Inflammatory Bowel Disease — Crohn's Disease, Ulcerative Colitis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Inflammatory bowel disease (IBD) is a group of chronic relapsing-remitting autoimmune conditions characterised by inflammation of the gastrointestinal (GI) tract. The two major forms are ulcerative colitis (UC) — continuous inflammation limited to the colonic mucosa, always involving the rectum and extending proximally — and Crohn's disease (CD) — transmural (full-thickness) inflammation that can affect any part of the GI tract from mouth to anus, with skip lesions and potential complications including strictures, fistulae, and abscesses. IBD affects approximately 10 million people worldwide, with the highest prevalence in Northern Europe (approximately 300-400 per 100,000) and North America, and rapidly increasing incidence in Asia and other developing regions. IBD typically presents in young adults (peak onset 15-35 years) and follows a relapsing-remitting course with significant impact on quality of life.

IBD results from inappropriate and sustained activation of the intestinal immune system in genetically susceptible individuals in response to the gut microbiome and environmental triggers. Genetic factors: over 240 IBD susceptibility loci identified — the most important include NOD2 (Crohn's disease), IL-23R (both UC and CD), and ATG16L1 (CD). Concordance in monozygotic twins: 50% for CD and 15% for UC, highlighting the interaction between genetics and environment. Environmental risk factors: smoking is a paradoxical risk factor — it increases CD risk (2-fold) but is protective in UC (smoking cessation increases UC flare risk); antibiotic use in childhood (dysbiosis); appendectomy (protective for UC); diet high in processed food, low in fibre; non-steroidal anti-inflammatory drugs (NSAIDs) trigger flares; stress exacerbates IBD via the gut-brain axis; and reduced environmental microbial exposure ('hygiene hypothesis' — explaining rising IBD incidence in high-income countries). Gut microbiome dysbiosis (reduced microbial diversity, increased pathobionts like Enterobacteriaceae) is consistently observed in IBD and likely plays a causal role.

Ulcerative colitis: bloody diarrhoea (the hallmark symptom — blood and mucus mixed in loose stools, urgency, tenesmus), abdominal cramping, and frequency (up to 10 or more bowel movements per day in severe disease). Symptoms correlate with disease extent. Proctitis (rectal-only) causes tenesmus and bleeding with minimal diarrhoea. Pan-colitis causes frequent watery bloody diarrhoea with systemic features. Crohn's disease: abdominal pain (typically right iliac fossa pain from terminal ileal disease), diarrhoea (non-bloody in many cases), weight loss, fatigue, fever, and perianal disease (fistulae, skin tags, fissures, abscesses — occurring in 30% of CD patients). Extra-intestinal manifestations affect both conditions: arthropathy (peripheral arthritis or axial spondyloarthritis — most common, correlates with disease activity in UC); skin (erythema nodosum, pyoderma gangrenosum); eyes (uveitis, episcleritis); liver (primary sclerosing cholangitis — more common in UC, 5-8% of patients; abnormal LFTs).

Diagnosis requires the combination of clinical, endoscopic, histological, and radiological findings. Blood tests: FBC (anaemia, thrombocytosis — active inflammation), CRP and ESR (elevated in active IBD — CRP correlates with CD activity better than UC), albumin (nutritional status), and LFTs. Faecal calprotectin (FC): a non-invasive marker of intestinal inflammation (normal less than 50 mcg/g; above 200 mcg/g suggests active mucosal inflammation); excellent for monitoring disease activity and treatment response, and for distinguishing IBD from IBS. Stool cultures and C. difficile toxin exclude infectious colitis before initiating immunosuppression. Colonoscopy with multiple biopsies (including from macroscopically normal mucosa): the gold standard — provides endoscopic grade of inflammation, tissue for histology, and biopsy for dysplasia surveillance in long-standing IBD. Ileal intubation is essential in CD. CT or MRI enterography: for small bowel CD (specifically MR enterography is preferred — no radiation, excellent soft tissue contrast for identifying strictures, fistulae, abscesses, and extramural disease).

