ref name="AR">{{cite web |title=Crohn's disease |url=https://www.autoimmuneregistry.org/crohns-disease |access-date=June 15, 2022 |website=Autoimmune Registry Inc. |archive-date=June 15, 2022 |archive-url=https://web.archive.org/web/20220615184526/https://www.autoimmuneregistry.org/crohns-disease |url-status=live}}</ref> | complications = Anemia (iron deficiency), skin rashes, arthritis, bowel cancer<ref name="Baumgart2012" /> | onset = 20–29 years<ref name="NIDDK2017" /> | duration = Long term<ref name="Baumgart2012" /> | causes = Uncertain | risks = Genetic predisposition, living in a developed country,<ref name="Baumgart2007">{{cite journal | vauthors = Baumgart DC, Carding SR | title = Inflammatory bowel disease: cause and immunobiology | journal = Lancet | volume = 369 | issue = 9573 | pages = 1627–1640 | date = May 2007 | pmid = 17499605 | doi = 10.1016/S0140-6736(07)60750-8 | bibcode = 2007Lanc..369.1627B }}</ref> stress,<ref>{{cite journal | vauthors = Mawdsley JE, Rampton DS | title = Psychological stress in IBD: new insights into pathogenic and therapeutic implications | journal = Gut | volume = 54 | issue = 10 | pages = 1481–1491 | date = October 2005 | pmid = 16162953 | pmc = 1774724 | doi = 10.1136/gut.2005.064261 }}</ref> tobacco smoking,<ref name="Cosnes2004" /> having undergone an appendectomy<ref>{{cite journal | vauthors = Koutroubakis IE, Vlachonikolis IG, Kapsoritakis A, Spanoudakis S, Roussomoustakaki M, Mouzas IA, Kouroumalis EA, Manousos ON | title = Appendectomy, tonsillectomy, and risk of inflammatory bowel disease: case-controlled study in Crete | journal = Diseases of the Colon and Rectum | volume = 42 | issue = 2 | pages = 225–230 | date = February 1999 | pmid = 10211500 | doi = 10.1007/BF02237133 | url = https://rd.springer.com/article/10.1007/BF02237133 | url-status = live | s2cid = 31528819 | archive-url = https://web.archive.org/web/20190613235036/https://rd.springer.com/article/10.1007/BF02237133 | archive-date = June 13, 2019 | url-access = subscription }}</ref><ref>{{cite journal | vauthors = Frisch M, Gridley G | title = Appendectomy in adulthood and the risk of inflammatory bowel diseases | journal = Scandinavian Journal of Gastroenterology | volume = 37 | issue = 10 | pages = 1175–1177 | date = October 2002 | pmid = 12408522 | doi = 10.1080/003655202760373380 }}</ref> or tonsillectomy<ref>{{cite journal | vauthors = Sun W, Han X, Wu S, Yang C | title = Tonsillectomy and the risk of inflammatory bowel disease: A systematic review and meta-analysis | journal = Journal of Gastroenterology and Hepatology | volume = 31 | issue = 6 | pages = 1085–1094 | date = June 2016 | pmid = 26678358 | doi = 10.1111/jgh.13273 | url = http://onlinelibrary.wiley.com/doi/10.1111/jgh.13273/abstract | access-date = February 9, 2024 | url-status = live | s2cid = 2625962 | archive-url = https://web.archive.org/web/20170816192410/http://onlinelibrary.wiley.com/doi/10.1111/jgh.13273/abstract | archive-date = August 16, 2017 | url-access = subscription }}</ref> | diagnosis = Biopsy, medical imaging<ref name="Baumgart2012" /> | differential = Irritable bowel syndrome, celiac disease, Behçet's disease, nonsteroidal anti-inflammatory drug enteropathy, intestinal tuberculosis<ref name="Baumgart2012" /><ref name="WGO-IBD" /> | prevention = | treatment = | medication = Corticosteroids, biological therapy, immunosuppressants such as azathioprine, methotrexate<ref name="Baumgart2012" /> | prognosis = Slightly increased risk of death<ref name="ACG_Guideline" /> | frequency = 3.2 per 1,000 (developed world)<ref name="Mol2012" /> | deaths = | alt = | named after = {{ubl|Burrill Bernard Crohn}} }} '''Crohn's disease''' is a type of inflammatory bowel disease (IBD) that may affect any segment of the gastrointestinal tract.<ref name="NIDDK2017" /> Symptoms often include abdominal pain, diarrhea, fever, abdominal distension, and weight loss.<ref name="Baumgart2012">{{cite journal | vauthors = Baumgart DC, Sandborn WJ | title = Crohn's disease | journal = Lancet | volume = 380 | issue = 9853 | pages = 1590–1605 | date = November 2012 | pmid = 22914295 | doi = 10.1016/S0140-6736(12)60026-9 | doi-access = free | title-link = doi }}</ref><ref name="NIDDK2017">{{cite web |title=Crohn's Disease |website=National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) |url=https://www.niddk.nih.gov/health-information/digestive-diseases/crohns-disease/all-content |archive-url=https://web.archive.org/web/20191208230827/https://www.niddk.nih.gov/health-information/digestive-diseases/crohns-disease/all-content |archive-date=December 8, 2019 |url-status=live |access-date=December 8, 2019}}</ref> Complications outside of the gastrointestinal tract may include anemia, skin rashes, arthritis, inflammation of the eye, and fatigue.<ref name="Baumgart2012" /> The skin rashes may be due to infections, as well as pyoderma gangrenosum or erythema nodosum.<ref name="Baumgart2012" /> Bowel obstruction may occur as a complication of chronic inflammation, and those with the disease are at much greater risk of colorectal cancer and small bowel cancer.<ref name="Baumgart2012" />

Although the precise causes of Crohn's disease (CD) are unknown, it is believed to be caused by a combination of environmental, immune, and bacterial factors in genetically susceptible individuals.<ref name="NIDDK2017" /><ref>{{cite journal | vauthors = Cho JH, Brant SR | title = Recent insights into the genetics of inflammatory bowel disease | journal = Gastroenterology | volume = 140 | issue = 6 | pages = 1704–1712 | date = May 2011 | pmid = 21530736 | pmc = 4947143 | doi = 10.1053/j.gastro.2011.02.046 }}</ref><ref name="Bact08" /><ref>{{cite journal | vauthors = Stefanelli T, Malesci A, Repici A, Vetrano S, Danese S | title = New insights into inflammatory bowel disease pathophysiology: paving the way for novel therapeutic targets | journal = Current Drug Targets | volume = 9 | issue = 5 | pages = 413–418 | date = May 2008 | pmid = 18473770 | doi = 10.2174/138945008784221170 }}</ref> It results in a chronic inflammatory disorder, in which the body's immune system defends the gastrointestinal tract, possibly targeting microbial antigens.<ref name="Bact08">{{cite journal | vauthors = Dessein R, Chamaillard M, Danese S | title = Innate immunity in Crohn's disease: the reverse side of the medal | journal = Journal of Clinical Gastroenterology | volume = 42 | issue = Suppl 3 Pt 1 | pages = S144–S147 | date = September 2008 | pmid = 18806708 | doi = 10.1097/MCG.0b013e3181662c90 }}</ref><ref name="pmid19437144">{{cite journal | vauthors = Marks DJ, Rahman FZ, Sewell GW, Segal AW | title = Crohn's disease: an immune deficiency state | journal = Clinical Reviews in Allergy & Immunology | volume = 38 | issue = 1 | pages = 20–31 | date = February 2010 | pmid = 19437144 | pmc = 4568313 | doi = 10.1007/s12016-009-8133-2 }}</ref> Although Crohn's is an immune-related disease, it does not seem to be an autoimmune disease (the immune system is not triggered by the body itself).<ref>{{cite journal | vauthors = Casanova JL, Abel L | title = Revisiting Crohn's disease as a primary immunodeficiency of macrophages | journal = The Journal of Experimental Medicine | volume = 206 | issue = 9 | pages = 1839–1843 | date = August 2009 | pmid = 19687225 | pmc = 2737171 | doi = 10.1084/jem.20091683 }}</ref> The exact underlying immune problem is not clear, though it may be immunodeficiency.<ref name="pmid19437144" /><ref>{{cite journal | vauthors = Lalande JD, Behr MA | title = Mycobacteria in Crohn's disease: how innate immune deficiency may result in chronic inflammation | journal = Expert Review of Clinical Immunology | volume = 6 | issue = 4 | pages = 633–641 | date = July 2010 | pmid = 20594136 | doi = 10.1586/eci.10.29 | s2cid = 25402952 }}</ref><ref>{{cite journal | vauthors = Yamamoto-Furusho JK, Korzenik JR | title = Crohn's disease: innate immunodeficiency? | journal = World Journal of Gastroenterology | volume = 12 | issue = 42 | pages = 6751–6755 | date = November 2006 | pmid = 17106921 | pmc = 4087427 | doi = 10.3748/wjg.v12.i42.6751 | doi-access = free | title-link = doi }}</ref>

About half of the overall risk is related to genetics, with more than 70 genes involved.<ref name="Baumgart2012" /><ref name="genetic_link">{{cite journal | vauthors = Barrett JC, Hansoul S, Nicolae DL, Cho JH, Duerr RH, Rioux JD, Brant SR, Silverberg MS, Taylor KD, Barmada MM, Bitton A, Dassopoulos T, Datta LW, Green T, Griffiths AM, Kistner EO, Murtha MT, Regueiro MD, Rotter JI, Schumm LP, Steinhart AH, Targan SR, Xavier RJ, Libioulle C, Sandor C, Lathrop M, Belaiche J, Dewit O, Gut I, Heath S, Laukens D, Mni M, Rutgeerts P, Van Gossum A, Zelenika D, Franchimont D, Hugot JP, de Vos M, Vermeire S, Louis E, Cardon LR, Anderson CA, Drummond H, Nimmo E, Ahmad T, Prescott NJ, Onnie CM, Fisher SA, Marchini J, Ghori J, Bumpstead S, Gwilliam R, Tremelling M, Deloukas P, Mansfield J, Jewell D, Satsangi J, Mathew CG, Parkes M, Georges M, Daly MJ | 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 | date = August 2008 | pmid = 18587394 | pmc = 2574810 | doi = 10.1038/ng.175 }}</ref> Tobacco smokers are three times as likely to develop Crohn's disease as non-smokers.<ref name="Cosnes2004">{{cite journal | vauthors = Cosnes J | title = Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice | journal = Best Practice & Research. Clinical Gastroenterology | volume = 18 | issue = 3 | pages = 481–496 | date = June 2004 | pmid = 15157822 | doi = 10.1016/j.bpg.2003.12.003 }}</ref> Crohn's disease is often triggered after a gastroenteritis episode.<ref name="Baumgart2012" /> Other conditions with similar symptoms include irritable bowel syndrome and Behçet's disease.<ref name="Baumgart2012" />

There is no known cure for Crohn's disease.<ref name="Baumgart2012" /><ref name="NIDDK2017" /> Treatment options are intended to help with symptoms, maintain remission, and prevent relapse.<ref name="Baumgart2012" /> In those newly diagnosed, a corticosteroid may be used for a brief period of time to improve symptoms rapidly, alongside another medication such as either methotrexate or a thiopurine to prevent recurrence.<ref name="Baumgart2012" /> Cessation of smoking is recommended for people with Crohn's disease.<ref name="Baumgart2012" /> One in five people with the disease is admitted to the hospital each year, and half of those with the disease will require surgery at some time during the next ten years.<ref name="Baumgart2012" /> Surgery is kept to a minimum whenever possible, but it is sometimes essential for treating abscesses, certain bowel obstructions, and cancers.<ref name="Baumgart2012" /> Checking for bowel cancer via colonoscopy is recommended every 1–3 years, starting eight years after the disease has begun.<ref name="Baumgart2012" />

Crohn's disease affects about 3.2 per 1,000 people in Europe and North America;<ref name="Mol2012">{{cite journal | vauthors = Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, Benchimol EI, Panaccione R, Ghosh S, Barkema HW, Kaplan GG | title = Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review | journal = Gastroenterology | volume = 142 | issue = 1 | pages = 46–54.e42; quiz e30 | date = January 2012 | pmid = 22001864 | doi = 10.1053/j.gastro.2011.10.001 | url = http://www.gastrojournal.org/article/S0016508511013783/pdf | access-date = October 7, 2022 | url-status = live | s2cid = 206223870 | archive-url = https://web.archive.org/web/20221007193457/https://www.gastrojournal.org/article/S0016-5085(11)01378-3/pdf | archive-date = October 7, 2022 | url-access = subscription }}</ref> it is less common in Asia and Africa.<ref>{{cite journal | vauthors = Prideaux L, Kamm MA, De Cruz PP, Chan FK, Ng SC | title = Inflammatory bowel disease in Asia: a systematic review | journal = Journal of Gastroenterology and Hepatology | volume = 27 | issue = 8 | pages = 1266–1280 | date = August 2012 | pmid = 22497584 | doi = 10.1111/j.1440-1746.2012.07150.x | s2cid = 205468282 | doi-access = free | title-link = doi }}</ref><ref name="Hov2012" /> It has historically been more common in the developed world.<ref name="Bur2013" /> Rates have, however, been increasing, particularly in the developing world, since the 1970s.<ref name="Hov2012">{{cite journal | vauthors = Hovde Ø, Moum BA | title = Epidemiology and clinical course of Crohn's disease: results from observational studies | journal = World Journal of Gastroenterology | volume = 18 | issue = 15 | pages = 1723–1731 | date = April 2012 | pmid = 22553396 | pmc = 3332285 | doi = 10.3748/wjg.v18.i15.1723 | doi-access = free | title-link = doi }}</ref><ref name="Bur2013">{{cite journal | vauthors = Burisch J, Munkholm P | title = Inflammatory bowel disease epidemiology | journal = Current Opinion in Gastroenterology | volume = 29 | issue = 4 | pages = 357–362 | date = July 2013 | pmid = 23695429 | doi = 10.1097/MOG.0b013e32836229fb | s2cid = 9538639 }}</ref> Inflammatory bowel disease resulted in 47,400 deaths in 2015,<ref>{{cite journal | vauthors = Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, etal | collaboration = GBD 2015 Mortality and Causes of Death Collaborators | title = Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1459–1544 | date = October 2016 | pmid = 27733281 | pmc = 5388903 | doi = 10.1016/S0140-6736(16)31012-1 }}</ref> and those with Crohn's disease have a slightly reduced life expectancy.<ref name="Baumgart2012" /> Onset of Crohn's disease tends to start in adolescence and young adulthood, though it can occur at any age.<ref>{{Cite journal | vauthors = Shih IL, Lee TC, Tu CH, Chang CC, Wang YF, Tseng YH, Chiu HM, Wu MS, Wang HP, Shih TT, Liu KL |date= December 2016 |title=Intraobserver and interobserver agreement for identifying extraluminal manifestations of Crohn's disease with magnetic resonance enterography |journal=Advances in Digestive Medicine |volume=3 |issue=4 |pages=174–180 |doi=10.1016/j.aidm.2015.05.004 |s2cid=70796090 |doi-access=free | title-link = doi }}</ref><ref name="Baumgart2012" /><ref name="NIDDK2017" /><ref name="eMedicineHealth" /> Males and females are affected roughly equally.<ref name="NIDDK2017" /> {{TOC limit}}

== Name controversy == The disease was named after gastroenterologist Burrill Bernard Crohn, who in 1932, together with Leon Ginzburg (1898–1988) and Gordon D. Oppenheimer (1900–1974) at Mount Sinai Hospital in New York, described a series of people with inflammation of the terminal ileum of the small intestine, the area most commonly affected by the illness.<ref name="CrohnBB">{{cite journal | vauthors = Crohn BB, Ginzburg L, Oppenheimer GD | title = Regional ileitis: a pathologic and clinical entity. 1932 | journal = The Mount Sinai Journal of Medicine, New York | volume = 67 | issue = 3 | pages = 263–268 | date = May 2000 | pmid = 10828911 }}</ref> The decision to name the disease after Crohn remains controversial.<ref>{{cite journal | vauthors = Van Hootegem P, Travis S | title = Is Crohn's Disease a Rightly Used Eponym? | journal = Journal of Crohn's & Colitis | volume = 14 | issue = 6 | pages = 867–871 | date = July 2020 | pmid = 31701137 | doi = 10.1093/ecco-jcc/jjz183 | url = https://academic.oup.com/ecco-jcc/article/14/6/867/5614546 | access-date = July 8, 2023 | url-status = live | doi-access = free | title-link = doi | archive-url = https://web.archive.org/web/20230708104800/https://academic.oup.com/ecco-jcc/article/14/6/867/5614546 | archive-date = July 8, 2023 }}</ref><ref>{{cite journal | vauthors = Mulder DJ, Noble AJ, Justinich CJ, Duffin JM | title = A tale of two diseases: the history of inflammatory bowel disease | journal = Journal of Crohn's & Colitis | volume = 8 | issue = 5 | pages = 341–348 | date = May 2014 | pmid = 24094598 | doi = 10.1016/j.crohns.2013.09.009 | s2cid = 13714394 | doi-access = free | title-link = doi }}</ref> While Crohn, in his memoir, describes his original investigation of the disease, Ginzburg provided strong evidence of how he and Oppenheimer were the first to study the disease.<ref>{{cite journal | vauthors = Ginzburg L | title = Regional enteritis: historical perspective (B. Crohn and L. Ginzburg) | journal = Gastroenterology | volume = 90 | issue = 5 Pt 1 | pages = 1310–1311 | date = May 1986 | pmid = 3514360 | doi = 10.1016/0016-5085(86)90419-1 | doi-access = free | title-link = doi }}</ref>

== Signs and symptoms == {{Symptoms in CD vs. UC}}

=== Gastrointestinal === Many people with Crohn's disease have symptoms for years before the diagnosis.<ref name="Pimentel">{{cite journal | vauthors = Pimentel M, Chang M, Chow EJ, Tabibzadeh S, Kirit-Kiriak V, Targan SR, Lin HC | title = Identification of a prodromal period in Crohn's disease but not ulcerative colitis | journal = The American Journal of Gastroenterology | volume = 95 | issue = 12 | pages = 3458–3462 | date = December 2000 | pmid = 11151877 | doi = 10.1111/j.1572-0241.2000.03361.x | s2cid = 2764694 }}</ref> The usual onset is in the teens and twenties, but can occur at any age.<ref name="eMedicineHealth">{{cite web |url=http://www.emedicinehealth.com/crohn_disease/article_em.htm |title=Crohn's Disease: Get Facts on Symptoms and Diet |website=eMedicineHealth|url-status=live|archive-url=https://web.archive.org/web/20071020184248/http://www.emedicinehealth.com/crohn_disease/article_em.htm|archive-date=October 20, 2007}}</ref><ref name="Baumgart2012" /> People with Crohn's disease experience chronic recurring periods of flare-ups and remission.<ref>{{cite book |author=National Research Council |title=Diagnosis and Control of Johne's Disease |year=2003 |chapter=Johne's Disease and Crohn's Disease |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK207651/ |publisher=National Academies Press |location=Washington, DC |doi=10.17226/10625 |pmid=25032299 |bibcode=2003nap..book10625N |isbn=978-0-309-08611-0 |id=NBK207651 |access-date=August 30, 2017 |archive-date=September 6, 2017 |archive-url=https://web.archive.org/web/20170906121542/https://www.ncbi.nlm.nih.gov/books/NBK207651/ |url-status=live }}</ref>

