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Crohn's disease

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 (left) compared to the areas affected by ulcerative colitis (colitis ulcerosa, right)
SpecialtyGastroenterology
SymptomsAbdominal pain, diarrhea (may be bloody), fever, weight loss,[1] fatigue, mouth sores, reduced appetite[2]
ComplicationsAnemia, skin rashes, arthritis, bowel cancer[1]
Usual onset20–29 years[3]
DurationLong term[1]
CausesUncertain
Risk factorsGenetic predisposition, living in a developed country,[4]
stress,[5] tobacco smoking,[6]
having undergone an appendectomy[7][8] or tonsillectomy[9]
Diagnostic methodBiopsy, medical imaging[1]
Differential diagnosisIrritable bowel syndrome, celiac disease, Behçet's disease, nonsteroidal anti-inflammatory drug enteropathy, intestinal tuberculosis[1][10]
MedicationCorticosteroids, biological therapy, immunosuppressants such as azathioprine, methotrexate[1]
PrognosisSlightly increased risk of death[11]
Frequency3.2 per 1,000 (developed world)[12]
Named after

Crohn's disease is a type of inflammatory bowel disease (IBD) that may affect any segment of the gastrointestinal tract.[3] Symptoms often include abdominal pain, diarrhea, fever, abdominal distension, and weight loss.[1][3] Complications outside of the gastrointestinal tract may include anemia, skin rashes, arthritis, inflammation of the eye, and fatigue.[1] The skin rashes may be due to infections as well as pyoderma gangrenosum or erythema nodosum.[1] Bowel obstruction may occur as a complication of chronic inflammation, and those with the disease are at greater risk of colon cancer and small bowel cancer.[1]

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.[3][13][14][15] It results in a chronic inflammatory disorder, in which the body's immune system defends the gastrointestinal tract, possibly targeting microbial antigens.[14][16] While 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).[17] The exact underlying immune problem is not clear; however, it may be an immunodeficiency state.[16][18][19]

About half of the overall risk is related to genetics, with more than 70 genes involved.[1][20] Tobacco smokers are three times as likely to develop Crohn's disease as non-smokers.[6] It often begins after gastroenteritis.[1] Other conditions with similar symptoms include irritable bowel syndrome and Behçet's disease.[1]

There is no known cure for Crohn's disease.[1][3] 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 improve symptoms rapidly, alongside another medication such as either methotrexate or a thiopurine used to prevent recurrence.[1] Cessation of smoking is recommended for people with Crohn's disease.[1] One in five people with the disease is admitted to the hospital each year, and half of those with the disease will require surgery at some time during 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;[12] it is less common in Asia and Africa.[21][22] It has historically been more common in the developed world.[23] Rates have, however, been increasing, particularly in the developing world, since the 1970s.[22][23] Inflammatory bowel disease resulted in 47,400 deaths in 2015,[24] and those with Crohn's disease have a slightly reduced life expectancy.[1] It tends to start in adolescence and young adulthood, though it can occur at any age.[25][1][3][26] Males and females are equally affected.[3]

  1. ^ a b c d e f g h i j k l m n o p q r s t u v Baumgart DC, Sandborn WJ (August 2012). "Crohn's disease". Lancet. 380 (9853): 1590–1605. doi:10.1016/S0140-6736(12)60026-9. PMID 22914295.
  2. ^ "Crohn's disease". Autoimmune Registry Inc. Archived from the original on June 15, 2022. Retrieved June 15, 2022.
  3. ^ a b c d e f g "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.
  4. ^ Baumgart DC, Carding SR (May 2007). "Inflammatory bowel disease: cause and immunobiology". Lancet. 369 (9573): 1627–40. doi:10.1016/S0140-6736(07)60750-8. PMID 17499605.
  5. ^ Mawdsley JE, Rampton DS (October 2005). "Psychological stress in IBD: new insights into pathogenic and therapeutic implications". Gut. 54 (10): 1481–91. doi:10.1136/gut.2005.064261. PMC 1774724. PMID 16162953.
  6. ^ a b Cosnes J (June 2004). "Tobacco and IBD: relevance in the understanding of disease mechanisms and clinical practice". Best Practice & Research. Clinical Gastroenterology. 18 (3): 481–496. doi:10.1016/j.bpg.2003.12.003. PMID 15157822.
  7. ^ Koutroubakis IE (February 1999). "Appendectomy, tonsillectomy, and risk of inflammatory bowel disease". Diseases of the Colon & Rectum. 42 (2): 225–230. doi:10.1007/BF02237133. PMID 10211500. S2CID 31528819. Archived from the original on June 13, 2019.{{cite journal}}: CS1 maint: date and year (link)
  8. ^ Frisch M, Gridley G (October 2002). "Appendectomy in adulthood and the risk of inflammatory bowel diseases". Scand J Gastroenterol. 37 (10): 1175–7. doi:10.1080/003655202760373380. PMID 12408522.
  9. ^ Weili Sun, Xiao Han, Siyuan Wu, Chuanhua Yang (June 1, 2016). "Tonsillectomy and the risk of inflammatory bowel disease: A systematic review and meta-analysis". Journal of Gastroenterology and Hepatology. 31 (6): 1085–94. doi:10.1111/jgh.13273. ISSN 1440-1746. PMID 26678358. S2CID 2625962.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Cite error: The named reference WGO-IBD was invoked but never defined (see the help page).
  11. ^ Cite error: The named reference ACG_Guideline was invoked but never defined (see the help page).
  12. ^ a b Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, et al. (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. Archived from the original on October 7, 2022. Retrieved October 7, 2022.
  13. ^ 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.
  14. ^ a b 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.
  15. ^ 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.
  16. ^ a b 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.
  17. ^ 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.
  18. ^ 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): 633–641. doi:10.1586/eci.10.29. PMID 20594136. S2CID 25402952.
  19. ^ 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.
  20. ^ 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. S2CID 205468282.
  21. ^ a b 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.
  22. ^ a b 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. S2CID 9538639.
  23. ^ 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.
  24. ^ Shih IL, Lee TC, Tu CH, Chang CC, Wang YF, Tseng YH, et al. (December 1, 2016). "Intraobserver and interobserver agreement for identifying extraluminal manifestations of Crohn's disease with magnetic resonance enterography". Advances in Digestive Medicine. 3 (4): 174–180. doi:10.1016/j.aidm.2015.05.004. S2CID 70796090.
  25. ^ Cite error: The named reference eMedicineHealth was invoked but never defined (see the help page).
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