Scroll down this page to learn more about the prevalence and incidence of Crohn’s disease as well as factors that contribute to its development.
In many countries in Europe, as well as in North America, over 0.3% of the population has been diagnosed with IBD (Ng et al., 2017). These regions are reported to have the highest prevalence of Crohn’s disease, one presentation of IBD, globally. A systematic review of population-based studies from around the world reported the prevalence of Crohn’s disease to be highest in Europe and North America; with the highest values for each region in Germany and Canada, with 319 and 322 cases, respectively, per 100,000 individuals (Ng et al., 2017).
While prevalence describes actual numbers of cases, incidence measures rates of new cases, and most epidemiological studies suggest that the incidence of IBD is increasing (Wehkamp et al., 2016).
Although the incidence may be stabilising in Europe and North America, it is rising in newly industrialised countries (Ng et al., 2017). For example, over recent years in Brazil, there has been an annual percentage increase of 11.1% (95% confidence interval 4.8–17.8) in the incidence of Crohn’s disease (Ng et al., 2017).
Crohn’s disease affects more women than men (Adams and Bornemann, 2013). It can develop at any point from early childhood (Wehkamp et al., 2016), but the median age of onset is 30 years (Feuerstein and Cheifitz, 2017). Onset tends to occur in two peaks — mainly between 20 and 30 years of age, but also around 50 years (Feuerstein and Cheifitz, 2017).
The precise aetiology of Crohn’s disease is unknown, but involves four factors (Zhou et al., 2017):
The prevalence of Crohn’s disease varies according to race: Caucasians, particularly Ashkenazi Jews, are among the most affected, while the condition occurs less often in Hispanic and Asian populations (Matricon et al., 2010; Gajendran et al., 2018). This suggests the possibility of a genetic component. This is supported by the presence of familial forms, with the relative risk of developing Crohn’s disease being 30-fold higher in siblings of patients with Crohn’s disease than the general population (Hedin et al., 2016). High rates of concordance in monozygotic twins provide further evidence of a genetic influence (Matricon et al., 2010; Gajendran et al., 2018). Twin studies also suggest that genetic disposition may play a greater role in the development of Crohn’s disease than ulcerative colitis with monozygotic concordance rates significantly higher in Crohn’s disease (Matricon et al., 2010).
As technology has advanced, genome-wide association studies have identified susceptibility loci for IBD. This research is ongoing, but over 200 such loci have been found (de Lange et al., 2017). In Crohn’s disease, these include polymorphisms in the NOD2 gene, which is expressed in a range of cell types and encodes a protein that helps to initiate innate immune responses, as well as in autophagy-related genes (Abraham and Cho, 2009).
Crohn’s disease is associated with loss of normal anaerobic bacteria from the intestine with patients exhibiting a 50% reduction in diversity compared with controls (Ott et al., 2004). This may enable the growth of other invasive species, and pathogenic strains of Crohn’s disease-associated Escherichia coli have been found (Matricon et al., 2010).
Exposure to antibiotics, such as penicillins, cephalosporins, metronidazole and fluoroquinolones, may be associated with the development of Crohn’s disease, but not ulcerative colitis (Theochari et al., 2018).
A range of other environmental factors also increase the risk of Crohn’s disease (Figure 3) (Feuerstein and Cheifitz, 2017; Zhang and Li, 2014).
See the pathophysiology section of the Knowledge Centre to learn about the mechanism by which the host immune response leads to disease development.
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