=== 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.<ref name="Baumgart2012" /> Perianal skin tags are also common in Crohn's disease, and may appear with or without the presence of colorectal polyps.<ref>{{cite journal | vauthors = Taylor BA, Williams GT, Hughes LE, Rhodes J | title = The histology of anal skin tags in Crohn's disease: an aid to confirmation of the diagnosis | journal = International Journal of Colorectal Disease | volume = 4 | issue = 3 | pages = 197–199 | date = August 1989 | pmid = 2769004 | doi = 10.1007/BF01649703 | s2cid = 7831833 }}</ref>

=== Intestines === The intestines, especially the colon and terminal ileum, are the areas of the body affected most commonly. Abdominal pain is a common initial symptom of Crohn's disease,<ref name="NIDDK2017" /> especially in the lower right abdomen.<ref name="ustekinumab">{{cite web |title=What I need to know about Crohn's Disease |url=http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/crohns-disease/Pages/ez.aspx#symptoms |website=www.niddk.nih.gov|access-date=December 11, 2015 |archive-url = https://web.archive.org/web/20151121213407/http://www.niddk.nih.gov/health-information/health-topics/digestive-diseases/crohns-disease/Pages/ez.aspx#symptoms|archive-date=November 21, 2015}}</ref> Flatulence, bloating, and abdominal distension are additional symptoms and may also add to the intestinal discomfort. Pain is often accompanied by non-bloody diarrhea; however, in some cases, the diarrhea can 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 greater 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="Baumgart2012" /><ref name="emed">{{EMedicine|article|172940|Crohn Disease}}</ref><ref name="Podolsky" /><ref>{{cite journal | vauthors = Mueller MH, Kreis ME, Gross ML, Becker HD, Zittel TT, Jehle EC | title = Anorectal functional disorders in the absence of anorectal inflammation in patients with Crohn's disease | journal = The British Journal of Surgery | volume = 89 | issue = 8 | pages = 1027–1031 | date = August 2002 | pmid = 12153630 | doi = 10.1046/j.1365-2168.2002.02173.x | s2cid = 42383375 | doi-access = free | title-link = doi }}</ref> Visible bleeding in the feces is less common in Crohn's disease than in ulcerative colitis, but is not unusual.<ref name="Baumgart2012" /> 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 bleed. In severe Crohn's colitis, bleeding may be copious.<ref name="emed" />

=== Stomach and esophagus=== The stomach is rarely the sole or predominant site of Crohn's disease. To date, there are only a few documented case reports of adults with isolated gastric Crohn's disease and no reports in the pediatric population. Isolated stomach involvement is a very unusual presentation accounting for less than 0.07% of all gastrointestinal Crohn's disease.<ref>{{cite journal | vauthors = Ingle SB, Hinge CR, Dakhure S, Bhosale SS | title = Isolated gastric Crohn's disease | journal = World Journal of Clinical Cases | volume = 1 | issue = 2 | pages = 71–73 | date = May 2013 | pmid = 24303469 | pmc = 3845940 | doi = 10.12998/wjcc.v1.i2.71 | doi-access = free | title-link = doi }}</ref> However, the esophagus and stomach are increasingly understood to be affected in people with intestinal Crohn's disease. Recent studies suggest upper GI involvement occurs in 13-16% of cases, typically presenting after distal symptoms.<ref>{{cite journal | vauthors = Greuter T, Piller A, Fournier N, Safroneeva E, Straumann A, Biedermann L, Godat S, Nydegger A, Scharl M, Rogler G, Vavricka SR, Schoepfer AM | title = Upper Gastrointestinal Tract Involvement in Crohn's Disease: Frequency, Risk Factors, and Disease Course | journal = Journal of Crohn's & Colitis | volume = 12 | issue = 12 | pages = 1399–1409 | date = November 2018 | pmid = 30165603 | doi = 10.1093/ecco-jcc/jjy121 | hdl = 2078.1/269513 | hdl-access = free }}</ref><ref>{{cite journal | vauthors = Laube R, Liu K, Schifter M, Yang JL, Suen MK, Leong RW | title = Oral and upper gastrointestinal Crohn's disease | journal = Journal of Gastroenterology and Hepatology | volume = 33 | issue = 2 | pages = 355–364 | date = February 2018 | pmid = 28708248 | doi = 10.1111/jgh.13866 }}</ref><ref>{{cite journal | vauthors = Pimentel AM, Rocha R, Santana GO | title = Crohn's disease of esophagus, stomach and duodenum | journal = World Journal of Gastrointestinal Pharmacology and Therapeutics | volume = 10 | issue = 2 | pages = 35–49 | date = March 2019 | pmid = 30891327 | pmc = 6422852 | doi = 10.4292/wjgpt.v10.i2.35 | doi-access = free | title-link = doi }}</ref> Upper gastrointestinal symptoms may include difficulty swallowing (dysphagia), painful swallowing (odynophagia), upper abdominal pain, and vomiting.<ref>{{cite journal | vauthors = Fix OK, Soto JA, Andrews CW, Farraye FA | title = Gastroduodenal Crohn's disease | journal = Gastrointestinal Endoscopy | volume = 60 | issue = 6 | page = 985 | date = December 2004 | pmid = 15605018 | doi = 10.1016/S0016-5107(04)02200-X }}</ref><ref>{{cite journal | vauthors = Pimentel AM, Rocha R, Santana GO | title = Crohn's disease of esophagus, stomach and duodenum | journal = World Journal of Gastrointestinal Pharmacology and Therapeutics | volume = 10 | issue = 2 | pages = 35–49 | date = March 2019 | pmid = 30891327 | pmc = 6422852 | doi = 10.4292/wjgpt.v10.i2.35 | doi-access = free | title-link = doi }}</ref>

===Oropharynx (mouth)=== [[File:Aphtha2.jpg|thumb|An aphthous ulcer on the mucous membrane of the mouth in Crohn's disease]] The mouth may be affected by recurrent canker 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 Crohn's disease, such as anti-inflammatory and sulfa-containing drugs, may cause lichenoid drug reactions in the mouth. Fungal infections, such as candidiasis, are 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 due to nutritional malabsorption.<ref name="pmid33477990">{{cite journal | vauthors = Antonelli E, Bassotti G, Tramontana M, Hansel K, Stingeni L, Ardizzone S, Genovese G, Marzano AV, Maconi G | title = Dermatological Manifestations in Inflammatory Bowel Diseases | journal = Journal of Clinical Medicine | volume = 10 | issue = 2 | page = 364 | date = January 2021 | pmid = 33477990 | pmc = 7835974 | doi = 10.3390/jcm10020364 | doi-access = free | title-link = doi }}</ref>

People with Crohn's disease are also susceptible to angular stomatitis, an inflammation of the corners of the mouth, and pyostomatitis vegetans.<ref name="Cutaneous">{{cite journal | vauthors = Aberumand B, Howard J, Howard J | title = Metastatic Crohn's Disease: An Approach to an Uncommon but Important Cutaneous Disorder | journal = BioMed Research International | volume = 2017 | article-number = 8192150 | date = January 3, 2017 | pmid = 28127561 | pmc = 5239966 | doi = 10.1155/2017/8192150 | doi-access = free | title-link = doi }}</ref>

=== Systemic === Like many other chronic, inflammatory diseases, Crohn's disease can cause a variety of systemic symptoms.<ref name="Baumgart2012" /> Among children, growth failure is common. Many children are first diagnosed with Crohn's disease based on inability to maintain growth.<ref name="Beattie" /> As it may manifest at the time of the growth spurt in puberty, as many as 30% of children with Crohn's disease may have retardation of growth.<ref>{{cite journal | vauthors = Büller HA | title = Problems in diagnosis of IBD in children | journal = The Netherlands Journal of Medicine | volume = 50 | issue = 2 | pages = S8-11 | date = February 1997 | pmid = 9050326 | doi = 10.1016/S0300-2977(96)00064-2 | url = http://dare.uva.nl/personal/pure/en/publications/problems-in-diagnosis-of-ibd-in-children(59612226-ecf5-49df-8848-d79d03f0c5c8).html | access-date = September 4, 2018 | url-status = live | type = Submitted manuscript | archive-url = https://web.archive.org/web/20210828051037/https://dare.uva.nl/search?identifier=59612226-ecf5-49df-8848-d79d03f0c5c8 | archive-date = August 28, 2021 }}</ref> 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.<ref name="Baumgart2012" /> 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.<ref name="Beattie">{{cite journal | vauthors = Beattie RM, Croft NM, Fell JM, Afzal NA, Heuschkel RB | title = Inflammatory bowel disease | journal = Archives of Disease in Childhood | volume = 91 | issue = 5 | pages = 426–432 | date = May 2006 | pmid = 16632672 | pmc = 2082730 | doi = 10.1136/adc.2005.080481 }}</ref> People with extensive small intestine disease may also have malabsorption of carbohydrates or lipids, which can further exacerbate weight loss.<ref name="pmid8898436">{{cite journal | vauthors = O'Keefe SJ | title = Nutrition and gastrointestinal disease | journal = Scandinavian Journal of Gastroenterology. Supplement | volume = 220 | pages = 52–59 | year = 1996 | pmid = 8898436 | doi = 10.3109/00365529609094750 }}</ref>

=== Extraintestinal === Crohn's disease can affect many organ systems beyond the gastrointestinal tract.<ref name="Harbord">{{cite journal | vauthors = Harbord M, Annese V, Vavricka SR, Allez M, Barreiro-de Acosta M, Boberg KM, Burisch J, De Vos M, De Vries AM, Dick AD, Juillerat P, Karlsen TH, Koutroubakis I, Lakatos PL, Orchard T, Papay P, Raine T, Reinshagen M, Thaci D, Tilg H, Carbonnel F | title = The First European Evidence-based Consensus on Extra-intestinal Manifestations in Inflammatory Bowel Disease | journal = Journal of Crohn's & Colitis | volume = 10 | issue = 3 | pages = 239–254 | date = March 2016 | pmid = 26614685 | pmc = 4957476 | doi = 10.1093/ecco-jcc/jjv213 }}</ref> {{Complications of CD vs. UC}}

====Visual====

Inflammation of the interior portion of the eye, known as uveitis, can cause blurred vision and eye pain, especially when exposed to light (photophobia).<ref name="Trikudanathan2012" /> Uveitis can lead to loss of vision if untreated.<ref name="Harbord" />

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.<ref name="Trikudanathan2012" />

Other very rare ophthalmological manifestations include: conjunctivitis, glaucoma, and retinal vascular disease.<ref name="Manifestations">{{cite journal | vauthors = Jose FA, Heyman MB | title = Extraintestinal manifestations of inflammatory bowel disease | journal = Journal of Pediatric Gastroenterology and Nutrition | volume = 46 | issue = 2 | pages = 124–133 | date = February 2008 | pmid = 18223370 | pmc = 3245880 | doi = 10.1097/MPG.0b013e318093f4b0 }}</ref>

The pathophysiology of ocular inflammation in people with Crohn's disease is complex and remains uncertain. The association between inflammatory conditions of the eye and Crohn's disease is due to many people with Crohn's disease having genetic markers such as HLA-B07, HLA-B27 and HLA-DRB1*0103.<ref>{{cite journal | vauthors = Orchard TR, Chua CN, Ahmad T, Cheng H, Welsh KI, Jewell DP | title = Uveitis and erythema nodosum in inflammatory bowel disease: clinical features and the role of HLA genes | journal = Gastroenterology | volume = 123 | issue = 3 | pages = 714–718 | date = September 2002 | pmid = 12198697 | doi = 10.1053/gast.2002.35396 }}</ref> Additionally, cytokines IL-6, IL-10, and IL-17 which are produced in the bowel enter the circulatory system and travel to the eyes to trigger inflammation.<ref>{{cite journal | vauthors = Migliorisi G, Vella G, Dal Buono A, Gabbiadini R, Busacca A, Loy L, Bezzio C, Vinciguerra P, Armuzzi A | title = Ophthalmological Manifestations in Inflammatory Bowel Diseases: Keep an Eye on It | journal = Cells | volume = 13 | issue = 2 | page = 142 | date = January 2024 | pmid = 38247834 | pmc = 10814681 | doi = 10.3390/cells13020142 | doi-access = free | title-link = doi }}</ref>

====Gallbladder and liver====

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, resulting in bile excretion in the stool. As a result, the cholesterol/bile ratio increases in the gallbladder, resulting in an increased risk for gallstones.<ref name="Trikudanathan2012" /> 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 |title=Robbins and Cotran: Pathologic Basis of Disease |vauthors=Kumar V, Abbas AK, Fausto N |date=July 30, 2004 |publisher=Elsevier Saunders |isbn=978-0-7216-0187-8 |edition=7th |location=Philadelphia, Pennsylvania |page=847 |chapter=The Gastrointestinal Tract}}</ref> Specifically, 0.96% of people with Crohn's disease also have primary sclerosing cholangitis.<ref>{{cite journal | vauthors = Barberio B, Massimi D, Cazzagon N, Zingone F, Ford AC, Savarino EV | title = Prevalence of Primary Sclerosing Cholangitis in Patients With Inflammatory Bowel Disease: A Systematic Review and Meta-analysis | journal = Gastroenterology | volume = 161 | issue = 6 | pages = 1865–1877 | date = December 2021 | pmid = 34425093 | doi = 10.1053/j.gastro.2021.08.032 | hdl = 11577/3401611 | hdl-access = free }}</ref>

Liver involvement of Crohn's disease can include cirrhosis and steatosis. Metabolic dysfunction–associated steatotic liver disease (MASLD) is relatively common and can slowly progress to end-stage liver disease. NAFLD sensitizes the liver to injury and increases the risk of developing acute or chronic liver failure following another liver injury.<ref name="Manifestations" />

Other rare hepatobiliary manifestations of Crohn's disease include: cholangiocarcinoma, granulomatous hepatitis, cholelithiasis, autoimmune hepatitis, hepatic abscess, and pericholangitis.<ref name="Manifestations" />

====Renal and urological====

Nephrolithiasis, obstructive uropathy, and fistulization of the urinary tract directly result from the underlying disease process. Nephrolithiasis is due to calcium oxalate or uric acid stones. Calcium oxalate stones due to hyperoxaluria are typically associated with either distal ileal Crohn's disease or ileal resection. Oxalate absorption increases in the presence of unabsorbed fatty acids in the colon. The fatty acids compete with oxalate to bind calcium, displacing the oxalate, which can then be absorbed as unbound sodium oxalate across colonocytes and excreted into the urine. Because sodium oxalate is only absorbed in the colon, calcium oxalate stones form only in people with an intact colon. People with an ileostomy are prone to the formation of uric acid stones because of frequent dehydration. The sudden onset of severe abdominal, back, or flank pain in patients with IBD, particularly if different from the usual discomfort, should lead to inclusion of a renal stone in the differential diagnosis.<ref name="Manifestations" />

Urological manifestations in people with IBD may include ureteral calculi, enterovesical fistula, perivesical infection, perinephric abscess, and obstructive uropathy with hydronephrosis. Ureteral compression is associated with retroperitoneal extension of the phlegmonous inflammatory process involving the terminal ileum and cecum, and may result in hydronephrosis severe enough to cause hypertension.<ref name="Manifestations" />

Immune complex glomerulonephritis presenting with proteinuria and hematuria has been described in children and adults with Crohn's disease or ulcerative colitis. Diagnosis is by renal biopsy, and treatment parallels the underlying IBD.<ref name="Manifestations" />

Amyloidosis (see endocrinological involvement) secondary to Crohn's disease has been described and is known to affect the kidneys.<ref name="Manifestations" />

====Pancreatic====

Pancreatitis may be associated with both ulcerative colitis and Crohn's disease. The most common cause is iatrogenic and involves sensitivity to medications used to treat IBD, including sulfasalazine, mesalamine, 6-mercaptopurine, and azathioprine. Pancreatitis may present as symptomatic or more commonly asymptomatic disease in adults with IBD.<ref name="Manifestations" />

====Cardiovascular and circulatory====

Children and adults with IBD have rarely (<1%) reported developing pleuropericarditis either at initial presentation or during active or quiescent disease. The pathogenesis of pleuropericarditis is unknown, although certain medications (e.g., sulfasalazine and mesalamine derivatives) have been implicated in some cases. The clinical presentation may include chest pain, dyspnea, or in severe cases pericardial tamponade requiring rapid drainage. Nonsteroidal anti-inflammatory drugs have been used as therapy, although this should be weighed against the hypothetical risk of exacerbating the underlying IBD.<ref name="Manifestations" />

In rare cases, cardiomyopathy, endocarditis, and myocarditis have been described.<ref name="Manifestations" />

Crohn's disease also increases the risk of blood clots;<ref name="Trikudanathan2012" /> painful swelling of the lower legs can be a sign of deep venous thrombosis, while difficulty breathing may be a result of pulmonary embolism.

