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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:
* Aggregation of ulcerative colitis in families.
* Twin concordance studies, although the evidence is less than for Crohn's disease
* Ethnic differences in incidence
* Genetic markers and linkages
Chromosome band 1p36 is linked to inflammatory bowel disease.
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. These highly environmentally and drug sensitive disorders have been associated with lupus, transient and sustained autoantibody production since the early 1950s.
Care must be taken with potential porphyrinogenic drugs, including sulfasalazine. Acute neurovisceral attacks and solar urticaria can occur with porphyrinogenic drugs. Complications can include syndrome of inappropriate antidiuretic hormone, focal and systemic neuropathy, ileus, pancreatitis, pericarditis and liver damage.
Testing must be appropriate for all neurovisceral and cutaneous porphyrias including porphyrin testing of urine, stool/bile and blood, enzyme or DNA testing if available. The urine screening test used for acute neurovisceral attacks is unreliable and inappropriate for hereditary coproporphyria, variegate porphyria and children.
[edit] 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.
* Smoking: unlike Crohn's disease, ulcerative colitis has a lesser prevalence in smokers than non-smokers.
* 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.
* Other childhood exposures, or infections
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. 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.
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Important notice:
The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other
qualified health provider with any questions you may have regarding a medical condition.
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