Crohn’s disease

Crohn’s disease is a chronic inflammatory bowel disease affecting any part of the gastrointestinal tract from the mouth to the anus, although the ileum, colon and perineum are most commonly involved. It is characterized by transmural granulomatous inflammation. Although the aetiology is unknown, Crohn’s disease is thought to result from a complex interplay of multiple genetic and environmental factors. There appears to be an immune dysregulation to microbiota in genetically predisposed individuals. Several genes involved in the interaction between microbiota and the host immune system, in particular the innate immune system, are defective in Crohn’s disease, including NOD2 and the autophagy genes ATG16L1 and IRGM. Diarrhoea, abdominal pain, fatigue, weight loss and fever are the hallmarks of Crohn’s disease. The clinical features depend on the location and behaviour of the disease in the gastrointestinal tract. Additionally there are extra-intestinal manifestations affecting joints, skin, eyes and the liver. Investigations are targeted at mapping the location, extent, and severity/behaviour (inflammatory, stricturing, penetrating) of disease. Treatment is usually with corticosteroids, immunomodulators (thiopurines, methotrexate), anti-tumour necrosis factor (TNF) therapy or surgery. Patients with poor prognostic features appear to benefit from early treatment with immunomodulator drugs and/or anti-TNF therapy.