====Respiratory====

Laryngeal involvement in inflammatory bowel disease is extremely rare. Only 12 cases of laryngeal involvement in Crohn's disease have been reported {{as of|2019|lc=y}}. Moreover, only one case of laryngeal manifestations in ulcerative colitis has been reported as of the same date.<ref>{{cite journal | vauthors = Loos E, Lemkens P, Poorten VV, Humblet E, Laureyns G | title = Laryngeal Manifestations of Inflammatory Bowel Disease | journal = Journal of Voice | volume = 33 | issue = 1 | pages = 1–6 | date = January 2019 | pmid = 29605161 | doi = 10.1016/j.jvoice.2017.09.021 | s2cid = 4565046 }}</ref> Nine people complained of difficulty in breathing due to edema and ulceration from the larynx to the hypopharynx.<ref>{{cite journal | vauthors = Hasegawa N, Ishimoto S, Takazoe M, Tsunoda K, Fujimaki Y, Shiraishi A, Kinoshita M, Okada K | title = Recurrent hoarseness due to inflammatory vocal fold lesions in a patient with Crohn's disease | journal = The Annals of Otology, Rhinology, and Laryngology | volume = 118 | issue = 7 | pages = 532–535 | date = July 2009 | pmid = 19708494 | doi = 10.1177/000348940911800713 | s2cid = 8472904 }}</ref> Hoarseness, sore throat, and odynophagia are other symptoms of laryngeal involvement of Crohn's disease.<ref>{{cite journal | vauthors = Li CJ, Aronowitz P | title = Sore throat, odynophagia, hoarseness, and a muffled, high-pitched voice | journal = Cleveland Clinic Journal of Medicine | volume = 80 | issue = 3 | pages = 144–145 | date = March 2013 | pmid = 23456463 | doi = 10.3949/ccjm.80a.12056 | s2cid = 31002546 | doi-access = free | title-link = doi }}</ref>

Considering extraintestinal manifestations of Crohn's disease, 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 Crohn's disease. 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.<ref>{{cite journal | vauthors = Lu DG, Ji XQ, Liu X, Li HJ, Zhang CQ | title = Pulmonary manifestations of Crohn's disease | journal = World Journal of Gastroenterology | volume = 20 | issue = 1 | pages = 133–141 | date = January 2014 | pmid = 24415866 | pmc = 3886002 | doi = 10.3748/wjg.v20.i1.133 | doi-access = free | title-link = doi }}</ref> A complete list of known pulmonary manifestations include: fibrosing alveolitis, pulmonary vasculitis, apical fibrosis, bronchiectasis, bronchitis, bronchiolitis, tracheal stenosis, granulomatous lung disease, and abnormal pulmonary function.<ref name="Manifestations" />

====Musculoskeletal====

Crohn's disease is associated with a type of rheumatologic disease known as seronegative spondyloarthropathy.<ref name="Trikudanathan2012" /> This group of diseases is characterized by inflammation of one or more joints (arthritis) or muscle insertions (enthesitis).<ref name="Trikudanathan2012" /> 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.<ref name="Trikudanathan2012" /> The second type symmetrically involves five or more of the small joints of the hands and feet.<ref name="Trikudanathan2012" /> 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.<ref name="Trikudanathan2012" />

Crohn's disease increases the risk of osteoporosis or thinning of the bones.<ref name="Trikudanathan2012" /><ref>{{cite journal | vauthors = van Bodegraven AA, Bravenboer N | title = Perspective on skeletal health in inflammatory bowel disease | journal = Osteoporosis International | volume = 31 | issue = 4 | pages = 637–646 | date = April 2020 | pmid = 31822927 | pmc = 7075921 | doi = 10.1007/s00198-019-05234-w }}</ref><ref>{{Cite web |title=Osteoporosis - IBD Journey - Complications of IBD - Osteoporosis |url=https://crohnsandcolitis.ca/About-Crohn-s-Colitis/IBD-Journey/Complications-and-Extraintestinal-Manifestations/Osteoporosis |access-date=February 14, 2025 |website=crohnsandcolitis.ca}}</ref> Individuals with osteoporosis are at increased risk of bone fractures.<ref name="Bernstein">{{cite journal | vauthors = Bernstein M, Irwin S, Greenberg GR | 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 = 2031–2035 | date = September 2005 | pmid = 16128948 | doi = 10.1111/j.1572-0241.2005.50219.x | s2cid = 28982700 }}</ref>

====Dermatological==== thumb|A single lesion of erythema nodosum

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.<ref name="Trikudanathan2012">{{cite journal | vauthors = Trikudanathan G, Venkatesh PG, Navaneethan U | title = Diagnosis and therapeutic management of extra-intestinal manifestations of inflammatory bowel disease | journal = Drugs | volume = 72 | issue = 18 | pages = 2333–2349 | date = December 2012 | pmid = 23181971 | doi = 10.2165/11638120-000000000-00000 | s2cid = 10078879 }}</ref><ref name="Thrash2013">{{cite journal | vauthors = Thrash B, Patel M, Shah KR, Boland CR, Menter A | title = Cutaneous manifestations of gastrointestinal disease: part II | journal = Journal of the American Academy of Dermatology | volume = 68 | issue = 2 | pages = 211.e1-33; quiz 244–6 | date = February 2013 | pmid = 23317981 | doi = 10.1016/j.jaad.2012.10.036 | s2cid = 1819416 }}</ref><ref name="PMID30682031">{{cite journal | vauthors = Roth N, Biedermann L, Fournier N, Butter M, Vavricka SR, Navarini AA, Rogler G, Scharl M | title = Occurrence of skin manifestations in patients of the Swiss Inflammatory Bowel Disease Cohort Study | journal = PLOS ONE | volume = 14 | issue = 1 | article-number = e0210436 | date = 2019 | pmid = 30682031 | pmc = 6347222 | doi = 10.1371/journal.pone.0210436 | s2cid = 59275029 | doi-access = free | title-link = doi | bibcode = 2019PLoSO..1410436R }}</ref> Erythema nodosum is due to inflammation of the underlying subcutaneous tissue, and is characterized by septal panniculitis.<ref name="Thrash2013" />

Pyoderma gangrenosum is a less common skin problem, occurring in under 2%,<ref name="PMID30682031" /> and is typically a painful ulcerating nodule.<ref name="Thrash2013" /><ref name="Harbord" />

Clubbing, a deformity of the ends of the fingers, may also be a result of Crohn's disease.<ref>{{cite journal | vauthors = Kitis G, Thompson H, Allan RN | title = Finger clubbing in inflammatory bowel disease: its prevalence and pathogenesis | journal = British Medical Journal | volume = 2 | issue = 6194 | pages = 825–828 | date = October 1979 | pmid = 509114 | pmc = 1596648 | doi = 10.1136/bmj.2.6194.825 }}</ref><ref>{{cite journal | vauthors = Kapsoritakis AN, Psychos AK, Sfiridaki A, Zintzaras E, Potamianos SP | title = Finger clubbing and erythropoietin serum levels in active IBD | journal = Inflammatory Bowel Diseases | volume = 12 | issue = 6 | pages = 535–536 | date = June 2006 | pmid = 16775499 | doi = 10.1097/00054725-200606000-00014 }}</ref>

Other very rare dermatological manifestations include: pyostomatitis vegetans, erythema multiforme, epidermolysis bullosa acquista (described in a case report), and metastatic Crohn's disease (the spread of Crohn's inflammation to the skin<ref name="Cutaneous" />).<ref name="Manifestations" /> It is unknown if Sweet's syndrome is connected to Crohn's disease.<ref name="Manifestations" />

====Neurological====

Crohn's disease can also cause neurological complications (reportedly in up to 15% of cases).<ref name="pro">[http://professionals.epilepsy.com/page/inflammatory_crohn.html Crohn's disease] {{webarchive|url=https://web.archive.org/web/20070805041654/http://professionals.epilepsy.com/page/inflammatory_crohn.html |date=August 5, 2007}}. professionals.epilepsy.com. Retrieved July 13, 2007.</ref> The most common of these are seizures, stroke, myopathy, peripheral neuropathy, headache, and depression.<ref name="pro" />

Central and peripheral neurological disorders are described in people with IBD and include peripheral neuropathies, myopathies, focal central nervous system defects, convulsions, confusional episodes, meningitis, syncope, optic neuritis, and sensorineural loss. Autoimmune mechanisms are proposed for involvement with IBD. Nutritional deficiencies associated with neurological manifestations, such as vitamin B12 deficiency, should be investigated. Spinal abscess has been reported in both a child and an adult with initial complaints of severe back pain due to extension of a psoas abscess from the epidural space to the subarachnoid space.<ref name="Manifestations" />

====Psychiatric and psychological====

Crohn's disease is linked to many psychological disorders, including depression and anxiety, denial of one's disease, the need for dependence or dependent behaviors, feeling overwhelmed, and having a poor self-image.<ref>{{Cite web |title=Mental and Emotional Well-Being |url=https://www.crohnscolitisfoundation.org/mental-health |access-date=September 6, 2021 |website=Crohn's & Colitis Foundation |archive-date=October 7, 2022 |archive-url=https://web.archive.org/web/20221007193457/https://www.crohnscolitisfoundation.org/mental-health |url-status=live}}</ref>

Many studies have found that people with IBD report a higher frequency of depressive and anxiety disorders than the general population; most studies confirm that women with IBD are more likely than men to develop affective disorders and show that up to 65% of them may have depression and anxiety disorder.<ref>{{cite journal | vauthors = Fracas E, Costantino A, Vecchi M, Buoli M | title = Depressive and Anxiety Disorders in Patients with Inflammatory Bowel Diseases: Are There Any Gender Differences? | journal = International Journal of Environmental Research and Public Health | volume = 20 | issue = 13 | page = 6255 | date = June 2023 | pmid = 37444101 | pmc = 10340762 | doi = 10.3390/ijerph20136255 | doi-access = free | title-link = doi }}</ref><ref>{{cite journal | vauthors = Barberio B, Zamani M, Black CJ, Savarino EV, Ford AC | title = Prevalence of symptoms of anxiety and depression in patients with inflammatory bowel disease: a systematic review and meta-analysis | journal = The Lancet. Gastroenterology & Hepatology | volume = 6 | issue = 5 | pages = 359–370 | date = May 2021 | pmid = 33721557 | doi = 10.1016/S2468-1253(21)00014-5 | hdl = 11577/3406430 | url = https://eprints.whiterose.ac.uk/173607/3/LGH_Manuscript_clean.pdf | access-date = May 26, 2024 | url-status = live | archive-url = https://web.archive.org/web/20231203051934/https://eprints.whiterose.ac.uk/173607/3/LGH_Manuscript_clean.pdf | archive-date = December 3, 2023 }}</ref>

====Endocrinological or hematological====

Leukocytosis and thrombocytopenia are usually due to immunosuppressant treatments or sulfasalazine. Plasma erythropoietin levels often are lower in patients with IBD than expected, in conjunction with severe anemia.<ref name="Manifestations" /> Anemia caused by iron deficiency is often a direct result of intestinal bleeding due to inflammation and interference with iron transport caused by inflammatory mediators.<ref name="Tsiolakidou">{{cite journal |last1=Tsiolakidou |first1=Georgia |last2=Koutroubakis |first2=Ioannis |title=Stimulating erythropoiesis |journal=World Journal of Gastroenterology |date=2007 |volume=13 |issue=36 |pages=4798–4806 |doi=10.3748/wjg.v13.i36.4798 |pmid=17828809 |pmc=4611757 |doi-access=free }}</ref>

Thrombocytosis and thromboembolic events resulting from a hypercoagulable state in people with IBD can lead to pulmonary embolism or thrombosis elsewhere in the body. Thrombosis has been reported in 1.8% of people with ulcerative colitis and 3.1% of people with Crohn's disease. Thromboembolism and thrombosis are less frequently reported among children, with three people with ulcerative colitis and one with Crohn's disease described in case reports.<ref name="Manifestations" />

In rare cases, hypercoagulation disorders and portal vein thrombosis have been described.<ref name="Manifestations" />

====Malnutrition symptoms====

People with Crohn's disease may develop anemia due to vitamin B12, folate, iron deficiency, or due to anemia of chronic disease.<ref name="Lomer2011">{{cite journal | vauthors = Lomer MC | title = Dietary and nutritional considerations for inflammatory bowel disease | journal = The Proceedings of the Nutrition Society | volume = 70 | issue = 3 | pages = 329–335 | date = August 2011 | pmid = 21450124 | doi = 10.1017/S0029665111000097 | doi-access = free | title-link = doi }}</ref><ref name="Gerasimidis2011">{{cite journal | vauthors = Gerasimidis K, McGrogan P, Edwards CA | title = The aetiology and impact of malnutrition in paediatric inflammatory bowel disease | journal = Journal of Human Nutrition and Dietetics | volume = 24 | issue = 4 | pages = 313–326 | date = August 2011 | pmid = 21564345 | doi = 10.1111/j.1365-277X.2011.01171.x | type = Review | doi-access = free | title-link = doi }}</ref> The most common is iron deficiency anemia from chronic blood loss,<ref name="Lomer2011" /> reduced dietary intake, and persistent inflammation leading to increased hepcidin levels, restricting iron absorption in the duodenum.<ref name="Gerasimidis2011" /> As Crohn's disease most commonly affects the terminal ileum where the vitamin B12/intrinsic factor complex is absorbed, B12 deficiency may be seen.<ref name="Gerasimidis2011" /> This is particularly common after one has had a surgical procedure to remove the ileum.<ref name="Lomer2011" /> 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.<ref>{{MedlinePlusEncyclopedia|000222|Small bowel bacterial overgrowth}}</ref><ref name="mimicking">{{cite journal | vauthors = Klaus J, Spaniol U, Adler G, Mason RA, Reinshagen M, von Tirpitz CC | title = Small intestinal bacterial overgrowth mimicking acute flare as a pitfall in patients with Crohn's Disease | journal = BMC Gastroenterology | volume = 9 | issue = 1 | article-number = 61 | date = July 2009 | pmid = 19643023 | pmc = 2728727 | doi = 10.1186/1471-230X-9-61 | doi-access = free | title-link = doi }} 50px Text was copied from this source, which is available under a [https://creativecommons.org/licenses/by/2.0/ Creative Commons Attribution 2.0 Generic (CC BY 2.0)] {{Webarchive|url=https://web.archive.org/web/20110223001542/http://creativecommons.org/licenses/by/2.0/ |date=February 23, 2011}} license.</ref>

=== Complications === ====Intestinal damage==== thumb|Histopathology of a non-necrotizing granuloma of colonic mucosa in a patient with Crohn's disease, H&E stain. It is seen as an aggregate of histiocytes in the center of the image, having ample eosinophilic cytoplasm. Crohn's disease can lead to several mechanical complications within the intestines, including obstruction,<ref>{{cite web | vauthors = Ansar P |url=http://www.merckmanuals.com/home/digestive-disorders/gastrointestinal-emergencies/intestinal-obstruction |title=Intestinal Obstruction |website=MERCK MANUAL Consumer Version|access-date=June 27, 2016|url-status=live|archive-url=https://web.archive.org/web/20160710102459/http://www.merckmanuals.com/home/digestive-disorders/gastrointestinal-emergencies/intestinal-obstruction|archive-date=July 10, 2016}}</ref> fistulae,<ref>{{cite web | vauthors = Ansar P |url=http://www.merckmanuals.com/home/digestive-disorders/anal-and-rectal-disorders/anorectal-fistula |title=Anorectal Fistula |website=MERCK MANUAL Consumer Version|access-date=June 27, 2016|url-status=live|archive-url=https://web.archive.org/web/20160710213544/http://www.merckmanuals.com/home/digestive-disorders/anal-and-rectal-disorders/anorectal-fistula|archive-date=July 10, 2016}}</ref> and abscesses.<ref>{{cite web | vauthors = Ansar P |url=http://www.merckmanuals.com/home/digestive-disorders/anal-and-rectal-disorders/anorectal-abscess |title=Anorectal Abscess |website=MERCK MANUAL Consumer Version|access-date=June 27, 2016|url-status=live|archive-url=https://web.archive.org/web/20160614095919/http://www.merckmanuals.com/home/digestive-disorders/anal-and-rectal-disorders/anorectal-abscess|archive-date=June 14, 2016}}</ref> 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.<ref>{{EMedicine|article|442000|Enterovesical Fistula}}</ref>

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.<ref name="emed" />

Intestinal granulomas are walled-off portions of the intestine by macrophages to isolate infections. Granuloma formation is more often seen in younger people, and mainly in the severe, active, penetrating disease.<ref name="granuloma">{{cite journal | vauthors = Molnár T, Tiszlavicz L, Gyulai C, Nagy F, Lonovics J | title = Clinical significance of granuloma in Crohn's disease | journal = World Journal of Gastroenterology | volume = 11 | issue = 20 | pages = 3118–3121 | date = May 2005 | pmid = 15918200 | pmc = 4305850 | doi = 10.3748/wjg.v11.i20.3118 | doi-access = free | title-link = doi }}</ref> Granuloma is considered the hallmark of microscopic diagnosis in Crohn's disease, but granulomas can be detected in only 21–60% of people with Crohn's disease.<ref name="granuloma" />

====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.<ref>{{cite journal | vauthors = Bye WA, Nguyen TM, Parker CE, Jairath V, East JE | title = Strategies for detecting colon cancer in patients with inflammatory bowel disease | journal = The Cochrane Database of Systematic Reviews | volume = 2017 | issue = 9 | article-number = CD000279 | date = September 2017 | pmid = 28922695 | pmc = 6483622 | doi = 10.1002/14651858.CD000279.pub4 }}</ref> Similarly, people with Crohn's colitis have a relative risk of 5.6 for developing colon cancer.<ref>{{cite journal | vauthors = Ekbom A, Helmick C, Zack M, Adami HO | title = Increased risk of large-bowel cancer in Crohn's disease with colonic involvement | journal = Lancet | volume = 336 | issue = 8711 | pages = 357–359 | date = August 1990 | pmid = 1975343 | doi = 10.1016/0140-6736(90)91889-I | url = https://zenodo.org/record/1258309 | access-date = September 4, 2018 | url-status = live | s2cid = 2046255 | archive-url = https://web.archive.org/web/20200805072047/https://zenodo.org/record/1258309 | archive-date = August 5, 2020 }}</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 | vauthors = Itzkowitz SH, Present DH | title = Consensus conference: Colorectal cancer screening and surveillance in inflammatory bowel disease | journal = Inflammatory Bowel Diseases | volume = 11 | issue = 3 | pages = 314–321 | date = March 2005 | pmid = 15735438 | doi = 10.1097/01.mib.0000160811.76729.d5 | collaboration = Crohn's and Colitis Foundation of America Colon Cancer in IBD Study Group }}</ref>

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.<ref>{{cite journal | vauthors = Zisman TL, Rubin DT | title = Colorectal cancer and dysplasia in inflammatory bowel disease | journal = World Journal of Gastroenterology | volume = 14 | issue = 17 | pages = 2662–2669 | date = May 2008 | pmid = 18461651 | pmc = 2709054 | doi = 10.3748/wjg.14.2662 | doi-access = free | title-link = doi }}</ref> Also, immunomodulators and biologic agents used to treat this disease may promote the development of extra-intestinal cancers.<ref>{{cite journal | vauthors = Axelrad JE, Lichtiger S, Yajnik V | title = Inflammatory bowel disease and cancer: The role of inflammation, immunosuppression, and cancer treatment | journal = World Journal of Gastroenterology | volume = 22 | issue = 20 | pages = 4794–4801 | date = May 2016 | pmid = 27239106 | pmc = 4873872 | doi = 10.3748/wjg.v22.i20.4794 | type = Review | doi-access = free | title-link = doi }}</ref>

Some cancers, such as acute myeloid leukemia, have been described in cases of Crohn's disease.<ref name="Manifestations" /> Hepatosplenic T-cell lymphoma (HSTCL) is a rare, lethal disease generally seen in young males with inflammatory bowel disease. TNF-α Inhibitor treatments (infliximab, adalimumab, certolizumab, natalizumab, and etanercept) are thought to be the cause of this rare disease.<ref>{{cite journal | vauthors = Parakkal D, Sifuentes H, Semer R, Ehrenpreis ED | title = Hepatosplenic T-cell lymphoma in patients receiving TNF-α inhibitor therapy: expanding the groups at risk | journal = European Journal of Gastroenterology & Hepatology | volume = 23 | issue = 12 | pages = 1150–1156 | date = November 2011 | pmid = 21941193 | doi = 10.1097/MEG.0b013e32834bb90a | s2cid = 27267004 }}</ref>

[[File:Colorectal cancer endo 2.jpg|thumb|Endoscopic image of colon cancer identified in the sigmoid colon on screening colonoscopy for Crohn's disease]]

