What are the causes of ulcerative colitis and how many people does it affect? Within this section of the Knowledge Centre you can gain insights into the prevalence and incidence of ulcerative colitis as well as the factors that underlie the condition.
Ulcerative colitis is more a common presentation of IBD than Crohn’s disease (Feuerstein and Cheifitz, 2014). As with Crohn’s disease, a systematic review revealed that, worldwide, the prevalence of ulcerative colitis is highest in Europe and North America (Figure 6). The countries with the highest reported prevalence in each region were Norway and the United States, with 505 and 286 cases per 100,000 individuals, respectively (Ng et al., 2017).
Globally, the incidence of ulcerative colitis is rising (Ungaro et al., 2017; Danese and Fiocchi, 2011) — with marked increases in newly industrialised countries (Ng et al., 2017). For example, Brazil has recently seen as an annual percentage change of 14.9% (95% confidence interval 10.4–19.6) (Ng et al., 2017).
Unlike Crohn’s disease, men and women tend to be equally affected by ulcerative colitis (Adams and Bornemann, 2013; Ungaro et al., 2017). Ulcerative colitis can develop from infancy onwards (Adams and Bornemann, 2013), but generally presents in teenagers and other patients under 30 years of age (Feurstein and Cheifitz, 2014). There is another, less pronounced, peak between the ages of 50 and 70 (Ordás et al., 2012).
As an alternative presentation of IBD to Crohn’s disease, the precise aetiology of ulcerative colitis remains to be elucidated but involves four factors (Zhou et al., 2017):
There is complex interplay between these factors and epigenetics may play a role (Zhou et al., 2017), affecting the way in which certain genes are expressed.
Genome-wide association studies to identify susceptibility loci are ongoing, but Dr Yingwei Chen and colleagues (Zhou et al., 2017) recently reviewed the prevailing situation. These researchers reported that over 200 susceptibility loci had been found, with 137 conferring risk for both ulcerative colitis and Crohn’s disease while an additional 27 were specific to ulcerative colitis (Zhou et al., 2017). They also stated that only around 8% of the disease variation in ulcerative colitis may be a result of “identified genetic factors” (Zhou et al., 2017). The situation will have changed slightly since these results were reported but is likely to have remained broadly similar.
In genetically predisposed individuals, it is possible that changes in the gut flora — dysbiosis — may trigger disease (Ordás et al., 2012; Wehkamp et al., 2016), and reduced microbial diversity is apparent in ulcerative colitis (Noor et al., 2010). For instance, the number of species of Bacteroides is decreased, and these bacteria may have a protective role (Noor et al., 2010). However, the extent of the dysbiosis is less than in Crohn’s disease, and whether this is a cause or consequence of mucosal inflammation remains to be definitively determined (Ungaro et al., 2017).
Interestingly, while Faecalibacterium prausnitzii exhibits defective gut colonisation in ulcerative colitis patients during remission, increasing populations of this bacteria after relapse are associated with maintaining remission (Varela et al., 2013). This suggests that increasing the Faecalibacterium prausnitzii population in the gut could be a useful strategy for maintaining remission in ulcerative colitis patients (Varela et al., 2013).
Gastrointestinal infections, such as with Campylobacter or Salmonella, can increase the risk of developing IBD (Garcia Rodriguez et al., 2006; Porter et al., 2008), although the risk is slightly lower for ulcerative colitis than Crohn’s disease (odds ratios (95% confidence intervals of 1.36 [1.08–1.72] and 1.54 [1.17–2.04], respectively) (Porter et al., 2008).
As with Crohn’s disease, other environmental factors may also play a role in the development of ulcerative colitis (Zhang and Li 2014). For instance, decreasing childhood intestinal infection as a consequence of improvements in sanitation might hamper the development of mucosal immunity (Ordás et al., 2012). However, in contrast to Crohn’s disease, smoking and appendicectomy may have protective effects in ulcerative colitis (Danese and Fiocchi 2011; Ordás et al., 2012).
The mechanism by which the immune response results in development of ulcerative colitis is considered in the pathophysiology section in this part of the Knowledge Centre.
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