An increase in the number of cases was seen up until the 1980s after which the number of patients seems to have stabilised. The most recent reports show a tendency towards declining numbers of Ulcerative Colitis (UC) patients, occurring at the same time as an increase in the number of Crohn's patients. The overall number of patients with IBD (UC + Crohn's Disease) is currently increasing.
Clearly, both UC and Crohn's Disease are caused by a combination of factors. Twin studies from Sweden, Denmark and UK have demonstrated that genetic factors explain approximately 6-16 % of UC cases. Environmental factors appear to be of more importance than genetic predisposition in the development of the disease. Strangely, in contrast to Crohn's Disease, UC is less prevalent among smokers compared to non-smokers. However health professionals strongly discourage smoking as they consider the risks of smoking heavily outweigh any benefits seen in UC. In addition, former smokers appear to have an increased risk of developing UC.
As with a wide range of diagnoses, the first case reports of inflammatory bowel disease date back to the Hippocratic writings, although it is impossible to make a statement regarding the exact diagnosis based on these reports.
Sir Samuel Wilks first used the term UC in a case report in 1859. Therapy in those days relied on a variety of different diets and surgical procedures, and mortality was very high. In fact an early publication reports a mortality rate of 43%. The first effective drug introduced was sulphasalazine in the 1940s, the use of which may be attributed to the Swedish professor Nanna Svartz. Steroid treatment was established in the 1950s.
Generally speaking, UC tends to present between the age of 20 and 30. However, infants as well as elderly people can present with UC. Current treatment options for moderately to severely active UC include oral or topical aminosalicylates (sulfasalazine, mesalazine, balsalazide or olsalazine), or treatment with corticosteroids if aminosalicylates are contraindicated or not tolerated.
Diarrhoea with rectal bleeding is typical for UC, often in combination with mild to moderate abdominal pain. Except in the most severe cases, weight loss is a rather uncommon symptom.
Approximately 10% of UC patients have disease manifestation outside the gastrointestinal tract. Joint pain and inflammation are the most common non-gastrointestinal manifestations. More rarely the skin, eyes or liver may be involved.
Diagnosis of UC is based on a typical medical history in combination with endoscopical or radiological examination. Blood samples may typically reveal signs of ongoing inflammation. Stool specimens may be needed in order to exclude an infectious origin.
Aminosalycylates: Are considered safe, but with limited effect in severe UC. Despite this profile, Aminosalycylates are considered to be a first-line drug, especially in mild forms of the disease.
Steroids: Have shown to be effective in the short-term perspective in inducing remission. Steroids are not used in maintenance therapy due to lack of effect in combination with high risk of side effects.
Immunosuppressants: Less documentation is available regarding the role of immunosuppressants in UC compared to Crohn's disease. Due to a more pronounced risk for severe side effects, immunomodulators are regarded as third-line drugs.
Biologicals: A TNF inhibitor is a pharmaceutical drug that suppresses response to tumour necrosis factor (TNF), which is part of the inflammatory response.
GMA apheresis: Is a non-pharmacological approach aimed at reducing the ongoing inflammation by removing over-activated white blood cells from the blood circulation, thereby reducing the inflammatory burden, without the risk of side effects attributed to drugs.
Surgical treatment: In approximately 50% of UC patients, surgical intervention will be needed at some time. It is believed that recent advances in the treatment of UC will reduce the number of patients in need of surgery.1
1. Targownik et al., Am J Gastroenterol. 2012;107(8):1228-1235
1. Baumgart DC, Carding SR. The Lancet 2007;369:1627-1640.
2. Hanai H et al., Clin Exp Immunol. 2011 Jan;163(1):50-8
3. Gerner et al.; Dig Dis. 2013;31(3-4):328-35