====Major complications==== Major complications of Crohn's disease include bowel obstruction, abscesses, free perforation, and hemorrhage, which in rare cases may be fatal.<ref name="pmid33399844">{{cite journal | vauthors = Cushing K, Higgins PD | title = Management of Crohn Disease: A Review | journal = JAMA | volume = 325 | issue = 1 | pages = 69–80 | date = January 2021 | pmid = 33399844 | pmc = 9183209 | doi = 10.1001/jama.2020.18936 }}</ref>

====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 with nutrition.<ref>{{cite journal | vauthors = Evans JP, Steinhart AH, Cohen Z, McLeod RS | title = Home total parenteral nutrition: an alternative to early surgery for complicated inflammatory bowel disease | journal = Journal of Gastrointestinal Surgery | volume = 7 | issue = 4 | pages = 562–566 | year = 2003 | pmid = 12763417 | doi = 10.1016/S1091-255X(02)00132-4 | s2cid = 195305419 }}</ref>

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, people with Crohn's disease are especially predisposed to develop SIBO. As a result, people with Crohn's disease may experience malabsorption and report symptoms such as weight loss, watery diarrhea, meteorism, flatulence, and abdominal pain, mimicking an acute flare.<ref name="mimicking" />

====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.<ref>{{cite web |url=http://www.ccfa.org/about/news/pregnancy |publisher=Crohn's and Colitis Foundation of America |date=October 21, 2005 |title=IBD and Pregnancy: What You Need to Know |vauthors=Kaplan C |access-date=November 7, 2009 |archive-url=https://web.archive.org/web/20120217151655/http://www.ccfa.org/about/news/pregnancy |archive-date=February 17, 2012}}</ref>

====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.<ref>{{Cite book | vauthors = Rodrigues FP, Novaes JA, Pinheiro MM, Martins P, Cunha-Melo JR | chapter = Intestinal Ostomy Complications and Care | title = Gastrointestinal Stomas |date=October 23, 2019 |publisher=IntechOpen | doi = 10.5772/intechopen.85633 | hdl = 1843/39797 |isbn=978-1-78984-186-2 |access-date=September 6, 2021 |archive-date=October 7, 2022 | chapter-url = https://www.intechopen.com/chapters/67036 |archive-url=https://web.archive.org/web/20221007193456/https://www.intechopen.com/chapters/67036 |url-status=live}}</ref>

== Etiology == The etiology of Crohn's disease is not fully understood. It is considered a complex, immune-mediated disorder that results from a combination of genetic susceptibility, environmental factors, and a dysregulated immune response to the gut microbiota in a susceptible host.<ref>{{Cite journal |last=Ananthakrishnan |first=Ashwin N. |date=April 2015|title=Epidemiology and risk factors for IBD |journal=Nature Reviews. Gastroenterology & Hepatology |volume=12 |issue=4 |pages=205–217 |doi=10.1038/nrgastro.2015.34 |issn=1759-5053 |pmid=25732745}}</ref><ref>{{Cite journal |last1=Jostins |first1=Luke |last2=Ripke |first2=Stephan |last3=Weersma |first3=Rinse K. |last4=Duerr |first4=Richard H. |last5=McGovern |first5=Dermot P. |last6=Hui |first6=Ken Y. |last7=Lee |first7=James C. |last8=Philip Schumm |first8=L. |last9=Sharma |first9=Yashoda |last10=Anderson |first10=Carl A. |last11=Essers |first11=Jonah |last12=Mitrovic |first12=Mitja |last13=Ning |first13=Kaida |last14=Cleynen |first14=Isabelle |last15=Theatre |first15=Emilie |date=Nov 2012|title=Host–microbe interactions have shaped the genetic architecture of inflammatory bowel disease |journal=Nature |language=en |volume=491 |issue=7422 |pages=119–124 |doi=10.1038/nature11582 |pmid=23128233 |issn=1476-4687|hdl=20.500.11820/aa67620e-007f-467b-8b0b-20a1912ccaec |hdl-access=free |pmc=3491803 |bibcode=2012Natur.491..119. }}</ref> This interaction leads to a chronic state of inflammation in the gastrointestinal tract. Crohn's disease involves both innate and adaptive immune pathways, though it is not classified as a classic autoimmune or autoinflammatory disease.<ref>{{Cite journal |last=de Souza |first=Heitor S. P. |date=July 2017|title=Etiopathogenesis of inflammatory bowel disease: today and tomorrow |journal=Current Opinion in Gastroenterology |volume=33 |issue=4 |pages=222–229 |doi=10.1097/MOG.0000000000000364 |issn=1531-7056 |pmid=28402995}}</ref> Instead, the prevailing model describes a breakdown in the normal homeostasis between the intestinal immune system and the commensal microbiome.<ref>{{Cite journal |last1=Maloy |first1=Kevin J. |last2=Powrie |first2=Fiona |date=June 2011 |title=Intestinal homeostasis and its breakdown in inflammatory bowel disease |url=https://www.nature.com/articles/nature10208 |journal=Nature |language=en |volume=474 |issue=7351 |pages=298–306 |doi=10.1038/nature10208 |pmid=21677746 |bibcode=2011Natur.474..298M |issn=1476-4687}}</ref>

=== Autoinflammatory theory === Crohn's disease can be described as a multifactorial autoinflammatory disease. The etiopathogenesis of Crohn's disease is still unknown, but a loss of immune regulation can be implicated in the onset of the disease. People with Crohn's disease have more frequent NOD2 gene mutations than the background population, making those mutations a risk factor. In contrast, a person with Blau's disease and a NOD2 mutation is likely to have the syndrome directly from that mutation, in addition to the mutation making them more susceptible to Crohn's. This pathogenesis of Crohn's disease allows it to be placed in the group of autoinflammatory syndromes.<ref name="Ciccarelli 261–269">{{cite journal |vauthors=Ciccarelli F, De Martinis M, Ginaldi L |date=January 2013 |title=An update on autoinflammatory diseases |journal=Current Medicinal Chemistry |volume=21 |issue=3 |pages=261–269 |doi=10.2174/09298673113206660303 |pmc=3905709 |pmid=24164192}}</ref>

Some examples of how the innate immune system affects bowel inflammation have been described.<ref name="Li 15–22">{{cite journal |vauthors=Li N, Shi RH |date=January 2018 |title=Updated review on immune factors in pathogenesis of Crohn's disease |journal=World Journal of Gastroenterology |volume=24 |issue=1 |pages=15–22 |doi=10.3748/wjg.v24.i1.15 |pmc=5757119 |pmid=29358878 |doi-access=free |title-link=doi}}</ref> A meta-analysis of Crohn's disease genome-wide association studies revealed 71 distinct Crohn's disease-susceptibility loci. Interestingly, three very important Crohn's disease-susceptibility genes (the intracellular pathogen-recognition receptor, NOD2; the autophagy-related 16-like 1, ATG16L1 and the immunity-related GTPase M, IRGM) are involved in innate immune responses against gut microbiota, while one (the X-box binding protein 1) is involved in regulation of the [adaptive] immune pathway via MHC class II,<ref>{{cite journal | vauthors = Roggenbuck D, Reinhold D, Baumgart DC, Schierack P, Conrad K, Laass MW | title = Autoimmunity in Crohn's Disease-A Putative Stratification Factor of the Clinical Phenotype | journal = Advances in Clinical Chemistry | volume = 77 | pages = 77–101 | date = January 1, 2016 | pmid = 27717419 | doi = 10.1016/bs.acc.2016.06.002 | publisher = Elsevier | isbn = 978-0-12-804686-9 | veditors = Makowski GS }}</ref> resulting in autoinflammatory inflammation. Studies have also found that increased ILC3 can overexpress major histocompatibility complex (MHC) II. MHC class II can induce CD4+ T cell apoptosis, thus avoiding the T cell response to normal bowel micro bacteria. Further studies of people with IBD compared with people without IBD found that the expression of MHC II by ILC3 was significantly reduced in people with IBD, thus causing an immune reaction against intestinal cells or normal bowel bacteria and damaging the intestines. This can also make the intestines more susceptible to environmental factors, such as food or bacteria.<ref name="Li 15–22" />

Together, defects in innate immune sensing and regulation, maladaptive adaptive immune responses, support the concept of Crohn's disease as a disorder of immune dysregulation rather than a purely autoinflammatory or autoimmune condition.<ref>{{Cite journal |last1=Strober |first1=Warren |last2=Fuss |first2=Ivan |last3=Mannon |first3=Peter |date=March 2007 |title=The fundamental basis of inflammatory bowel disease |journal=The Journal of Clinical Investigation |volume=117 |issue=3 |pages=514–521 |doi=10.1172/JCI30587 |issn=0021-9738 |pmc=1804356 |pmid=17332878 |bibcode=2007JCliI.117..514S }}</ref>

=== Integrated Immunological Model === As previously stated, current evidence supports an integrated immunological model of Crohn's disease in which defects in immune regulation at the intestinal mucosa lead to chronic inflammation, rather than a single primary immunodeficiency or a classic autoimmune mechanism.<ref>{{Cite web |date=2025-11-24 |title=Inflammatory bowel disease {{!}} Nature Immunology |url=https://www.nature.com/subjects/inflammatory-bowel-disease/ni |access-date=2025-12-21 |website=www.nature.com |language=en}}</ref><ref>{{Cite journal |last1=Abraham |first1=Clara |last2=Cho |first2=Judy H. |date=2009-11-19 |title=Inflammatory Bowel Disease |journal=New England Journal of Medicine |volume=361 |issue=21 |pages=2066–2078 |doi=10.1056/NEJMra0804647 |issn=0028-4793 |pmc=3491806 |pmid=19923578}}</ref> Genetic studies have identified risk variants affecting innate immune pathways involved in microbial sensing, autophagy, and epithelial defense, indicating that impaired early immune responses contribute to defective control of the intestinal microbiota and disruption of mucosal homeostasis.<ref>{{Cite journal |last1=Jostins |first1=Luke |last2=Ripke |first2=Stephan |last3=Weersma |first3=Rinse K. |last4=Duerr |first4=Richard H. |last5=McGovern |first5=Dermot P. |last6=Hui |first6=Ken Y. |last7=Lee |first7=James C. |last8=Philip Schumm |first8=L. |last9=Sharma |first9=Yashoda |last10=Anderson |first10=Carl A. |last11=Essers |first11=Jonah |last12=Mitrovic |first12=Mitja |last13=Ning |first13=Kaida |last14=Cleynen |first14=Isabelle |last15=Theatre |first15=Emilie |date=Nov 2012|title=Host–microbe interactions have shaped the genetic architecture of inflammatory bowel disease |journal=Nature |language=en |volume=491 |issue=7422 |pages=119–124 |doi=10.1038/nature11582 |pmid=23128233 |issn=1476-4687|hdl=20.500.11820/aa67620e-007f-467b-8b0b-20a1912ccaec |hdl-access=free |pmc=3491803 |bibcode=2012Natur.491..119. }}</ref>

Impaired innate immune function results in persistent antigenic stimulation within the gut, which promotes maladaptive activation of the adaptive immune system, particularly Th1- and Th17-mediated responses.<ref>{{Cite journal |last=Neurath |first=Markus F. |date=May 2014 |title=Cytokines in inflammatory bowel disease |url=https://www.nature.com/articles/nri3661 |journal=Nature Reviews Immunology |language=en |volume=14 |issue=5 |pages=329–342 |doi=10.1038/nri3661 |pmid=24751956 |bibcode=2014NatRI..14..329N |issn=1474-1741|url-access=subscription }}</ref> These responses fail to restore immune tolerance and instead perpetuate tissue damage and inflammation. Together, these findings support the previously mentioned classification of Crohn's disease as a disorder of immune dysregulation involving coordinated dysfunction of both innate and adaptive immune pathways, rather than a purely autoinflammatory or autoimmune disease.<ref>{{Cite journal |last1=Geremia |first1=Alessandra |last2=Biancheri |first2=Paolo |last3=Allan |first3=Philip |last4=Corazza |first4=Gino R. |last5=Di Sabatino |first5=Antonio |date=Jan 2014|title=Innate and adaptive immunity in inflammatory bowel disease |journal=Autoimmunity Reviews |volume=13 |issue=1 |pages=3–10 |doi=10.1016/j.autrev.2013.06.004 |issn=1873-0183 |pmid=23774107}}</ref>

== Risk factors == {{Risk factors in CD vs. UC}} While the exact cause or causes are unknown, Crohn's disease seems to be due to a combination of environmental factors and genetic predisposition.<ref>{{cite journal | vauthors = Braat H, Peppelenbosch MP, Hommes DW | title = Immunology of Crohn's disease | journal = Annals of the New York Academy of Sciences | volume = 1072 | issue = 1 | pages = 135–154 | date = August 2006 | pmid = 17057196 | doi = 10.1196/annals.1326.039 | s2cid = 2627465 | bibcode = 2006NYASA1072..135B }}</ref> 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.<ref>{{cite journal | vauthors = Henckaerts L, Figueroa C, Vermeire S, Sans M | title = The role of genetics in inflammatory bowel disease | journal = Current Drug Targets | volume = 9 | issue = 5 | pages = 361–368 | date = May 2008 | pmid = 18473763 | doi = 10.2174/138945008784221161 }}</ref> Each 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.<ref name="Marks2006"> {{cite journal | vauthors = 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 = 668–678 | date = February 2006 | pmid = 16503465 | doi = 10.1016/S0140-6736(06)68265-2 | s2cid = 13898663 }}</ref> 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.<ref>{{cite journal | vauthors = Comalada M, Peppelenbosch MP | title = Impaired innate immunity in Crohn's disease | journal = Trends in Molecular Medicine | volume = 12 | issue = 9 | pages = 397–399 | date = September 2006 | pmid = 16890491 | doi = 10.1016/j.molmed.2006.07.005 }}</ref>

=== Genetics === [[File:NOD2 structure model domain diagram.png|thumb|upright=1.4|NOD2 protein model with schematic diagram. Two N-terminal CARD domains (red) connected via helical linker (blue) with central NBD domain (green). At the 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.<ref>{{cite journal | vauthors = Nakagome S, Mano S, Kozlowski L, Bujnicki JM, Shibata H, Fukumaki Y, Kidd JR, Kidd KK, Kawamura S, Oota H | title = Crohn's disease risk alleles on the NOD2 locus have been maintained by natural selection on standing variation | journal = Molecular Biology and Evolution | volume = 29 | issue = 6 | pages = 1569–1585 | date = June 2012 | pmid = 22319155 | pmc = 3697811 | doi = 10.1093/molbev/mss006 }}</ref>]] Crohn's has a genetic component.<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=April 16, 2007 |access-date=November 7, 2009 |archive-url = https://web.archive.org/web/20070502210012/http://www.ccfa.org/reuters/geneticlink |archive-date=May 2, 2007}}</ref> Because of this, siblings of known people with Crohn's are 30 times more likely to develop Crohn's than the general population.<ref>{{cite journal | vauthors = Liu JZ, Anderson CA | title = Genetic studies of Crohn's disease: past, present and future | journal = Best Practice & Research. Clinical Gastroenterology | volume = 28 | issue = 3 | pages = 373–386 | date = June 2014 | pmid = 24913378 | pmc = 4075408 | doi = 10.1016/j.bpg.2014.04.009 }}</ref>

The first mutation found to be associated with Crohn's was a frameshift in the NOD2 gene (also known as the CARD15 gene),<ref>{{cite journal | vauthors = Ogura Y, Bonen DK, Inohara N, Nicolae DL, Chen FF, Ramos R, Britton H, Moran T, Karaliuskas R, Duerr RH, Achkar JP, Brant SR, Bayless TM, Kirschner BS, Hanauer SB, Nuñez G, Cho JH | title = A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease | journal = Nature | volume = 411 | issue = 6837 | pages = 603–606 | date = May 2001 | pmid = 11385577 | doi = 10.1038/35079114 | hdl-access = free | s2cid = 205017657 | bibcode = 2001Natur.411..603O | hdl = 2027.42/62856 }}</ref> followed by the discovery of point mutations.<ref>{{cite journal | vauthors = Cuthbert AP, Fisher SA, Mirza MM, King K, Hampe J, Croucher PJ, Mascheretti S, Sanderson J, Forbes A, Mansfield J, Schreiber S, Lewis CM, Mathew CG | 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 = 867–874 | date = April 2002 | pmid = 11910337 | doi = 10.1053/gast.2002.32415 }}</ref> 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.<ref>{{cite journal | vauthors = Kaser A, Lee AH, Franke A, Glickman JN, Zeissig S, Tilg H, Nieuwenhuis EE, Higgins DE, Schreiber S, Glimcher LH, Blumberg RS | title = XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease | journal = Cell | volume = 134 | issue = 5 | pages = 743–756 | date = September 2008 | pmid = 18775308 | pmc = 2586148 | doi = 10.1016/j.cell.2008.07.021 }}</ref><ref>{{cite journal | vauthors = Clevers H | title = Inflammatory bowel disease, stress, and the endoplasmic reticulum | journal = The New England Journal of Medicine | volume = 360 | issue = 7 | pages = 726–727 | date = February 2009 | pmid = 19213688 | doi = 10.1056/NEJMcibr0809591 }}</ref> The gene variants of NOD2/CARD15 seem to be related with small-bowel involvement.<ref>{{cite journal | vauthors = Vermeire S | title = NOD2/CARD15: relevance in clinical practice | journal = Best Practice & Research. Clinical Gastroenterology | volume = 18 | issue = 3 | pages = 569–575 | date = June 2004 | pmid = 15157828 | doi = 10.1016/j.bpg.2003.12.008 | type = Review }}</ref> Other well documented genes which increase the risk of developing Crohn's disease are ATG16L1,<ref name="Prescott NJ, Fisher SA, Franke A, Hampe J, Onnie CM, Soars D, Bagnall R, Mirza MM, Sanderson J, Forbes A, Mansfield JC, Lewis CM, Schreiber S, Mathew CG 2007 1665–71">{{cite journal | vauthors = Prescott NJ, Fisher SA, Franke A, Hampe J, Onnie CM, Soars D, Bagnall R, Mirza MM, Sanderson J, Forbes A, Mansfield JC, Lewis CM, Schreiber S, Mathew CG | 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 = 1665–1671 | date = May 2007 | pmid = 17484864 | doi = 10.1053/j.gastro.2007.03.034 | doi-access = free | title-link = doi }}</ref> IL23R,<ref>{{cite journal | vauthors = Diegelmann J, Czamara D, Le Bras E, Zimmermann E, Olszak T, Bedynek A, Göke B, Franke A, Glas J, Brand S | title = Intestinal DMBT1 expression is modulated by Crohn's disease-associated IL23R variants and by a DMBT1 variant which influences binding of the transcription factors CREB1 and ATF-2 | journal = PLOS ONE | volume = 8 | issue = 11 | article-number = e77773 | year = 2013 | pmid = 24223725 | pmc = 3818382 | doi = 10.1371/journal.pone.0077773 | doi-access = free | title-link = doi | bibcode = 2013PLoSO...877773D }}</ref> IRGM,<ref>{{cite journal | vauthors = Prescott NJ, Dominy KM, Kubo M, Lewis CM, Fisher SA, Redon R, Huang N, Stranger BE, Blaszczyk K, Hudspith B, Parkes G, Hosono N, Yamazaki K, Onnie CM, Forbes A, Dermitzakis ET, Nakamura Y, Mansfield JC, Sanderson J, Hurles ME, Roberts RG, Mathew CG | title = Independent and population-specific association of risk variants at the IRGM locus with Crohn's disease | journal = Human Molecular Genetics | volume = 19 | issue = 9 | pages = 1828–1839 | date = May 2010 | pmid = 20106866 | pmc = 2850616 | doi = 10.1093/hmg/ddq041 }}</ref> and SLC11A1.<ref>{{cite journal | vauthors = Chermesh I, Azriel A, Alter-Koltunoff M, Eliakim R, Karban A, Levi BZ | title = Crohn's disease and SLC11A1 promoter polymorphism | journal = Digestive Diseases and Sciences | volume = 52 | issue = 7 | pages = 1632–1635 | date = July 2007 | pmid = 17385031 | doi = 10.1007/s10620-006-9682-3 | s2cid = 11429585 }}</ref> There is considerable overlap between susceptibility loci for IBD and mycobacterial infections.<ref name="pmid23128233">{{cite journal | vauthors = Jostins L, Ripke S, Weersma RK, Duerr RH, McGovern DP, Hui KY, Lee JC, Schumm LP, Sharma Y, Anderson CA, Essers J, Mitrovic M, Ning K, Cleynen I, Theatre E, Spain SL, Raychaudhuri S, Goyette P, Wei Z, Abraham C, Achkar JP, Ahmad T, Amininejad L, Ananthakrishnan AN, Andersen V, Andrews JM, Baidoo L, Balschun T, Bampton PA, Bitton A, Boucher G, Brand S, Büning C, Cohain A, Cichon S, D'Amato M, De Jong D, Devaney KL, Dubinsky M, Edwards C, Ellinghaus D, Ferguson LR, Franchimont D, Fransen K, Gearry R, Georges M, Gieger C, Glas J, Haritunians T, Hart A, Hawkey C, Hedl M, Hu X, Karlsen TH, Kupcinskas L, Kugathasan S, Latiano A, Laukens D, Lawrance IC, Lees CW, Louis E, Mahy G, Mansfield J, Morgan AR, Mowat C, Newman W, Palmieri O, Ponsioen CY, Potocnik U, Prescott NJ, Regueiro M, Rotter JI, Russell RK, Sanderson JD, Sans M, Satsangi J, Schreiber S, Simms LA, Sventoraityte J, Targan SR, Taylor KD, Tremelling M, Verspaget HW, De Vos M, Wijmenga C, Wilson DC, Winkelmann J, Xavier RJ, Zeissig S, Zhang B, Zhang CK, Zhao H, Silverberg MS, Annese V, Hakonarson H, Brant SR, Radford-Smith G, Mathew CG, Rioux JD, Schadt EE, Daly MJ, Franke A, Parkes M, Vermeire S, Barrett JC, Cho JH | title = Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease | journal = Nature | volume = 491 | issue = 7422 | pages = 119–124 | date = November 2012 | pmid = 23128233 | pmc = 3491803 | doi = 10.1038/nature11582 | bibcode = 2012Natur.491..119. }}</ref> Genome-wide association studies have shown that Crohn's disease is genetically linked to coeliac disease.<ref>{{cite journal | vauthors = Walker MM, Murray JA | title = An update in the diagnosis of coeliac disease | journal = Histopathology | volume = 59 | issue = 2 | pages = 166–179 | date = August 2011 | pmid = 21054494 | doi = 10.1111/j.1365-2559.2010.03680.x | type = Review | s2cid = 5196629 | quote = Recent genome-wide association studies have shown that chronic inflammatory and autoimmune diseases are linked genetically to coeliac disease; for example, type 1 diabetes mellitus, Grave's disease and Crohn's disease. }}</ref>

