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Crohn's disease
Other namesCrohn disease, Crohn syndrome, granulomatous enteritis, regional enteritis, Leśniowski-Crohn disease
The three most common sites of intestinal involvement in Crohn's disease
Medical specialtyGastroenterology
SymptomsAbdominal pain, diarrhea (may be bloody), fever, weight loss[1]
ComplicationsAnemia, skin rashes, arthritis, bowel cancer[1]
Usual onset20 to 30[2]
DurationLong term[1]
Risk factorsTobacco smoking[3]
Diagnostic methodBiopsy, medical imaging[1]
Differential diagnosisIrritable bowel syndrome, celiac disease, Behçet's disease, nonsteroidal anti-inflammatory drug enteropathy, intestinal tuberculosis[1]
MedicationCorticosteroids, methotrexate[1]
PrognosisSlightly reduced life expectancy[1]
Frequency3.2 per 1,000 (developed world)[4]

Crohn's disease is a type of inflammatory bowel disease (IBD) that may affect any segment of the gastrointestinal tract from the mouth to the anus.[2] Symptoms often include abdominal pain, diarrhea (which may be bloody if inflammation is severe), fever, and weight loss.[1][2] Other complications outside the gastrointestinal tract may include anemia, skin rashes, arthritis, inflammation of the eye, and tiredness.[1] The skin rashes may be due to infections as well as pyoderma gangrenosum or erythema nodosum.[1] Bowel obstruction may occur as a complication of chronic inflammation, and those with the disease are at greater risk of colon cancer and small bowel cancer.[1]

While the causes of Crohn's disease are unknown, it is believed to be caused by a combination of environmental, immune, and bacterial factors in genetically susceptible individuals.[5][6][7][2] It results in a chronic inflammatory disorder, in which the body's immune system attacks the gastrointestinal tract, possibly targeting microbial antigens.[6][8] While Crohn's is an immune-related disease, it does not appear to be an autoimmune disease (in that the immune system is not being triggered by the body itself).[9] The exact underlying immune problem is not clear; however, it may be an immunodeficiency state.[8][10][11] About half of the overall risk is related to genetics, with more than 70 genes having been found to be involved.[1][12] Tobacco smokers are twice as likely to develop Crohn's disease as nonsmokers.[3] It also often begins after gastroenteritis.[1] Diagnosis is based on a number of findings including biopsy and appearance of the bowel wall, medical imaging, and description of the disease.[1] Other conditions that can present similarly include irritable bowel syndrome and Behçet's disease.[1]

There are not any medications or surgical procedures that can cure Crohn's disease.[1][2] Treatment options are intended to help with symptoms, maintain remission, and prevent relapse.[1] In those newly diagnosed, a corticosteroid may be used for a brief period of time to rapidly improve symptoms, alongside another medication such as either methotrexate or a thiopurine used to prevent recurrence.[1] Stopping smoking is recommended in people with Crohn's disease.[1] One in five people with the disease is admitted to hospital each year, and half of those with the disease will require surgery for the disease at some point over a ten-year period.[1] While surgery should be used as little as possible, it is necessary to address some abscesses, certain bowel obstructions, and cancers.[1] Checking for bowel cancer via colonoscopy is recommended every few years, starting eight years after the disease has begun.[1]

Crohn's disease affects about 3.2 per 1,000 people in Europe and North America.[4] It is less common in Asia and Africa.[13][14] It has historically been more common in the developed world.[15] Rates have, however, been increasing, particularly in the developing world, since the 1970s.[14][15] Inflammatory bowel disease resulted in 47,400 deaths in 2015[16] and those with Crohn's disease have a slightly reduced life expectancy.[1] It tends to start in the teens and twenties, though it can occur at any age.[1][2] Males and females are equally affected.[2] The disease was named after gastroenterologist Burrill Bernard Crohn, who in 1932, together with two colleagues at Mount Sinai Hospital in New York, described a series of patients with inflammation of the terminal ileum of the small intestine, the area most commonly affected by the illness.[17]

