Inflammatory bowel disease comprises the chronic relapsing-remitting intestinal inflammatory disorders Crohn’s disease (CD) and ulcerative colitis (UC). Strong abdominal pain, bloody diarrhoea, fever, weight loss, complications including malignancies, peak of disease-onset in the second to third decade of life and the lack of causative treatments are some factors that explain the high individual affliction associated with these diseases. The most important economic factors that influence the cost profiles of both diseases are long-term productivity losses due to an ongoing inability to work and the cost of medication. Family history is a risk factor for developing IBD, with a first-degree relative risk (S) of 10-60 and a monozygotic twin concordance rate of 60-70%. IBD is thought to result from an inappropriate and continuing inflammatory response to commensal microbes in a genetically susceptible host.
UC is characterized by inflammation that is limited to the colon: it begins in the rectum, spreads proximally in a continuous fashion and frequently involves the periappendiceal region. By contrast, CD involves any part of the gastrointestinal tract — most commonly the terminal ileum or the perianal region — in a non-continuous fashion and, unlike UC, is commonly associated with complications such as strictures, abscesses and fistulas. Histologically, UC shows superficial inflammatory changes limited to the mucosa and submucosa with cryptitis and crypt abscesses. The microscopic features of CD include thickened submucosa, transmural inflammation, fissuring ulceration and non-caseating granulomas.
The prevalence of CD and UC is highest in North America, northern Europe and the United Kingdom, with the average number of cases ranging from 100 to 200 cases per 100,000 persons. The changes in prevalence over a few generations obviously cannot be attributed to underlying population genetic factors. It is hypothesized that the steep rise in incidence may rather be explained by the drastic environmental changes throughout the last century and the not yet adapted – and therefore predisposing – genetic background in a sub-fraction of the population. Environmental suspects are the increased level of hygiene (hence a significant decrease in antigen contacts), nutritional habits, smoking and the industrialization of both food production and preservation. Recent advances have been made in the description of genetic risk factors and formal pathophysiology (e.g. the description of inflammatory signal transduction), yet the complex questions why the disease manifests at a specific time and how the disease perpetuates over time in a given individual are completely unresolved.