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.<ref>{{cite news |vauthors=Coghlan A |title=A single gene can either raise or lower Crohn's disease risk |url=https://www.newscientist.com/article/single-gene-can-either-raise-lower-crohns-disease-risk/ |work=New Scientist |date=January 10, 2018 |access-date=November 5, 2020 |archive-date=November 9, 2020 |archive-url=https://web.archive.org/web/20201109041205/https://www.newscientist.com/article/single-gene-can-either-raise-lower-crohns-disease-risk/ |url-status=live}}</ref>

=== Immune system === There was a prevailing view that Crohn's disease is a primary T cell autoimmune disorder; however, a newer theory (published in 2008) hypothesizes that Crohn's results from an impaired innate immunity.<ref>{{cite journal | vauthors = Marks DJ, Segal AW | title = Innate immunity in inflammatory bowel disease: a disease hypothesis | journal = The Journal of Pathology | volume = 214 | issue = 2 | pages = 260–266 | date = January 2008 | pmid = 18161747 | pmc = 2635948 | doi = 10.1002/path.2291 }}</ref> 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.<ref name="Bact08" /><ref name="Marks2006" /> Another theory is that the inflammation of Crohn's was caused by an overactive Th1 and Th17 cytokine response.<ref>{{cite journal | vauthors = Cobrin GM, Abreu MT | title = Defects in mucosal immunity leading to Crohn's disease | journal = Immunological Reviews | volume = 206 | issue = 1 | pages = 277–295 | date = August 2005 | pmid = 16048555 | doi = 10.1111/j.0105-2896.2005.00293.x | s2cid = 37353838 }}</ref><ref>{{cite journal | vauthors = Elson CO, Cong Y, Weaver CT, Schoeb TR, McClanahan TK, Fick RB, Kastelein RA | title = Monoclonal anti-interleukin 23 reverses active colitis in a T cell-mediated model in mice | journal = Gastroenterology | volume = 132 | issue = 7 | pages = 2359–2370 | date = June 2007 | pmid = 17570211 | doi = 10.1053/j.gastro.2007.03.104 }}</ref>

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.<ref name="Prescott NJ, Fisher SA, Franke A, Hampe J, Onnie CM, Soars D, Bagnall R, Mirza MM, Sanderson J, Forbes A, Mansfield JC, Lewis CM, Schreiber S, Mathew CG 2007 1665–71" /> 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 responses.<ref>{{cite news |url=https://www.nytimes.com/2008/06/29/magazine/29wwln-essay-t.html |work=The New York Times |title=The Worm Turns |vauthors=Velasquez-Manoff M |date=June 29, 2008 |url-status=live |archive-url = https://web.archive.org/web/20170107144610/http://www.nytimes.com/2008/06/29/magazine/29wwln-essay-t.html |archive-date=January 7, 2017}}</ref>

=== Microbes === It is hypothesized that maintenance of commensal microorganism growth in the GI tract is dysregulated, either as a result or cause of immune dysregulation.<ref>{{cite journal | vauthors = Sartor RB | title = Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis | journal = Nature Clinical Practice. Gastroenterology & Hepatology | volume = 3 | issue = 7 | pages = 390–407 | date = July 2006 | pmid = 16819502 | doi = 10.1038/ncpgasthep0528 | s2cid = 3329677 }}</ref><ref name="pmid22508665">{{cite journal | vauthors = Dogan B, Scherl E, Bosworth B, Yantiss R, Altier C, McDonough PL, Jiang ZD, Dupont HL, Garneau P, Harel J, Rishniw M, Simpson KW | title = Multidrug resistance is common in Escherichia coli associated with ileal Crohn's disease | journal = Inflammatory Bowel Diseases | volume = 19 | issue = 1 | pages = 141–150 | date = January 2013 | pmid = 22508665 | doi = 10.1002/ibd.22971 | s2cid = 25518704 | doi-access = free | title-link = doi }}</ref>

There is an apparent connection between Crohn's disease, ''Mycobacterium'', other pathogenic bacteria, and genetic markers.<ref>{{cite journal | vauthors = Subramanian S, Roberts CL, Hart CA, Martin HM, Edwards SW, Rhodes JM, Campbell BJ | 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 | issue = 2 | pages = 427–434 | date = February 2008 | pmid = 18070962 | pmc = 2224732 | doi = 10.1128/AAC.00375-07 }}</ref><ref>{{cite journal | vauthors = Mpofu CM, Campbell BJ, Subramanian S, Marshall-Clarke S, Hart CA, Cross A, Roberts CL, McGoldrick A, Edwards SW, Rhodes JM | title = Microbial mannan inhibits bacterial killing by macrophages: a possible pathogenic mechanism for Crohn's disease | journal = Gastroenterology | volume = 133 | issue = 5 | pages = 1487–1498 | date = November 2007 | pmid = 17919633 | doi = 10.1053/j.gastro.2007.08.004 }}</ref> For instance, the genetic predisposition to Crohn's disease overlaps with susceptibility to leprosy, a mycobacterial disease.<ref>{{Cite journal |last1=Fava |first1=Vinicius M. |last2=Dallmann-Sauer |first2=Monica |last3=Schurr |first3=Erwin |date=2019-11-11 |title=Genetics of leprosy: today and beyond |url=http://link.springer.com/10.1007/s00439-019-02087-5 |journal=Human Genetics |language=en |volume=139 |issue=6–7 |pages=835–846 |doi=10.1007/s00439-019-02087-5 |pmid=31713021 |issn=0340-6717 |access-date=2025-07-29|url-access=subscription }}</ref> Several studies have suggested a causal role for ''Mycobacterium avium'' subspecies ''paratuberculosis'' (MAP), which causes a similar disease, Johne's disease, in cattle.<ref name="pmid16306778">{{cite journal | vauthors = Naser SA, Collins MT | title = Debate on the lack of evidence of Mycobacterium avium subsp. paratuberculosis in Crohn's disease | journal = Inflammatory Bowel Diseases | volume = 11 | issue = 12 | page = 1123 | date = December 2005 | pmid = 16306778 | doi = 10.1097/01.MIB.0000191609.20713.ea | doi-access = free | title-link = doi }}</ref><ref name="PMC4064085">{{cite journal | vauthors = Naser SA, Sagramsingh SR, Naser AS, Thanigachalam S | title = Mycobacterium avium subspecies paratuberculosis causes Crohn's disease in some inflammatory bowel disease patients | journal = World Journal of Gastroenterology | volume = 20 | issue = 23 | pages = 7403–7415 | date = June 2014 | pmid = 24966610 | pmc = 4064085 | doi = 10.3748/wjg.v20.i23.7403 | doi-access = free | title-link = doi }}</ref> 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.<ref>{{cite web |title=New insights into Crohn's Disease |url=http://www.liv.ac.uk/researchintelligence/issue33/crohns.htm|archive-url=https://web.archive.org/web/20130923151342/http://www.liv.ac.uk/researchintelligence/issue33/crohns.htm|archive-date=September 23, 2013}}</ref>

Other studies have linked Adherent-invasive Escherichia coli (AIEC) to the disease.<ref>{{cite journal | vauthors = Barnich N, Darfeuille-Michaud A | title = Adherent-invasive Escherichia coli and Crohn's disease | journal = Current Opinion in Gastroenterology | volume = 23 | issue = 1 | pages = 16–20 | date = January 2007 | pmid = 17133079 | doi = 10.1097/MOG.0b013e3280105a38 | s2cid = 23564986 }}</ref>

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.<ref name="pmid14683664">{{cite journal | vauthors = Hugot JP, Alberti C, Berrebi D, Bingen E, Cézard JP | title = Crohn's disease: the cold chain hypothesis | journal = Lancet | volume = 362 | issue = 9400 | pages = 2012–2015 | date = December 2003 | pmid = 14683664 | doi = 10.1016/S0140-6736(03)15024-6 | s2cid = 10254395 }}</ref><ref>{{cite news |title=Fridges blamed for Crohn's disease rise |work=Medical News Today |date=December 12, 2003 |url=http://www.medicalnewstoday.com/articles/4849.php |url-status=live |archive-url = https://web.archive.org/web/20090103190132/http://www.medicalnewstoday.com/articles/4849.php |archive-date=January 3, 2009}}</ref><ref>{{cite journal | vauthors = Forbes A, Kalantzis T | title = Crohn's disease: the cold chain hypothesis | journal = International Journal of Colorectal Disease | volume = 21 | issue = 5 | pages = 399–401 | date = July 2006 | pmid = 16059694 | doi = 10.1007/s00384-005-0003-7 | s2cid = 13271176 }}</ref>

There is also a tentative association between ''Candida'' colonization and Crohn's disease.<ref>{{cite journal | vauthors = Kumamoto CA | title = Inflammation and gastrointestinal Candida colonization | journal = Current Opinion in Microbiology | volume = 14 | issue = 4 | pages = 386–391 | date = August 2011 | pmid = 21802979 | pmc = 3163673 | doi = 10.1016/j.mib.2011.07.015 }}</ref>

Still, these relationships between specific pathogens and Crohn's disease remain unclear.<ref name="scah_out38">{{cite web |title=Possible links between Crohn's disease and Paratuberculosis |url=http://ec.europa.eu/food/fs/sc/scah/out38_en.pdf|archive-url=https://web.archive.org/web/20081217094053/http://ec.europa.eu/food/fs/sc/scah/out38_en.pdf|archive-date=December 17, 2008|access-date=November 7, 2009 |publisher=European Commission Directorate-General Health & Consumer Protection}}</ref><ref>{{cite journal | vauthors = 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 = The Journal of Antimicrobial Chemotherapy | volume = 39 | issue = 3 | pages = 393–400 | date = March 1997 | pmid = 9096189 | doi = 10.1093/jac/39.3.393 | doi-access = free | title-link = doi }}</ref>

=== Environmental factors === The increased incidence of Crohn's disease 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.<ref name="Shoda"> {{cite journal | vauthors = Shoda R, Matsueda K, Yamato S, Umeda N | 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 = The American Journal of Clinical Nutrition | volume = 63 | issue = 5 | pages = 741–745 | date = May 1996 | pmid = 8615358 | doi = 10.1093/ajcn/63.5.741 | doi-access = free | title-link = doi }}</ref> Those who consume vegetable proteins appear to have a lower incidence of Crohn's disease. Consumption of fish protein has no association.<ref name="Shoda" /> Smoking increases the risk of the return of active disease (flares).<ref name="Cosnes2004" /> 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.<ref> {{cite journal | vauthors = Lesko SM, Kaufman DW, Rosenberg L, Helmrich SP, Miller DR, Stolley PD, Shapiro S | title = Evidence for an increased risk of Crohn's disease in oral contraceptive users | journal = Gastroenterology | volume = 89 | issue = 5 | pages = 1046–1049 | date = November 1985 | pmid = 4043662 | doi = 10.1016/0016-5085(85)90207-0 }}</ref> Isotretinoin is associated with Crohn's.<ref>{{cite journal | vauthors = Reddy D, Siegel CA, Sands BE, Kane S | title = Possible association between isotretinoin and inflammatory bowel disease | journal = The American Journal of Gastroenterology | volume = 101 | issue = 7 | pages = 1569–1573 | date = July 2006 | pmid = 16863562 | doi = 10.1111/j.1572-0241.2006.00632.x | s2cid = 27663573 }}</ref><ref>{{cite journal | vauthors = Borobio E, Arín A, Valcayo A, Iñarrairaegui M, Nantes O, Prieto C | title = [Isotretinoin and ulcerous colitis] | language = es | journal = Anales del Sistema Sanitario de Navarra | volume = 27 | issue = 2 | pages = 241–243 | year = 2004 | pmid = 15381956 | doi = 10.4321/S1137-66272004000300009 | doi-access = free | title-link = doi }}</ref><ref>{{cite journal | vauthors = Reniers DE, Howard JM | title = Isotretinoin-induced inflammatory bowel disease in an adolescent | journal = The Annals of Pharmacotherapy | volume = 35 | issue = 10 | pages = 1214–1216 | date = October 2001 | pmid = 11675849 | doi = 10.1345/aph.10368 | s2cid = 22216642 |type=Case report}}</ref>

Although stress is sometimes claimed to exacerbate Crohn's disease, there is no concrete evidence to support such claim.<ref name="NIDDK2017" /> Still, it is well known that immune function is related to stress.<ref>{{cite journal | vauthors = Segerstrom SC, Miller GE | title = Psychological stress and the human immune system: a meta-analytic study of 30 years of inquiry | journal = Psychological Bulletin | volume = 130 | issue = 4 | pages = 601–630 | date = July 2004 | pmid = 15250815 | pmc = 1361287 | doi = 10.1037/0033-2909.130.4.601 }}</ref> 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 people with Crohn's.<ref>{{cite journal | vauthors = Lomer MC, Hutchinson C, Volkert S, Greenfield SM, Catterall A, Thompson RP, Powell JJ | title = Dietary sources of inorganic microparticles and their intake in healthy subjects and patients with Crohn's disease | journal = The British Journal of Nutrition | volume = 92 | issue = 6 | pages = 947–955 | date = December 2004 | pmid = 15613257 | doi = 10.1079/bjn20041276 | doi-access = free | title-link = doi | bibcode = 2004BrJN...92..947L }}</ref><ref>{{cite journal | vauthors = Powell JJ, Thoree V, Pele LC | title = Dietary microparticles and their impact on tolerance and immune responsiveness of the gastrointestinal tract | journal = The British Journal of Nutrition | volume = 98 | issue = Suppl 1 | pages = S59–S63 | date = October 2007 | pmid = 17922962 | pmc = 2737314 | doi = 10.1017/S0007114507832922 | bibcode = 2007BrJN...98S..59P }}</ref> The use of doxycycline has also been associated with increased risk of developing inflammatory bowel diseases.<ref>{{cite journal | vauthors = Lee TW, Russell L, Deng M, Gibson PR | title = Association of doxycycline use with the development of gastroenteritis, irritable bowel syndrome and inflammatory bowel disease in Australians deployed abroad | journal = Internal Medicine Journal | volume = 43 | issue = 8 | pages = 919–926 | date = August 2013 | pmid = 23656210 | doi = 10.1111/imj.12179 | s2cid = 9418654 }}</ref><ref name="tetracycline">{{cite journal | vauthors = Margolis DJ, Fanelli M, Hoffstad O, Lewis JD | title = Potential association between the oral tetracycline class of antimicrobials used to treat acne and inflammatory bowel disease | journal = The American Journal of Gastroenterology | volume = 105 | issue = 12 | pages = 2610–2616 | date = December 2010 | pmid = 20700115 | doi = 10.1038/ajg.2010.303 | s2cid = 20085592 }}</ref><ref>{{cite journal |vauthors=Garrett JP, Margolis DJ |title=Impact of Long-Term Antibiotic Use for Acne on Bacterial Ecology and Health Outcomes: A Review of Observational Studies |journal=Current Dermatology Reports |date=March 2012 |volume=1 |issue=1 |pages=23–28 |doi=10.1007/s13671-011-0001-7 |doi-access=free | title-link = doi }}</ref> In one large retrospective study, participants who were prescribed doxycycline for their acne had a 2.25-fold greater risk of developing Crohn's disease.<ref name="tetracycline" />

