Inflammatory Bowel Disease

Inflammatory bowel disease covers Crohn's disease and ulcerative colitis, two chronic immune-mediated conditions in which the mucosal immune system attacks the gut in genetically susceptible people. The distinction matters clinically: ulcerative colitis is confined to the colon with continuous mucosal inflammation from the rectum upward, while Crohn's can affect any part of the gastrointestinal tract, is patchy, and is transmural, which is why it produces strictures, fistulas and abscesses that colitis does not. Modern management is built around a treat-to-target philosophy. The target is no longer symptom relief but objective remission — normalised faecal calprotectin and mucosal healing on endoscopy — because symptoms correlate poorly with inflammation and untreated inflammation accumulates irreversible bowel damage. Early effective therapy with biologics or small molecules in high-risk patients outperforms step-up escalation. Steroids are for induction only; using them repeatedly is a marker of inadequate maintenance therapy. Nutritional consequences are common and frequently under-treated. Terminal ileal Crohn's impairs B12 and bile acid absorption, chronic blood loss and inflammation produce iron deficiency, and steroid exposure plus malabsorption threaten bone density. Curcumin has randomised evidence as an add-on to mesalazine in ulcerative colitis, and multi-strain probiotics have data in pouchitis and mild colitis. Neither replaces disease-modifying therapy.

• •Chronic diarrhoea
• •Blood or mucus in stool
• •Abdominal pain and cramping
• •Urgency and night-time bowel motions
• •Unintended weight loss
• •Fatigue
• •Mouth ulcers, joint pain or eye inflammation

• •Genetic susceptibility
• •Dysregulated mucosal immunity
• •Microbial dysbiosis
• •Impaired epithelial barrier
• •Smoking (Crohn's)
• •NSAID use
• •Prior infectious gastroenteritis

Genetic susceptibility including NOD2 variants in Crohn's, dysregulated mucosal immune response to gut microbiota, impaired epithelial barrier function, microbial dysbiosis with reduced diversity, smoking which worsens Crohn's, prior gastroenteritis, non-steroidal anti-inflammatory use triggering flares, and Western dietary patterns including emulsifiers.