Chronic inflammatory and ulcerating condition of the GI tract that can affect anywhere from mouth to anus, most commonly the terminal ileum and colon

Aetiology

• Genetic predisposition - NOD2 gene found in 10-20% of Caucasian patients with Crohn’s (involved in bacterial recognition)
• Dysbiosis
• Faulty immune response
• Environmental factors - aggravated by smoking and NSAIDs

Pathophysiology

1. Bacterial lipopolysaccharide triggers persistent activation of T cells and macrophages in a genetically susceptible individual
2. Normally the reaction against the lipopolysaccharide is self-limiting, but in IBD patients once the inflammation starts it does not stop
3. Excess pro-inflammatory cytokine production and bystander damage due to neutrophilic inflammation

Disease phenotypes

• Ileal and/or colonic chronic active mucosal inflammation including cryptitis and crypt abscesses
• Any area of GI tract can be affected
• Intestinal strictures - bowel narrowing by scar tissue from inflammation
• Fissure ulcers - from inflammation
• Fistula - left behind from draining of fissure ulcer
• Skip lesions - unaffected areas of bowel (vs. UC - bowel continually affected)

Clinical features

Symptoms

• Symptoms are variable but often include diarrhoea (which may be bloody and become chronic - i.e. present for more than six weeks), abdominal pain and/or weight loss