== Pathophysiology == {{Pathophysiology in CD vs. UC}} 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. Common features include a transmural pattern of inflammation, meaning the inflammation may span the entire depth of the intestinal wall.<ref name="Baumgart2012" /> Recent work has found that changes in NOD2 and in autophagy-related genes such as ATG16L1 can interfere with how immune cells in the gut recognize microbes and carry out normal cleanup processes. When this doesn't happen correctly, the intestine struggles to clear bacteria and leftover cellular material, which keeps inflammatory signals active. Researchers have also found that reduced ATG16L1 activity affects the development and stability of innate lymphoid cells and dendritic cells, both of which are important for keeping the gut's immune environment steady. When these cells aren't functioning properly, cytokine signaling becomes unbalanced and can eventually lead to tissue fibrosis. These findings help connect genetic risk factors with the ongoing inflammation that defines Crohn's disease.<ref>'''Parkes, M., Barrett, J. C., Prescott, N. J., Tremelling, M., Anderson, C. A., Fisher, S. A., and colleagues. "Sequence Variants in the Autophagy Gene ATG16L1 Influence Susceptibility to Crohn's Disease." ''Nature Genetics'', vol. 39, no. 2, 2007, pp. 207–211.'''</ref>

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.{{Citation needed|date=April 2025}} 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.<ref>{{cite book |vauthors=Crawford JM |chapter=17. The Gastrointestinal tract |veditors=Cotran RS, Kumar V, Robbins SL |title=Robbins Pathologic Basis of Disease |publisher=W.B. Saunders |edition=5th |date=1994 |isbn=0-7216-5032-5 |oclc=29702821}}</ref><ref>{{Cite journal |last1=Singh |first1=Rajbir |last2=Balasubramanian |first2=Iyshwarya |last3=Zhang |first3=Lanjing |last4=Gao |first4=Nan |date=March 31, 2020 |title=Metaplastic Paneth Cells in Extra-Intestinal Mucosal Niche Indicate a Link to Microbiome and Inflammation |journal=Frontiers in Physiology |volume=11 |article-number=280 |doi=10.3389/fphys.2020.00280 |doi-access=free | title-link = doi |pmid=32296343 |pmc=7138011 |issn=1664-042X}}</ref>

== Diagnosis == The diagnosis of Crohn's disease can sometimes be challenging,<ref name="Pimentel" /> and many 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 allows access to only the colon and lower portions of the small intestines; introduction of the capsule endoscopy<ref>{{Cite web|url=http://www.givenimaging.com/en-us/HealthcareProfessionals/Pages/pageHCP.aspx|archive-url=https://web.archive.org/web/20080616005419/http://www.givenimaging.com/en-us/HealthCareProfessionals/Pages/pageHCP.aspx|title=HCP: Pill Cam, Capsule Endoscopy, Esophageal Endoscopy|archive-date=June 16, 2008}}</ref> aids in endoscopic diagnosis. Intestinal ultrasound should be considered an early step in the diagnosis and follow-up of people with Crohn's disease, even in people with a proximal small bowel localization of the disease.<ref name="Novak_2021">{{cite journal | vauthors = Novak KL, Nylund K, Maaser C, Petersen F, Kucharzik T, Lu C, Allocca M, Maconi G, de Voogd F, Christensen B, Vaughan R, Palmela C, Carter D, Wilkens R | title = Expert Consensus on Optimal Acquisition and Development of the International Bowel Ultrasound Segmental Activity Score [IBUS-SAS]: A Reliability and Inter-rater Variability Study on Intestinal Ultrasonography in Crohn's Disease | journal = Journal of Crohn's & Colitis | volume = 15 | issue = 4 | pages = 609–616 | date = April 2021 | pmid = 33098642 | pmc = 8023841 | doi = 10.1093/ecco-jcc/jjaa216 }}</ref><ref name="Elli_2022">{{cite journal | vauthors = Elli L, Centorrino E, Costantino A, Vecchi M, Orlando S, Fraquelli M | title = Capsule enteroscopy versus small-bowel ultrasonography for the detection and differential diagnosis of intestinal diseases | journal = Clinical Endoscopy | volume = 55 | issue = 4 | pages = 532–539 | date = July 2022 | pmid = 35898151 | pmc = 9329643 | doi = 10.5946/ce.2021.224 }}</ref> Giant (multinucleate) cells, a common finding in the lesions of Crohn's disease, are less common in the lesions of lichen nitidus.<ref>{{cite journal | vauthors = Scheinfeld NS, Teplitz E, McClain SA | title = Crohn's disease and lichen nitidus: a case report and comparison of common histopathologic features | journal = Inflammatory Bowel Diseases | volume = 7 | issue = 4 | pages = 314–318 | date = November 2001 | pmid = 11720321 | doi = 10.1097/00054725-200111000-00006 | s2cid = 35892792 | doi-access = free | title-link = doi }}</ref> <gallery widths=180> CD colitis.jpg|Endoscopic image of Crohn's colitis showing deep ulceration CT scan gastric CD.jpg|CT scan showing Crohn's disease in the fundus of the stomach Crohn's transmural path.jpg|Section of colectomy showing transmural inflammation ResectedIleum.jpg|Resected ileum from a person with Crohn's disease </gallery>

=== Classification === thumb|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.

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.<ref>{{cite journal | vauthors = Tan WC, Allan RN | title = Diffuse jejunoileitis of Crohn's disease | journal = Gut | volume = 34 | issue = 10 | pages = 1374–1378 | date = October 1993 | pmid = 8244104 | pmc = 1374544 | doi = 10.1136/gut.34.10.1374 }}</ref> The disease can attack any part of the digestive tract, from the mouth to the anus. However, individuals affected by the disease rarely fall outside these three classifications, with presentations in other areas.<ref name="Baumgart2012" />

Crohn's disease may also be categorized by the behavior of the disease as it progresses. These categorizations are formalized in the Vienna classification of the disease.<ref name="Vienna">{{cite journal | vauthors = Gasche C, Scholmerich J, Brynskov J, D'Haens G, Hanauer SB, Irvine EJ, Jewell DP, Rachmilewitz D, Sachar DB, Sandborn WJ, Sutherland LR | title = A simple classification of Crohn's disease: report of the Working Party for the World Congresses of Gastroenterology, Vienna 1998 | journal = Inflammatory Bowel Diseases | volume = 6 | issue = 1 | pages = 8–15 | date = February 2000 | pmid = 10701144 | doi = 10.1002/ibd.3780060103 }}</ref> 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.<ref name="Vienna" /><ref>{{cite journal | vauthors = Dubinsky MC, Fleshner PP | title = Treatment of Crohn's Disease of Inflammatory, Stenotic, and Fistulizing Phenotypes | journal = Current Treatment Options in Gastroenterology | volume = 6 | issue = 3 | pages = 183–200 | date = June 2003 | pmid = 12744819 | doi = 10.1007/s11938-003-0001-1 | s2cid = 21302609 }}</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 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,<ref name="Baumgart2012" /> 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.<ref name="Hara2006" /> The utility of capsule endoscopy for this, however, is still uncertain.<ref>{{cite journal |vauthors = Triester SL, Leighton JA, Leontiadis GI, Gurudu SR, Fleischer DE, Hara AK, Heigh RI, Shiff AD, Sharma VK | title = A meta-analysis of the yield of capsule endoscopy compared to other diagnostic modalities in people with non-stricturing small bowel Crohn's disease | journal = The American Journal of Gastroenterology | volume = 101 | issue = 5 | pages = 954–964 | date = May 2006 | pmid = 16696781 | doi = 10.1111/j.1572-0241.2006.00506.x | s2cid = 25684863 }}</ref> A 2025 clinical guideline indicated that video capsule endoscopy is a useful adjunct in the diagnosis of people with small bowel Crohn's disease.<ref>{{Cite journal |last1=Lichtenstein |first1=Gary R. |last2=Loftus |first2=Edward V. |last3=Afzali |first3=Anita |last4=Long |first4=Millie D. |last5=Barnes |first5=Edward L. |last6=Isaacs |first6=Kim L. |last7=Ha |first7=Christina Y. |date=June 2025 |title=ACG Clinical Guideline: Management of Crohn's Disease in Adults |url=https://journals.lww.com/ajg/fulltext/2025/06000/acg_clinical_guideline__management_of_crohn_s.14.aspx |journal=American Journal of Gastroenterology |volume=120 |issue=6 |pages=1225–1264 |doi=10.14309/ajg.0000000000003465 |pmid=40701562 |issn=0002-9270|url-access=subscription }}</ref>

=== Radiologic tests === 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.<ref name="Hara2006">{{cite journal | vauthors = Hara AK, Leighton JA, Heigh RI, Sharma VK, Silva AC, De Petris G, Hentz JG, Fleischer DE | 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 = 128–134 | date = January 2006 | pmid = 16373764 | doi = 10.1148/radiol.2381050296 }}</ref><ref>{{cite journal | vauthors = Dixon PM, Roulston ME, Nolan DJ | title = The small bowel enema: a ten year review | journal = Clinical Radiology | volume = 47 | issue = 1 | pages = 46–48 | date = January 1993 | pmid = 8428417 | doi = 10.1016/S0009-9260(05)81213-9 }}</ref> 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).<ref>{{cite journal | vauthors = Carucci LR, Levine MS | title = Radiographic imaging of inflammatory bowel disease | journal = Gastroenterology Clinics of North America | volume = 31 | issue = 1 | pages = 93–117, ix | date = March 2002 | pmid = 12122746 | doi = 10.1016/S0889-8553(01)00007-3 }}</ref>

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols.<ref>{{cite journal | vauthors = Rajesh A, Maglinte DD | title = Multislice CT enteroclysis: technique and clinical applications | journal = Clinical Radiology | volume = 61 | issue = 1 | pages = 31–39 | date = January 2006 | pmid = 16356814 | doi = 10.1016/j.crad.2005.08.006 }}</ref> They are also useful for looking for intra-abdominal complications of Crohn's disease, such as abscesses, small bowel obstructions, or fistulae.<ref>{{cite journal | vauthors = Zissin R, Hertz M, Osadchy A, Novis B, Gayer G | 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 | date = February 2005 | pmid = 15835588 | url = https://www.proquest.com/openview/d36a211b9091938911c873b3ed55d0dc/1 | access-date = May 18, 2022 | url-status = live | archive-url = https://web.archive.org/web/20221007193456/https://www.proquest.com/openview/d36a211b9091938911c873b3ed55d0dc/1 | archive-date = October 7, 2022 }}</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 | vauthors = Mackalski BA, Bernstein CN | title = New diagnostic imaging tools for inflammatory bowel disease | journal = Gut | volume = 55 | issue = 5 | pages = 733–741 | date = May 2006 | pmid = 16609136 | pmc = 1856109 | doi = 10.1136/gut.2005.076612 }}</ref> MRI techniques such as diffusion-weighted imaging and high-resolution imaging are more sensitive in detecting ulceration and inflammation compared to CT.<ref>{{cite journal | vauthors = Sinha R, Rajiah P, Murphy P, Hawker P, Sanders S | title = Utility of high-resolution MR imaging in demonstrating transmural pathologic changes in Crohn disease | journal = Radiographics | volume = 29 | issue = 6 | pages = 1847–1867 | date = October 2009 | pmid = 19959525 | doi = 10.1148/rg.296095503 }}</ref><ref>{{cite journal | vauthors = Sinha R, Rajiah P, Ramachandran I, Sanders S, Murphy PD | title = Diffusion-weighted MR imaging of the gastrointestinal tract: technique, indications, and imaging findings | journal = Radiographics | volume = 33 | issue = 3 | pages = 655–76; discussion 676–80 | date = May 2013 | pmid = 23674768 | doi = 10.1148/rg.333125042 | doi-access = free | title-link = doi }}</ref>

=== Pediatrics considerations === Imaging in pediatric Crohn's disease requires careful consideration to minimize radiation exposure while ensuring accurate diagnosis and monitoring. Magnetic Resonance Enterography (MRE) is favored over Computed Tomography Enterography (CTE) due to its lack of ionizing radiation and superior soft tissue contrast. MRE effectively assesses bowel wall thickening, inflammation, and complications such as strictures or fistulas. However, it demands longer scan times and patient cooperation, which can be challenging for younger children.<ref>{{Cite journal |last=Casciani |first=Emanuele |date=2014 |title=Imaging of the small bowel: Crohn's disease in paediatric patients |journal=World Journal of Radiology |volume=6 |issue=6 |pages=313–328 |doi=10.4329/wjr.v6.i6.313 |doi-access=free | title-link = doi |issn=1949-8470 |pmc=4072817 |pmid=24976933}}</ref>

Ultrasound (US), particularly contrast-enhanced ultrasound, serves as a valuable, radiation-free alternative for evaluating bowel wall thickness, vascularity, and inflammatory changes. It is especially useful for initial assessments and ongoing disease monitoring, though its effectiveness can be operator-dependent.<ref>{{Cite journal |last=Chiorean |first=Liliana |date=2015 |title=Ultrasonographic imaging of inflammatory bowel disease in pediatric patients |journal=World Journal of Gastroenterology |volume=21 |issue=17 |pages=5231–5241 |doi=10.3748/wjg.v21.i17.5231 |doi-access=free | title-link = doi |issn=1007-9327 |pmc=4419063 |pmid=25954096}}</ref>

In urgent situations where rapid imaging is necessary to evaluate severe disease complications, such as bowel perforation or abscess formation, CTE may be utilized despite its associated radiation exposure.<ref>{{Cite journal |last1=Moore |first1=Michael M. |last2=Gee |first2=Michael S. |last3=Iyer |first3=Ramesh S. |last4=Chan |first4=Sherwin S. |last5=Ayers |first5=Travis D. |last6=Bardo |first6=Dianna M.E. |last7=Chandra |first7=Tushar |last8=Cooper |first8=Matthew L. |last9=Dotson |first9=Jennifer L. |last10=Gadepalli |first10=Samir K. |last11=Gill |first11=Anne E. |last12=Levin |first12=Terry L. |last13=Nadel |first13=Helen R. |last14=Schooler |first14=Gary R. |last15=Shet |first15=Narendra S. |date=May 2022 |title=ACR Appropriateness Criteria® Crohn Disease-Child |url=https://linkinghub.elsevier.com/retrieve/pii/S1546144022001909 |journal=Journal of the American College of Radiology |volume=19 |issue=5 |pages=S19–S36 |doi=10.1016/j.jacr.2022.02.020|pmid=35550801 |url-access=subscription }}</ref>

Regular imaging follow-ups should be guided by clinical symptoms and biomarkers to minimize unnecessary scans.<ref>{{Cite journal |last1=Gee |first1=Michael S. |last2=Nimkin |first2=Katherine |last3=Hsu |first3=Maylee |last4=Israel |first4=Esther J. |last5=Biller |first5=Jeffrey A. |last6=Katz |first6=Aubrey J. |last7=Mino-Kenudson |first7=Mari |last8=Harisinghani |first8=Mukesh G. |date=July 2011 |title=Prospective Evaluation of MR Enterography as the Primary Imaging Modality for Pediatric Crohn Disease Assessment |journal=American Journal of Roentgenology |volume=197 |issue=1 |pages=224–231 |doi=10.2214/AJR.10.5970 |issn=0361-803X |pmc=3711021 |pmid=21701034}}</ref> Emerging imaging techniques continue to improve the safety and efficacy of pediatric Crohn's disease evaluation.

=== Blood tests === A complete blood count may reveal anemia, which commonly is caused by blood loss leading to iron deficiency or by vitamin B{{sub|12}} deficiency, usually caused by ileal disease impairing vitamin B{{sub|12}} absorption. Rarely, autoimmune hemolysis may occur.<ref>{{cite journal | vauthors = Goh J, O'Morain CA | title = Review article: nutrition and adult inflammatory bowel disease | journal = Alimentary Pharmacology & Therapeutics | volume = 17 | issue = 3 | pages = 307–320 | date = February 2003 | pmid = 12562443 | doi = 10.1046/j.1365-2036.2003.01482.x | s2cid = 72099458 | doi-access = free | title-link = doi }}</ref> 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.<ref>{{cite journal | vauthors = Chamouard P, Richert Z, Meyer N, Rahmi G, Baumann R | title = Diagnostic value of C-reactive protein for predicting activity level of Crohn's disease | journal = Clinical Gastroenterology and Hepatology | volume = 4 | issue = 7 | pages = 882–887 | date = July 2006 | pmid = 16630759 | doi = 10.1016/j.cgh.2006.02.003 }}</ref>

Other causes of anemia include medication used in the 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<ref>{{cite journal | vauthors = Kaila B, Orr K, Bernstein CN | 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 = Canadian Journal of Gastroenterology | volume = 19 | issue = 12 | pages = 717–721 | date = December 2005 | pmid = 16341311 | doi = 10.1155/2005/147681 | doi-access = free | title-link = doi }}</ref> and to differentiate Crohn's disease from ulcerative colitis.<ref>{{cite journal | vauthors = Israeli E, Grotto I, Gilburd B, Balicer RD, Goldin E, Wiik A, Shoenfeld Y | title = Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease | journal = Gut | volume = 54 | issue = 9 | pages = 1232–1236 | date = September 2005 | pmid = 16099791 | pmc = 1774672 | doi = 10.1136/gut.2004.060228 }}</ref> 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.<ref>{{cite journal | vauthors = Ferrante M, Henckaerts L, Joossens M, Pierik M, Joossens S, Dotan N, Norman GL, Altstock RT, Van Steen K, Rutgeerts P, Van Assche G, Vermeire S | title = New serological markers in inflammatory bowel disease are associated with complicated disease behaviour | journal = Gut | volume = 56 | issue = 10 | pages = 1394–1403 | date = October 2007 | pmid = 17456509 | pmc = 2000264 | doi = 10.1136/gut.2006.108043 | first12 = S }}</ref><ref>{{cite journal | vauthors = Papp M, Altorjay I, Dotan N, Palatka K, Foldi I, Tumpek J, Sipka S, Udvardy M, Dinya T, Lakatos L, Kovacs A, Molnar T, Tulassay Z, Miheller P, Norman GL, Szamosi T, Papp J, Lakatos PL | 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 = The American Journal of Gastroenterology | volume = 103 | issue = 3 | pages = 665–681 | date = March 2008 | pmid = 18047543 | doi = 10.1111/j.1572-0241.2007.01652.x | s2cid = 6015339 }}</ref><ref>{{cite journal | vauthors = Seow CH, Stempak JM, Xu W, Lan H, Griffiths AM, Greenberg GR, Steinhart AH, Dotan N, Silverberg MS | title = Novel anti-glycan antibodies related to inflammatory bowel disease diagnosis and phenotype | journal = The American Journal of Gastroenterology | volume = 104 | issue = 6 | pages = 1426–1434 | date = June 2009 | pmid = 19491856 | doi = 10.1038/ajg.2009.79 | s2cid = 25021606 }}</ref><ref>{{cite journal | vauthors = Dotan I | title = Serologic markers in inflammatory bowel disease: tools for better diagnosis and disease stratification | journal = Expert Review of Gastroenterology & Hepatology | volume = 1 | issue = 2 | pages = 265–274 | date = December 2007 | pmid = 19072419 | doi = 10.1586/17474124.1.2.265 | s2cid = 32035337 }}</ref>