References

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  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 Baumgart DC, Sandborn WJ (August 2012). "Crohn's disease". Lancet. 380 (9853): 1590–605. doi:10.1016/S0140-6736(12)60026-9. PMID 22914295.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 "Crohn's Disease". National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Archived from the original on December 8, 2019. Retrieved December 8, 2019.
  3. 3.0 3.1 Cosnes J (June 2004). "Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice". Best Practice & Research. Clinical Gastroenterology. 18 (3): 481–96. doi:10.1016/j.bpg.2003.12.003. PMID 15157822.
  4. 4.0 4.1 Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, Benchimol EI, Panaccione R, Ghosh S, Barkema HW, Kaplan GG (January 2012). "Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review". Gastroenterology. 142 (1): 46–54.e42, quiz e30. doi:10.1053/j.gastro.2011.10.001. PMID 22001864. S2CID 206223870.[permanent dead link]
  5. Cho JH, Brant SR (May 2011). "Recent insights into the genetics of inflammatory bowel disease". Gastroenterology. 140 (6): 1704–12. doi:10.1053/j.gastro.2011.02.046. PMC 4947143. PMID 21530736.
  6. 6.0 6.1 Dessein R, Chamaillard M, Danese S (September 2008). "Innate immunity in Crohn's disease: the reverse side of the medal". Journal of Clinical Gastroenterology. 42 Suppl 3 Pt 1: S144–7. doi:10.1097/MCG.0b013e3181662c90. PMID 18806708.
  7. Stefanelli T, Malesci A, Repici A, Vetrano S, Danese S (May 2008). "New insights into inflammatory bowel disease pathophysiology: paving the way for novel therapeutic targets". Current Drug Targets. 9 (5): 413–8. doi:10.2174/138945008784221170. PMID 18473770.
  8. 8.0 8.1 Marks DJ, Rahman FZ, Sewell GW, Segal AW (February 2010). "Crohn's disease: an immune deficiency state". Clinical Reviews in Allergy & Immunology. 38 (1): 20–31. doi:10.1007/s12016-009-8133-2. PMC 4568313. PMID 19437144.
  9. Casanova JL, Abel L (August 2009). "Revisiting Crohn's disease as a primary immunodeficiency of macrophages". The Journal of Experimental Medicine. 206 (9): 1839–43. doi:10.1084/jem.20091683. PMC 2737171. PMID 19687225.
  10. Lalande JD, Behr MA (July 2010). "Mycobacteria in Crohn's disease: how innate immune deficiency may result in chronic inflammation". Expert Review of Clinical Immunology. 6 (4): 633–41. doi:10.1586/eci.10.29. PMID 20594136.
  11. Yamamoto-Furusho JK, Korzenik JR (November 2006). "Crohn's disease: innate immunodeficiency?". World Journal of Gastroenterology. 12 (42): 6751–5. doi:10.3748/wjg.v12.i42.6751. PMC 4087427. PMID 17106921. Archived from the original on June 6, 2013.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. Prideaux L, Kamm MA, De Cruz PP, Chan FK, Ng SC (August 2012). "Inflammatory bowel disease in Asia: a systematic review". Journal of Gastroenterology and Hepatology. 27 (8): 1266–80. doi:10.1111/j.1440-1746.2012.07150.x. PMID 22497584.
  13. 14.0 14.1 Hovde Ø, Moum BA (April 2012). "Epidemiology and clinical course of Crohn's disease: results from observational studies". World Journal of Gastroenterology. 18 (15): 1723–31. doi:10.3748/wjg.v18.i15.1723. PMC 3332285. PMID 22553396.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. 15.0 15.1 Burisch J, Munkholm P (July 2013). "Inflammatory bowel disease epidemiology". Current Opinion in Gastroenterology. 29 (4): 357–62. doi:10.1097/MOG.0b013e32836229fb. PMID 23695429.
  15. GBD 2015 Mortality Causes of Death Collaborators (October 2016). "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". The Lancet. 388 (10053): 1459–1544. doi:10.1016/S0140-6736(16)31012-1. PMC 5388903. PMID 27733281. {{cite journal}}: |author1= has generic name (help)CS1 maint: numeric names: authors list (link)
  16. Crohn BB, Ginzburg L, Oppenheimer GD (May 2000). "Regional ileitis: a pathologic and clinical entity. 1932". The Mount Sinai Journal of Medicine, New York. 67 (3): 263–8. PMID 10828911.