Treatment aims for mucosal healing (endoscopic remission) as the target. Ulcerative colitis: 5-aminosalicylates (mesalazine — oral and rectal suppositories/enemas) are first-line for mild-moderate UC — induction and maintenance of remission; topical mesalazine is more effective than oral for proctitis. Corticosteroids (prednisolone 40 mg/day) for acute flares — not for long-term maintenance. Thiopurines (azathioprine 2-2.5 mg/kg/day or mercaptopurine): immunomodulators for steroid-dependent or frequently relapsing UC; require TPMT testing before initiation. Biologic therapy for moderate-severe UC: anti-TNF antibodies (infliximab IV, adalimumab SC, golimumab SC); anti-integrin (vedolizumab — gut-selective, favourable safety profile); anti-IL-12/23 (ustekinumab). JAK inhibitors (tofacitinib, filgotinib, upadacitinib — oral agents) for moderate-severe UC refractory to biologics. Colectomy (total proctocolectomy with ileal pouch-anal anastomosis, IPAA) for medically refractory UC or dysplasia/cancer. Crohn's disease: exclusive enteral nutrition (EEN) is first-line remission induction in paediatric CD. Early biologic therapy ('top-down' approach) for moderate-severe CD; metronidazole/ciprofloxacin for perianal CD; anti-TNF plus azathioprine combination improves remission rates in CD ('SONIC trial').

Untreated or inadequately controlled IBD causes serious gastrointestinal and systemic complications. Toxic megacolon — acute colonic dilatation (transverse colon diameter above 6 cm) — is a life-threatening complication of severe ulcerative colitis or Crohn's colitis, causing transmural necrosis, bacteraemia, and a mortality of up to 20-40% without emergency colectomy. Intestinal perforation from toxic megacolon or transmural Crohn's inflammation causes peritonitis requiring emergency surgery. Colorectal cancer risk increases significantly with longstanding extensive colitis — cumulative risk of approximately 2% at 10 years, 8% at 20 years, and 18% at 30 years in untreated extensive UC. Crohn's disease causes progressive bowel strictures from transmural fibrosis, causing bowel obstruction requiring surgery in approximately 70% of patients over 20 years; enteroenteric and enterocutaneous fistulae cause chronic sepsis, abscesses, and malnutrition. Chronic active IBD causes iron deficiency anaemia, vitamin B12 and folate deficiency, vitamin D deficiency, and protein malnutrition — contributing to growth failure in children. Primary sclerosing cholangitis (PSC), occurring in 5-8% of UC patients, progresses to biliary cirrhosis and hepatic failure. Severe anaemia, hypoalbuminaemia, and malnutrition from active IBD increase surgical risk and peri-operative complications.

There is no established primary prevention for IBD. For relapse prevention: maintain prescribed maintenance therapy even in remission — stopping mesalazine in UC or thiopurines in CD significantly increases relapse risk. Monitor faecal calprotectin every 3-6 months as a non-invasive marker of disease activity — rising FC predicts endoscopic relapse weeks before symptoms. Dietary modification: a high-fibre, Mediterranean-style diet rich in fruits, vegetables, and legumes supports gut microbiome diversity; avoid processed foods and excessive red meat; identify personal food triggers. Psychological support: IBD has a strong bidirectional relationship with anxiety and depression — cognitive behavioural therapy and IBD nurse support lines significantly improve quality of life and outcomes. Vaccinations: ensure all indicated vaccines (influenza, pneumococcal, COVID-19, varicella) are given before starting immunosuppression. Colorectal cancer surveillance: colonoscopy every 1-5 years for patients with extensive colitis for more than 10 years (risk is 2-8 times higher than general population in longstanding extensive disease).

Seek emergency care for: large-volume rectal bleeding; fever with abdominal distension (risk of toxic megacolon — a life-threatening complication of severe colitis); severe abdominal pain suggesting perforation; or signs of sepsis. Attend urgent review if you have bloody diarrhoea more than 6 times per day, cannot maintain oral intake, or have lost more than 10% of body weight. Contact your gastroenterologist if you notice a change in your usual IBD pattern, develop new perianal symptoms, or if your symptoms are not controlled despite prescribed therapy. All patients with IBD should have regular gastroenterology follow-up every 6-12 months, with colonoscopy according to surveillance intervals based on disease extent and duration.