Low serum levels of vitamin D are associated with Crohn's disease.<ref name="IBD2015">{{cite journal | vauthors = Del Pinto R, Pietropaoli D, Chandar AK, Ferri C, Cominelli F | title = Association Between Inflammatory Bowel Disease and Vitamin D Deficiency: A Systematic Review and Meta-analysis | journal = Inflammatory Bowel Diseases | volume = 21 | issue = 11 | pages = 2708–2717 | date = November 2015 | pmid = 26348447 | pmc = 4615394 | doi = 10.1097/MIB.0000000000000546 }}</ref> Further studies are required to determine the significance of this association.<ref name="IBD2015" />

=== 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 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="Baumgart2012" /><ref name="emed" /><ref name="Podolsky" /> {{Findings in CD vs. UC}}

=== Differential diagnosis === 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.<ref name="WGO-IBD">{{cite web |url=http://www.worldgastroenterology.org/UserFiles/file/guidelines/inflammatory-bowel-disease-english-2015.pdf |title=Inflammatory Bowel Disease |date=August 2015 |publisher=World Gastroenterology Organization|access-date=March 13, 2016|archive-url=https://web.archive.org/web/20160314014940/http://www.worldgastroenterology.org/UserFiles/file/guidelines/inflammatory-bowel-disease-english-2015.pdf|archive-date=March 14, 2016}}</ref> Irritable bowel syndrome is excluded when there are inflammatory changes.<ref name="WGO-IBD" /> Celiac disease cannot be excluded if specific antibodies (anti-transglutaminase antibodies) are negative,<ref>{{cite journal | vauthors = Lewis NR, Scott BB | title = Systematic review: the use of serology to exclude or diagnose coeliac disease (a comparison of the endomysial and tissue transglutaminase antibody tests) | journal = Alimentary Pharmacology & Therapeutics | volume = 24 | issue = 1 | pages = 47–54 | date = July 2006 | pmid = 16803602 | doi = 10.1111/j.1365-2036.2006.02967.x | type = Review | s2cid = 16823218 | doi-access = free | title-link = doi | quote = Both the endomysial antibody and tissue transglutaminase antibody have very high sensitivities (93% for both) and specificities (>99% and >98% respectively) for the diagnosis of typical coeliac disease with villous atrophy. (...) As the detection of at least partial villous atrophy was used to make a diagnosis of coeliac disease in the vast majority of studies, we can't assume that the same LRs apply to coeliac patients with lesser abnormality, such as an increase in intraepithelial lymphocytes or electron-microscopic changes only. In fact, if such lesser abnormalities were used as criteria for diagnosing (and excluding) coeliac disease, the sensitivity of the tests could be lower (i.e. more false negatives), especially since a number of studies suggest that the EMA and tTG antibody tests are less sensitive with lesser degrees of mucosal abnormality }}</ref><ref>{{cite journal | vauthors = Rodrigo L, Garrote JA, Vivas S | title = [Celiac disease] | language = es | journal = Medicina Clinica | volume = 131 | issue = 7 | pages = 264–270 | date = September 2008 | pmid = 18775218 | doi = 10.1016/S0025-7753(08)72247-4 | url = http://www.elsevier.es/es-revista-medicina-clinica-2-articulo-enfermedad-celiaca-13125306 | access-date = March 13, 2016 | type = Review | archive-url = https://web.archive.org/web/20160319224000/http://www.elsevier.es/es-revista-medicina-clinica-2-articulo-enfermedad-celiaca-13125306 | quote = Estos marcadores presentan en general una elevada sensibilidad y especificidad (cercanas al 90%) en presencia de atrofia marcada de las vellosidades intestinales. Sin embargo, muestran una notable disminución de la sensibilidad (del orden del 40-50%) en casos con atrofia vellositaria leve o cambios mínimos. "These markers generally have high sensitivity and specificity (around 90%) in the presence of marked atrophy of the villi. However, they show a marked decrease in sensitivity (of the order of 40-50%) in cases with mild villous atrophy or minimal changes. | archive-date = March 19, 2016 | url-access = subscription }}</ref> nor in the absence of intestinal villi atrophy.<ref>{{cite journal | vauthors = Rostami Nejad M, Hogg-Kollars S, Ishaq S, Rostami K | title = Subclinical celiac disease and gluten sensitivity | journal = Gastroenterology and Hepatology from Bed to Bench | volume = 4 | issue = 3 | pages = 102–108 | date = 2011 | pmid = 24834166 | pmc = 4017418 | type = Review }}</ref><ref>{{cite journal | vauthors = Bold J, Rostami K | title = Gluten tolerance; potential challenges in treatment strategies | journal = Gastroenterology and Hepatology from Bed to Bench | volume = 4 | issue = 2 | pages = 53–57 | date = 2011 | pmid = 24834157 | pmc = 4017406 | type = Review }}</ref>

== Management == {{Main|Management of Crohn's disease}} {{Treatment in CD vs. UC}} 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 relapse. 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 |website=WebMD |vauthors=Fries WS, Nazario B |date=May 16, 2007 |access-date=February 14, 2008 |url-status=live |archive-url = https://web.archive.org/web/20080208234633/http://www.webmd.com/digestive-disorders/features/crohns-disease-54-tips-to-help-you-manage |archive-date=February 8, 2008}}</ref> Treatment for Crohn's disease involves first treating the acute problem and its symptoms, then maintaining remission of the disease.

=== Lifestyle changes === Certain lifestyle changes can reduce symptoms, including dietary adjustments, elemental diet, proper hydration, and smoking cessation. Some reviews underlined the importance of adopting diets that are best supported by evidence, even if little is known about the impact of diets on these people.<ref>{{cite journal | vauthors = Roncoroni L, Gori R, Elli L, Tontini GE, Doneda L, Norsa L, Cuomo M, Lombardo V, Scricciolo A, Caprioli F, Costantino A, Scaramella L, Vecchi M | title = Nutrition in Patients with Inflammatory Bowel Diseases: A Narrative Review | journal = Nutrients | volume = 14 | issue = 4 | page = 751 | date = February 2022 | pmid = 35215401 | pmc = 8879392 | doi = 10.3390/nu14040751 | doi-access = free | title-link = doi }}</ref><ref>{{cite journal | vauthors = Ananthakrishnan AN, Kaplan GG, Bernstein CN, Burke KE, Lochhead PJ, Sasson AN, Agrawal M, Tiong JH, Steinberg J, Kruis W, Steinwurz F, Ahuja V, Ng SC, Rubin DT, Colombel JF, Gearry R | title = Lifestyle, behaviour, and environmental modification for the management of patients with inflammatory bowel diseases: an International Organization for Study of Inflammatory Bowel Diseases consensus | journal = The Lancet. Gastroenterology & Hepatology | volume = 7 | issue = 7 | pages = 666–678 | date = July 2022 | pmid = 35487235 | doi = 10.1016/S2468-1253(22)00021-8 | url = https://pure.amsterdamumc.nl/en/publications/021ce789-c2f2-4d1f-b8c1-0b25da701b09 }}</ref> 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.<ref>{{cite journal | vauthors = Hou JK, Abraham B, El-Serag H | title = Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature | journal = The American Journal of Gastroenterology | volume = 106 | issue = 4 | pages = 563–573 | date = April 2011 | pmid = 21468064 | doi = 10.1038/ajg.2011.44 | s2cid = 10337669 }}</ref> 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. Despite the recognized importance of dietary fiber for intestinal health, some people should follow a low residue diet to control acute symptoms, especially if foods high in insoluble fiber cause symptoms, e.g., due to obstruction or irritation of the bowel.<ref name="WebMD" /> 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), for example, lactose.<ref>{{cite book |vauthors=Escott-Stump S |title=Nutrition and Diagnosis-Related Care, 7th edition |year=2008 |publisher=Lippincott Williams & Wilkins |location=Baltimore, MD |isbn=978-1-60831-017-3 |pages=1020 (pp 431)}}</ref> Fatigue can be helped with regular exercise, a healthy diet, and enough sleep, and for those with malabsorption of vitamin B12 due to disease or surgical resection of the terminal ileum, cobalamin injections. Smoking may worsen symptoms and the course of the disease, and stopping is recommended. Alcohol consumption can also worsen symptoms, and moderation or cessation is advised.<ref name="WebMD" /> Many patients with Crohn's disease tend to follow restrictive diets to control symptoms. Usually, lactose-free diets are the most common diet followed by patients with Crohn's disease (17.4% vs 11.6% controls), followed by Gluten-free diet (13.4% CD vs 9.3% in controls). Low-FODMAP diet adoption is usually minimal. Fibre avoidance is higher in patients with Crohn's disease (52%) compared to controls (5%).<ref>Scricciolo, A., Lombardo, V., Bascuñán, K.A. et al. Assessment of nutritional status and eating behaviours in patients with chronic inflammatory bowel disease: a pilot study. Eur J Clin Nutr (2025). https://doi.org/10.1038/s41430-025-01645-7</ref>

=== Medication === Acute treatment uses medications to treat any infection (normally antibiotics) and to reduce inflammation (normally corticosteroids). When symptoms are in remission, treatment enters maintenance, intending to avoid 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 can maintain the treatment, and many require immunosuppressive drugs.<ref name="HanauerCrohns" /> It has also been suggested that antibiotics change the enteric flora, and their continuous use may pose the risk of overgrowth with pathogens such as ''Clostridioides difficile''.<ref name="Shanahan">{{cite journal | vauthors = Shanahan F | title = Crohn's disease | journal = Lancet | volume = 359 | issue = 9300 | pages = 62–69 | date = January 2002 | pmid = 11809204 | doi = 10.1016/S0140-6736(02)07284-7 | s2cid = 743620 }}</ref>

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,<ref name="pmid29338679">{{cite journal | vauthors = Djurić Z, Šaranac L, Budić I, Pavlović V, Djordjević J | title = Therapeutic role of methotrexate in pediatric Crohn's disease | journal = Bosnian Journal of Basic Medical Sciences | volume = 18 | issue = 3 | pages = 211–216 | date = August 2018 | pmid = 29338679 | pmc = 6087553 | doi = 10.17305/bjbms.2018.2792 }}</ref> and anti-TNF therapies and monoclonal antibodies, such as infliximab, adalimumab,<ref name="Podolsky">{{cite journal | vauthors = Podolsky DK | title = Inflammatory bowel disease | journal = The New England Journal of Medicine | volume = 347 | issue = 6 | pages = 417–429 | date = August 2002 | pmid = 12167685 | doi = 10.1056/NEJMra020831 | url = http://gut.bmj.com/cgi/content/short/39/Suppl_1/A15 | access-date = September 4, 2018 | url-status = live | type = Submitted manuscript | archive-url = https://web.archive.org/web/20210428151606/https://gut.bmj.com/cgi/content/short/39/Suppl_1/A15 | archive-date = April 28, 2021 | url-access = subscription }}</ref> certolizumab,<ref>{{cite press release |url=https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116882.htm |title=FDA Approves Cimzia to Treat Crohn's Disease |publisher=Food and Drug Administration (FDA) |date=April 22, 2008 |access-date=November 5, 2009 |archive-url=https://web.archive.org/web/20091020111256/https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116882.htm |archive-date=October 20, 2009}}</ref> vedolizumab, ustekinumab,<ref>{{cite web |title=Prescribing information ustekinumab |url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/125261s147lbl.pdf |website=FDA |access-date=May 23, 2019 |archive-date=October 18, 2020 |archive-url=https://web.archive.org/web/20201018151109/https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/125261s147lbl.pdf |url-status=live}}</ref> natalizumab,<ref>{{cite journal | vauthors = Sandborn WJ, Colombel JF, Enns R, Feagan BG, Hanauer SB, Lawrance IC, Panaccione R, Sanders M, Schreiber S, Targan S, van Deventer S, Goldblum R, Despain D, Hogge GS, Rutgeerts P | title = Natalizumab induction and maintenance therapy for Crohn's disease | journal = The New England Journal of Medicine | volume = 353 | issue = 18 | pages = 1912–1925 | date = November 2005 | pmid = 16267322 | doi = 10.1056/NEJMoa043335 | collaboration = International Efficacy of Natalizumab as Active Crohn's Therapy (ENACT-1) Trial Group; Evaluation of Natalizumab as Continuous Therapy (ENACT-2) Trial Group | doi-access = free | title-link = doi }}</ref><ref>{{cite journal | vauthors = Nelson SM, Nguyen TM, McDonald JW, MacDonald JK | title = Natalizumab for induction of remission in Crohn's disease | journal = The Cochrane Database of Systematic Reviews | volume = 2018 | issue = 8 | article-number = CD006097 | date = August 2018 | pmid = 30068022 | pmc = 6513248 | doi = 10.1002/14651858.CD006097.pub3 }}</ref> risankizumab-rzaa, and upadacitinib<ref>{{Cite web |title=Discover RINVOQ® (upadacitinib) |url=https://www.rinvoq.com/ |access-date=May 29, 2023 |website=RINVOQ |archive-date=May 18, 2023 |archive-url=https://web.archive.org/web/20230518231109/https://www.rinvoq.com/ |url-status=live}}</ref> Hydrocortisone should be used in severe attacks of Crohn's disease.<ref name="OHCM">{{cite book |vauthors=Longmore M, Wilkinson I, Turmezei T, Cheung CK |title=Oxford Handbook of Clinical Medicine |edition=7th |publisher=Oxford University Press |year=2007 |pages=266–7 |isbn=978-0-19-856837-7}}</ref> Biological therapies are medications used to avoid long-term steroid use, decrease inflammation, and treat people who have fistulas with abscesses.<ref name="ustekinumab" /> The monoclonal antibody ustekinumab appears to be a safe treatment option, and may help people with moderate to severe active Crohn's disease.<ref name=":0">{{Cite journal |last1=Hasskamp |first1=Johannes |last2=Meinhardt |first2=Christian |last3=Timmer |first3=Antje |date=2025-05-13 |title=Anti-IL-12/23p40 antibodies for induction of remission in Crohn's disease |journal=The Cochrane Database of Systematic Reviews |volume=2025 |issue=5 |article-number=CD007572 |doi=10.1002/14651858.CD007572.pub4 |issn=1469-493X |pmc=12070676 |pmid=40357993 }}</ref> The long term safety and effectiveness of monoclonal antibody treatment is not known.<ref name=":0" /> The monoclonal antibody briakinumab is not effective for people with active Crohn's disease and it is no longer being manufactured.<ref name=":0" />

The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routine monitoring for this.<ref name="Mowat2011">{{cite journal | vauthors = Mowat C, Cole A, Windsor A, Ahmad T, Arnott I, Driscoll R, Mitton S, Orchard T, Rutter M, Younge L, Lees C, Ho GT, Satsangi J, Bloom S | title = Guidelines for the management of inflammatory bowel disease in adults | journal = Gut | volume = 60 | issue = 5 | pages = 571–607 | date = May 2011 | pmid = 21464096 | doi = 10.1136/gut.2010.224154 | s2cid = 8269837 | url = https://discovery.dundee.ac.uk/en/publications/fd12256b-cdfa-44b8-843c-46d0d3b1f238 | collaboration = IBD Section of the British Society of Gastroenterology }}</ref><ref name="ReferenceA">{{cite journal | vauthors = Goddard AF, James MW, McIntyre AS, Scott BB | title = Guidelines for the management of iron deficiency anaemia | journal = Gut | volume = 60 | issue = 10 | pages = 1309–1316 | date = October 2011 | pmid = 21561874 | doi = 10.1136/gut.2010.228874 | doi-access = free | title-link = doi }}</ref><ref name="ReferenceB">{{cite journal | vauthors = Gasche C, Berstad A, Befrits R, Beglinger C, Dignass A, Erichsen K, Gomollon F, Hjortswang H, Koutroubakis I, Kulnigg S, Oldenburg B, Rampton D, Schroeder O, Stein J, Travis S, Van Assche G | title = Guidelines on the diagnosis and management of iron deficiency and anemia in inflammatory bowel diseases | journal = Inflammatory Bowel Diseases | volume = 13 | issue = 12 | pages = 1545–1553 | date = December 2007 | pmid = 17985376 | doi = 10.1002/ibd.20285 | doi-access = free | title-link = doi }}</ref>

=== Immunosuppressant therapies, infection risks, and vaccinations ===

Many people affected by Crohn's disease need immunosuppressant therapies, which are known to be associated with a higher risk of contracting opportunistic infectious diseases and of pre-neoplastic or neoplastic lesions such as cervical high-grade dysplasia and cancer.<ref>{{cite journal | vauthors = Beaugerie L, Itzkowitz SH | title = Cancers complicating inflammatory bowel disease | journal = The New England Journal of Medicine | volume = 372 | issue = 15 | pages = 1441–1452 | date = April 2015 | pmid = 25853748 | doi = 10.1056/NEJMra1403718 }}</ref><ref>{{cite journal | vauthors = Toruner M, Loftus EV, Harmsen WS, Zinsmeister AR, Orenstein R, Sandborn WJ, Colombel JF, Egan LJ | title = Risk factors for opportunistic infections in patients with inflammatory bowel disease | journal = Gastroenterology | volume = 134 | issue = 4 | pages = 929–936 | date = April 2008 | pmid = 18294633 | doi = 10.1053/j.gastro.2008.01.012 }}</ref> Many of these potentially harmful diseases, such as Hepatitis B, Influenza, herpes zoster virus, pneumococcal pneumonia, or human papilloma virus, can be prevented by vaccines.<ref>{{cite journal | vauthors = Farraye FA, Melmed GY, Lichtenstein GR, Kane SV | title = ACG Clinical Guideline: Preventive Care in Inflammatory Bowel Disease | journal = The American Journal of Gastroenterology | volume = 112 | issue = 2 | pages = 241–258 | date = February 2017 | pmid = 28071656 | doi = 10.1038/ajg.2016.537 }}</ref> Compared to the rest of the population, people affected by IBD are known to be at higher risk of contracting some vaccine-preventable diseases such as the flu and pneumonia.<ref>{{cite journal | vauthors = Ananthakrishnan AN, McGinley EL | title = Infection-related hospitalizations are associated with increased mortality in patients with inflammatory bowel diseases | journal = Journal of Crohn's & Colitis | volume = 7 | issue = 2 | pages = 107–112 | date = March 2013 | pmid = 22440891 | doi = 10.1016/j.crohns.2012.02.015 }}</ref> Nevertheless, despite the increased risk of infections, vaccination rates in people with IBD are known to be suboptimal and may also be lower than vaccination rates in the general population.<ref>{{cite journal | vauthors = Malhi G, Rumman A, Thanabalan R, Croitoru K, Silverberg MS, Hillary Steinhart A, Nguyen GC | title = Vaccination in inflammatory bowel disease patients: attitudes, knowledge, and uptake | journal = Journal of Crohn's & Colitis | volume = 9 | issue = 6 | pages = 439–444 | date = June 2015 | pmid = 25908717 | doi = 10.1093/ecco-jcc/jjv064 }}</ref><ref>{{cite journal | vauthors = Costantino A, Michelon M, Noviello D, Macaluso FS, Leone S, Bonaccorso N, Costantino C, Vecchi M, Caprioli F | title = Attitudes towards Vaccinations in a National Italian Cohort of Patients with Inflammatory Bowel Disease | journal = Vaccines | volume = 11 | issue = 10 | page = 1591 | date = October 2023 | pmid = 37896993 | pmc = 10611209 | doi = 10.3390/vaccines11101591 | doi-access = free | title-link = doi }}</ref>

