Ulcerative colitis causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2]
Overview
The exact cause of ulcerative colitis is still unknown. Several possible causes have been suggested including genetic, environmental and autoimmune factors.[1][2]
Causes
While the cause of ulcerative colitis is unknown, several possibly interrelated causes have been suggested.
Genetic factors
A genetic component to the etiology of ulcerative colitis can be hypothesized based on the following:[3]
- 20-25 patients with IBD have relatives having IBD.[4]
- Aggregation of ulcerative colitis in families
- Identical twin concordance rate of 10% and dizygotic twin concordance rate of 3%[5]
- Ethnic differences in incidence
- Genetic markers and linkages
There are 12 regions of the genome which may be linked to ulcerative colitis. This includes chromosomes 16, 12, 6, 14, 5, 19, 1, 16, and 3 in the order of their discovery.[6] However, none of these loci has been consistently shown to be at fault, suggesting that the disorder arises from the combination of multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease.[7] Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There are even HLA associations which may be at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.[6]
Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn's disease, celiac disease, dermatitis herpetiformis, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren's disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with potential porphyrinogenic drugs, including sulfasalazine.
Environmental factors
Many hypotheses have been raised for environmental contributants to the pathogenesis of ulcerative colitis. They include the following:
- Diet: As the colon is exposed to many different dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. There have been few studies to investigate such an association, but one study showed no association of refined sugar on the prevalence of ulcerative colitis.[8]
- Smoking: Unlike Crohn's disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers.[9]
- Breastfeeding: There have been conflicting reports of the protection of breastfeeding in the development of inflammatory bowel disease. One Italian study showed a potential protective effect.[10]
- Other childhood exposures, or infections
- Use of NSAIDs
- Stress
Autoimmune disease
Some sources list ulcerative colitis as an autoimmune disease, a disease in which the immune system malfunctions, attacking some part of the body. As discussed above, ulcerative colitis is a systemic disease that affects many areas of the body outside the digestive system. Surgical removal of the large intestine often cures the disease, including the manifestations outside the digestive system.[11] This suggests that the cause of the disease is in the colon itself, and not in the immune system or some other part of the body.
Alternative theories
Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis. This could mean that there are higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine.[12][13]
References
- ↑ Orholm M, Binder V, Sorensen TI, Rasmussen LP, Kyvik KO. Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study. Scand J Gastroenterol 2000;35:1075-81. PMID 11099061.
- ↑ Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B (1988). ""Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking". Gut. 29: 990–996.
- ↑ Orholm M, Binder V, Sorensen TI, Rasmussen LP, Kyvik KO. Concordance of inflammatory bowel disease among Danish twins. Results of a nationwide study. Scand J Gastroenterol 2000;35:1075-81. PMID 11099061.
- ↑ "online.ccfa.org" (PDF).
- ↑ Tysk C, Lindberg E, Jarnerot G, Floderus-Myrhed B (1988). ""Ulcerative colitis and Crohn's disease in an unselected population of monozygotic and dizygotic twins. A study of heritability and the influence of smoking". Gut. 29: 990–996.
- ↑ 6.0 6.1 Baumgart DC, Carding SF (May 2007). ""Inflammatory bowel disease: cause and immunobiology"". Lancet. 369 (9573). doi:10.1016/S0140-6736(07)60750-8. Unknown parameter
|Pages=ignored (|pages=suggested) (help) - ↑ Cho JH, Nicolae DL, Ramos R, Fields CT, Rabenau K, Corradino S, Brant SR, Espinosa R, LeBeau M, Hanauer SB, Bodzin J, Bonen DK. Linkage and linkage disequilibrium in chromosome band 1p36 in American Chaldeans with inflammatory bowel disease. Hum Mol Genet 2000;9:1425-32. Fulltext. PMID 10814724.
- ↑ Jarnerot G, Jarnmark I, Nilsson K. Consumption of refined sugar by patients with Crohn's disease, ulcerative colitis, or irritable bowel syndrome. Scand J Gastroenterol 1983;18:999-1002. PMID 6673083.
- ↑ Calkins BM. A meta-analysis of the role of smoking in inflammatory bowel disease. Dig Dis Sci 1989;34:1841-54. PMID 2598752.
- ↑ Corrao G, Tragnone A, Caprilli R, Trallori G, Papi C, Andreoli A, Di Paolo M, Riegler G, Rigo GP, Ferrau O, Mansi C, Ingrosso M, Valpiani D. Risk of inflammatory bowel disease attributable to smoking, oral contraception and breastfeeding in Italy: a nationwide case-control study. Cooperative Investigators of the Italian Group for the Study of the Colon and the Rectum (GISC). Int J Epidemiol 1998;27:397-404. PMID 9698126.
- ↑ Ulcerative Colitis Practice Guidelines in Adults, Am. Coll. Gastroenterology, 2004. PDF
- ↑ Roediger WE, Moore J, Babidge W. Colonic sulfide in pathogenesis and treatment of ulcerative colitis. Dig Dis Sci 1997;42:1571-9. PMID 9286219.
- ↑ Levine J, Ellis CJ, Furne JK, Springfield J, Levitt MD. Fecal hydrogen sulfide production in ulcerative colitis. Am J Gastroenterol 1998;93:83-7. PMID 9448181.