A Review of Crohn’s Disease - European Medical Journal

A Review of Crohn’s Disease

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Philip Hendy,1 Ailsa Hart2

No potential conflict of interest.

EMJ Gastroenterol. ;[1]:116-123. DOI/10.33590/emjgastroenterol/10311850. https://doi.org/10.33590/emjgastroenterol/10311850.
Anti-tumour necrosis factor alpha (anti–TNFα), autophagy genes, Crohn’s disease, immunomodulators, inflammatory bowel disease, metabolomics, metagenomics, NOD2

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Crohn’s disease is a chronic relapsing inflammatory bowel disease that may affect any part of the gastrointestinal tract. The ileum, colon, and perineum are most commonly affected. It is characterised by transmural inflammation, and granulomata may be present. Whilst the aetiology of Crohn’s disease is not completely understood, it is thought to be caused by the complex interplay between genetic, immunological, microbiological, and environmental factors. Current opinion is that, in genetically susceptible individuals, there is an immune dysregulation to an environmental factor, and the intestinal microbiota plays a central role. Genetic studies of patients with Crohn’s disease have found several gene mutations which affect the innate immune system. Two important mutations contributing towards the pathogenesis of Crohn’s disease are Nucleotide-binding oligomerisation domain-containing protein 2 (NOD2) and autophagyrelated 16-like 1 (ATG16L1). The most common symptoms of Crohn’s disease are diarrhoea, abdominal pain, weight loss, and fatigue. Symptoms reflect the site and behaviour of disease, and the presence or absence of strictures and fistulae. Extraintestinal manifestations may be present and typically affect the eyes, skin, joints, or biliary tree. Investigations are performed to map the disease location, assess disease severity, and survey for complications of the disease or treatment. Management is with smoking cessation, steroids, immunomodulators, anti-tumour necrosis factor (TNF) therapy, or surgery.

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