=== Surgery === 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.<ref>{{cite journal | vauthors = Kristo I, Stift A, Bergmann M, Riss S | title = Surgical recurrence in Crohn's disease: Are we getting better? | journal = World Journal of Gastroenterology | volume = 21 | issue = 20 | pages = 6097–6100 | date = May 2015 | pmid = 26034346 | pmc = 4445088 | doi = 10.3748/wjg.v21.i20.6097 | doi-access = free | title-link = doi }}</ref> 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.{{Citation needed|date=February 2025}} For people with an obstruction due to a stricture, two options for treatment are strictureplasty and resection of that portion of the 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.<ref name="pmid8918424">{{cite journal | vauthors = Ozuner G, Fazio VW, Lavery IC, Milsom JW, Strong SA | title = Reoperative rates for Crohn's disease following strictureplasty. Long-term analysis | journal = Diseases of the Colon and Rectum | volume = 39 | issue = 11 | pages = 1199–1203 | date = November 1996 | pmid = 8918424 | doi = 10.1007/BF02055108 | s2cid = 33628350 }}</ref>

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 "Rutgeerts score" is an endoscopic scoring system for postoperative disease recurrence in Crohn's disease. Postsurgical remission per the Rutgeerts score is graded as i0; while mild postsurgical recurrences are graded i1 and i2, and moderate to severe recurrences are graded i3 and i4.<ref name="pmid2394349">{{cite journal | vauthors = Rutgeerts P, Geboes K, Vantrappen G, Beyls J, Kerremans R, Hiele M | title = Predictability of the postoperative course of Crohn's disease | journal = Gastroenterology | volume = 99 | issue = 4 | pages = 956–963 | date = October 1990 | pmid = 2394349 | doi = 10.1016/0016-5085(90)90613-6 | doi-access = free | title-link = doi }}</ref> 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.<ref name="pmid24917974">{{cite journal | vauthors = Yamamoto T, Bamba T, Umegae S, Matsumoto K | title = The impact of early endoscopic lesions on the clinical course of patients following ileocolonic resection for Crohn's disease: A 5-year prospective cohort study | journal = United European Gastroenterology Journal | volume = 1 | issue = 4 | pages = 294–298 | date = August 2013 | pmid = 24917974 | pmc = 4040796 | doi = 10.1177/2050640613495197 }}</ref>

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 people who have had half or more of their small intestines removed.<ref>{{cite web |title=Short Bowel Syndrome |website=National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) |date=July 2015 |url=https://www.niddk.nih.gov/health-information/digestive-diseases/short-bowel-syndrome |archive-url=https://web.archive.org/web/20191209002943/https://www.niddk.nih.gov/health-information/digestive-diseases/short-bowel-syndrome |archive-date=December 9, 2019 |access-date=December 8, 2019}}</ref> 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.<ref>{{cite web |url=http://www.revolutionhealth.com/conditions/digestive/crohns-disease/surgery/intestinal-transplant |title=Intestinal transplant for Crohn's disease |vauthors=Rhodes M |date=October 24, 2006 |publisher=Everyday Health|access-date=March 22, 2009|url-status=live|archive-url=https://web.archive.org/web/20081008034121/http://www.revolutionhealth.com/conditions/digestive/crohns-disease/surgery/intestinal-transplant|archive-date=October 8, 2008}}</ref>

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.<ref>{{cite journal | vauthors = Hofmann AF | title = The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy | journal = Gastroenterology | volume = 52 | issue = 4 | pages = 752–757 | date = April 1967 | pmid = 5337211 | doi = 10.1016/S0016-5085(67)80140-9 | doi-access = free | title-link = doi }}</ref>

=== Microbiome modification === The use of oral probiotic supplements to modify the composition and behaviour of the gastrointestinal microbiome has been researched to understand whether it may help to improve remission rates in people with Crohn's disease. However, only two controlled trials were available in 2020, with no clear overall evidence of higher remission nor lower adverse effects, in people with Crohn's disease receiving probiotic supplementation.<ref>{{cite journal | vauthors = Limketkai BN, Akobeng AK, Gordon M, Adepoju AA | title = Probiotics for induction of remission in Crohn's disease | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 7 | article-number = CD006634 | date = July 2020 | pmid = 32678465 | pmc = 7389339 | doi = 10.1002/14651858.CD006634.pub3 | collaboration = Cochrane Gut Group }}</ref>

=== Mental health === Crohn's may result in anxiety or mood disorders, especially in young people who may have stunted growth or embarrassment from fecal incontinence.<ref name="Szigethy">{{cite journal | vauthors = Szigethy E, McLafferty L, Goyal A | title = Inflammatory bowel disease | journal = Child and Adolescent Psychiatric Clinics of North America | volume = 19 | issue = 2 | pages = 301–18, ix | date = April 2010 | pmid = 20478501 | doi = 10.1016/j.chc.2010.01.007 | url = http://gut.bmj.com/cgi/content/short/39/Suppl_1/A15 | access-date = September 4, 2018 | url-status = live | type = Submitted manuscript | archive-url = https://web.archive.org/web/20210428151606/https://gut.bmj.com/cgi/content/short/39/Suppl_1/A15 | archive-date = April 28, 2021 | url-access = subscription }}</ref> Counselling as well as antidepressant or anxiolytic medication may help some people manage.<ref name="Szigethy" />

{{as of|2017}} there is a small amount of research looking at mindfulness-based therapies, hypnotherapy, and cognitive behavioural therapy.<ref>{{cite journal | vauthors = Ballou S, Keefer L | title = Psychological Interventions for Irritable Bowel Syndrome and Inflammatory Bowel Diseases | journal = Clinical and Translational Gastroenterology | volume = 8 | issue = 1 | pages = e214 | date = January 2017 | pmid = 28102860 | pmc = 5288603 | doi = 10.1038/ctg.2016.69 }}</ref> A meta-analysis of interventions to improve mood (including talking therapy, antidepressants, and exercise) in people with inflammatory bowel disease found that they reduced inflammatory markers such as C-reactive protein and faecal calprotectin. Psychological therapies reduced inflammation more than antidepressants or exercise.<ref>{{cite journal | vauthors = Seaton N, Hudson J, Harding S, Norton S, Mondelli V, Jones AS, Moss-Morris R | title = Do interventions for mood improve inflammatory biomarkers in inflammatory bowel disease?: a systematic review and meta-analysis | journal = eBioMedicine | volume = 100 | article-number = 104910 | date = February 2024 | pmid = 38272759 | pmc = 10878994 | doi = 10.1016/j.ebiom.2023.104910 }}</ref><ref>{{Cite journal |date=July 17, 2024 |title=Improving mood reduces inflammation in inflammatory bowel disease |url=https://evidence.nihr.ac.uk/alert/improving-mood-reduces-inflammation-in-inflammatory-bowel-disease/ |journal=NIHR Evidence|doi=10.3310/nihrevidence_63192 |url-access=subscription |doi-access=free }}</ref>

=== Alternative medicine === It is common for people with Crohn's disease to try complementary or alternative therapy.<ref name="Caprilli_2006">{{cite journal | vauthors = Caprilli R, Gassull MA, Escher JC, Moser G, Munkholm P, Forbes A, Hommes DW, Lochs H, Angelucci E, Cocco A, Vucelic B, Hildebrand H, Kolacek S, Riis L, Lukas M, de Franchis R, Hamilton M, Jantschek G, Michetti P, O'Morain C, Anwar MM, Freitas JL, Mouzas IA, Baert F, Mitchell R, Hawkey CJ | title = European evidence based consensus on the diagnosis and management of Crohn's disease: special situations | journal = Gut | volume = 55 | issue = Suppl 1 | pages = i36–i58 | date = March 2006 | pmid = 16481630 | pmc = 1859996 | doi = 10.1136/gut.2005.081950c | quote = the colitis activity index fell significantly in the treatment group compared to the sham acupuncture group. However, recruitment did not reach its target, and the number of patients was small. | collaboration = European Crohn's Colitis Organisation }}</ref> These include diets, probiotics, fish oil, and other herbal and nutritional supplements. 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.<ref>{{cite journal | vauthors = Joos S | title = Review on efficacy and health services research studies of complementary and alternative medicine in inflammatory bowel disease | journal = Chinese Journal of Integrative Medicine | volume = 17 | issue = 6 | pages = 403–409 | date = June 2011 | pmid = 21660673 | doi = 10.1007/s11655-011-0758-3 | s2cid = 207298246 }}</ref> * There is insufficient evidence to recommend the use of acupuncture.<ref name="Caprilli_2006" /> * Homeopathic preparations are of no benefit with this or any other condition.<ref>{{cite journal |vauthors=Smith K |title=Homeopathy is Unscientific and Unethical |journal=Bioethics |volume=26 |issue=9 |doi=10.1111/j.1467-8519.2011.01956.x |pages=508–512 |year=2012 |s2cid=143067523 |url=https://zenodo.org/record/1035885 |access-date=October 28, 2017 |archive-date=October 29, 2017 |archive-url=https://web.archive.org/web/20171029012949/https://zenodo.org/record/1035885 |url-status=live}}</ref> * There is no good evidence that cannabis or cannabis oil is an effective or safe treatment.<ref>{{cite journal | vauthors = Kafil TS, Nguyen TM, MacDonald JK, Chande N | title = Cannabis for the treatment of Crohn's disease | journal = The Cochrane Database of Systematic Reviews | volume = 11 | issue = 11 | article-number = CD012853 | date = November 2018 | pmid = 30407616 | pmc = 6517156 | doi = 10.1002/14651858.CD012853.pub2 }}</ref>

== Prognosis == 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 recurs, 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.<ref name="ACG_Guideline">{{cite journal | vauthors = Lichtenstein GR, Loftus EV, Isaacs KL, Regueiro MD, Gerson LB, Sands BE | title = ACG Clinical Guideline: Management of Crohn's Disease in Adults | journal = The American Journal of Gastroenterology | volume = 113 | issue = 4 | pages = 481–517 | date = April 2018 | pmid = 29610508 | doi = 10.1038/ajg.2018.27 | s2cid = 4568430 }}</ref> Most people diagnosed with Crohn's require surgery for complications or symptoms of the disease within their lifetime, although the rate associated with this is decreasing with better access to modern treatments.<ref>{{Cite journal |last1=Dittrich |first1=Alexandra E. |last2=Sutton |first2=Reed Taylor |last3=Haynes |first3=Kate |last4=Wang |first4=Haili |last5=Fedorak |first5=Richard N. |last6=Kroeker |first6=Karen I. |date=2020-11-19 |title=Incidence Rates for Surgery in Crohn's Disease Have Decreased: A Population-based Time-trend Analysis |journal=Inflammatory Bowel Diseases |volume=26 |issue=12 |pages=1909–1916 |doi=10.1093/ibd/izz315 |issn=1536-4844 |pmid=31895949}}</ref> Most people with Crohn's live a normal lifespan.<ref>{{cite web |url=http://www.umm.edu/patiented/articles/who_gets_crohns_disease_000103_5.htm |title=Crohn's disease - Prognosis |publisher=University of Maryland Medical Centre|access-date=October 19, 2012|url-status=live|archive-url=https://web.archive.org/web/20120829165909/http://www.umm.edu/patiented/articles/who_gets_crohns_disease_000103_5.htm|archive-date=August 29, 2012}}</ref> However, Crohn's disease is associated with a much greater increase in risk of small bowel and colorectal carcinoma (bowel cancer).<ref>{{cite journal | vauthors = Canavan C, Abrams KR, Mayberry J | title = Meta-analysis: colorectal and small bowel cancer risk in patients with Crohn's disease | journal = Alimentary Pharmacology & Therapeutics | volume = 23 | issue = 8 | pages = 1097–1104 | date = April 2006 | pmid = 16611269 | doi = 10.1111/j.1365-2036.2006.02854.x | s2cid = 25193522 | doi-access = free | title-link = doi }}</ref>

== Epidemiology == 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 & Colitis Foundation of America cites this number as approx 149:100,000; NIH cites 28 to 199 per 100,000.<ref name="Hiatt">{{cite journal | vauthors = Hiatt RA, Kaufman L | title = Epidemiology of inflammatory bowel disease in a defined northern California population | journal = The Western Journal of Medicine | volume = 149 | issue = 5 | pages = 541–546 | date = November 1988 | pmid = 3250100 | pmc = 1026530 }}</ref><ref>{{cite journal | vauthors = Moum B, Vatn MH, Ekbom A, Aadland E, Fausa O, Lygren I, Stray N, Sauar J, Schulz T | 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 = 355–361 | date = April 1996 | pmid = 8726303 | doi = 10.3109/00365529609006410 }}</ref> Crohn's disease is more common in northern countries, and with higher rates still in the northern areas of these countries.<ref>{{cite journal | vauthors = Shivananda S, Lennard-Jones J, Logan R, Fear N, Price A, Carpenter L, van Blankenstein M | 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 = 690–697 | date = November 1996 | pmid = 9014768 | pmc = 1383393 | doi = 10.1136/gut.39.5.690 }}</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="Baumgart2012" /><ref>{{cite journal | vauthors = Yang H, McElree C, Roth MP, Shanahan F, Targan SR, Rotter JI | title = Familial empirical risks for inflammatory bowel disease: differences between Jews and non-Jews | journal = Gut | volume = 34 | issue = 4 | pages = 517–524 | date = April 1993 | pmid = 8491401 | pmc = 1374314 | doi = 10.1136/gut.34.4.517 }}</ref> and smokers.<ref name="pmid19067428">{{cite journal | vauthors = Seksik P, Nion-Larmurier I, Sokol H, Beaugerie L, Cosnes J | title = Effects of light smoking consumption on the clinical course of Crohn's disease | journal = Inflammatory Bowel Diseases | volume = 15 | issue = 5 | pages = 734–741 | date = May 2009 | pmid = 19067428 | doi = 10.1002/ibd.20828 | s2cid = 10988974 | doi-access = free | title-link = doi }}</ref>

Crohn's disease begins most commonly in people in their teens and 20s, and people in their 50s through to their 70s.<ref name="Baumgart2012" /><ref name="emed" /><ref name="eMedicineHealth" /> It is rarely diagnosed in early childhood. It usually affects female children more severely than males.<ref>{{cite web |url=http://www.ccfa.org/reuters/ibdboysgirls |title=Crohn's disease manifests differently in boys and girls |publisher=Crohn's and Colitis Foundation of America |archive-url=https://web.archive.org/web/20080216141623/http://www.ccfa.org/reuters/ibdboysgirls |archive-date=February 16, 2008}}</ref> However, only slightly more women than men have Crohn's disease.<ref>{{cite web | vauthors = Rhodes M, Romito K, Vanagunas AD | date = October 24, 2006 | veditors = Ariss KM, Cronen M, Truman P, Vail T |url=http://www.webmd.com/hw-popup/who-is-affected-by-crohns-disease |title=Who is affected by Crohn's disease |publisher=Healthwise |archive-url=https://web.archive.org/web/20090123043717/http://www.webmd.com/hw-popup/who-is-affected-by-crohns-disease |archive-date=January 23, 2009}}</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 | vauthors = Satsangi J, Jewell DP, Bell JI | title = The genetics of inflammatory bowel disease | journal = Gut | volume = 40 | issue = 5 | pages = 572–574 | date = May 1997 | pmid = 9203931 | pmc = 1027155 | doi = 10.1136/gut.40.5.572 }}</ref> Twin studies find that if one has the disease, there is a 55% chance the other will too.<ref>{{cite journal | vauthors = 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 = 990–996 | date = July 1988 | pmid = 3396969 | pmc = 1433769 | doi = 10.1136/gut.29.7.990 }}</ref>

The incidence of Crohn's disease is increasing in Europe<ref name="BurischJess2013">{{cite journal | vauthors = Burisch J, Jess T, Martinato M, Lakatos PL | title = The burden of inflammatory bowel disease in Europe | journal = Journal of Crohn's & Colitis | volume = 7 | issue = 4 | pages = 322–337 | date = May 2013 | pmid = 23395397 | doi = 10.1016/j.crohns.2013.01.010 | doi-access = free | title-link = doi }}</ref> and in newly industrialised countries.<ref name="Ng2017">{{cite journal | vauthors = Ng SC, Shi HY, Hamidi N, Underwood FE, Tang W, Benchimol EI, Panaccione R, Ghosh S, Wu JC, Chan FK, Sung JJ, Kaplan GG | title = Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies | journal = Lancet | volume = 390 | issue = 10114 | pages = 2769–2778 | date = December 2017 | pmid = 29050646 | doi = 10.1016/S0140-6736(17)32448-0 | s2cid = 32940 | doi-access = free | title-link = doi }}</ref> For example, in Brazil, there has been an annual increase of 11% in the incidence of Crohn's disease since 1990.<ref name="Ng2017" />

== History == {{main|List of people diagnosed with Crohn's disease}}

Inflammatory bowel diseases were described by Giovanni Battista Morgagni (1682–1771) and by Scottish physician Thomas Kennedy Dalziel in 1913.<ref>{{cite journal | vauthors = Kirsner JB | title = Historical aspects of inflammatory bowel disease | journal = Journal of Clinical Gastroenterology | volume = 10 | issue = 3 | pages = 286–297 | date = June 1988 | pmid = 2980764 | doi = 10.1097/00004836-198806000-00012 }}</ref>

''Ileitis terminalis'' was first described by Polish surgeon Antoni Leśniowski in 1904, although it was not conclusively distinguished from intestinal tuberculosis.<ref>{{cite journal | vauthors = Lichtarowicz AM, Mayberry JF | title = Antoni Lésniowski and his contribution to regional enteritis (Crohn's disease) | journal = Journal of the Royal Society of Medicine | volume = 81 | issue = 8 | pages = 468–470 | date = August 1988 | pmid = 3047387 | pmc = 1291720 | doi = 10.1177/014107688808100817 }}</ref> In Poland, it is still called Leśniowski-Crohn's disease ({{langx|pl|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.<ref name="CrohnBB" />

== References == {{Reflist}}

== External links == * {{cite web |url=https://medlineplus.gov/crohnsdisease.html |publisher=U.S. National Library of Medicine |work=MedlinePlus |title=Crohn's disease}} *{{commons category-inline}} {{Medical condition classification and resources | ICD11 = {{ICD11|DD70}} | ICD10 = {{ICD10|K50}} | ICD9 = {{ICD9|555}} | ICDO = | OMIM = 266600 | MeshID = D003424 | DiseasesDB = 3178 | MedlinePlus = 000249 | eMedicineSubj = med | eMedicineTopic = 477 | eMedicine_mult = {{eMedicine2|ped|507}} {{eMedicine2|radio|197}} }}

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