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Inflammatory Bowel Disease — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Updated: 2026-07-06
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Quick Facts

Type
Chronic idiopathic inflammatory bowel disease (Crohn's disease and ulcerative colitis)
Specialist
Gastroenterologist / IBD Specialist Nurse
Key Treatment
UC: mesalazine (5-ASA), corticosteroids, azathioprine, anti-TNF biologics. Crohn's: corticosteroids, azathioprine, anti-TNF (infliximab, adalimumab), vedolizumab, ustekinumab
Prevalence
Affects over 10 million people globally; highest incidence in Western Europe, North America, and Australasia; incidence rising in newly industrialised nations

What Is Inflammatory Bowel Disease?

Inflammatory bowel disease (IBD) is a group of chronic idiopathic inflammatory conditions affecting the gastrointestinal tract. The two main forms are ulcerative colitis (UC) and Crohn's disease. Ulcerative colitis involves continuous mucosal inflammation restricted to the colon and rectum (extends proximally from the rectum; always involves the rectum). Crohn's disease can affect any part of the GI tract from mouth to anus, with transmural (full-thickness) inflammation and skip lesions (areas of healthy bowel between inflamed segments); it most commonly affects the terminal ileum and ileocaecal region. A third category, IBD unclassified (IBDU or indeterminate colitis), applies when features of both conditions are present. IBD affects over 10 million people globally, with peak onset in the second and third decades of life, causing a significant chronic disease burden in young adults.

Causes & Risk Factors

IBD results from an inappropriate chronic immune response to the gut microbiome in genetically susceptible individuals. Genetic factors: over 200 susceptibility gene loci identified (NOD2 — Crohn's disease; HLA loci — UC); concordance in identical twins: 50% for Crohn's (strong genetic component) and 15% for UC (environmental factors more important). Environmental factors: smoking — paradoxically, smoking protects against UC but nearly doubles the risk of Crohn's disease; appendectomy reduces UC risk; antibiotic use in childhood; altered gut microbiome (reduced microbial diversity); Western diet (low fibre, high processed food); urban dwelling (hygiene hypothesis); and vitamin D deficiency. The gut microbiome dysbiosis — reduced Faecalibacterium prausnitzii (anti-inflammatory commensal) and increased adherent-invasive Escherichia coli — is characteristic of Crohn's disease. IBD is more common in Ashkenazi Jewish populations.

Symptoms & Signs

Ulcerative colitis: bloody diarrhoea (the cardinal symptom — present in virtually all UC), rectal urgency and tenesmus, mucus in stool, abdominal cramping (left-sided or generalised), and nocturnal diarrhoea. Severity ranges from mild (fewer than 4 stools per day, no systemic upset) to severe/fulminant (more than 6-8 bloody stools daily with fever, tachycardia, anaemia, and hypoalbuminaemia — Truelove and Witts criteria). Crohn's disease: right lower quadrant pain (terminal ileal disease), non-bloody diarrhoea (unless colonic involvement), weight loss, malnutrition, and fatigue. Perianal disease (fistulae, skin tags, perianal abscesses) is highly specific for Crohn's. Extra-intestinal manifestations (both conditions): peripheral arthropathy, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis (more common in UC), uveitis/episcleritis, and ankylosing spondylitis.

How IBD Is Diagnosed

Diagnosis requires clinical assessment combined with endoscopic, histological, and cross-sectional imaging. Blood tests: FBC (anaemia — iron deficiency from bleeding/malabsorption), CRP and ESR (elevated in active inflammation), albumin (low in severe disease/malnutrition), vitamin B12 and folate (terminal ileal Crohn's malabsorption). Faecal calprotectin (FC): highly sensitive marker for intestinal inflammation — FC above 100-250 mcg/g strongly suggests active IBD and guides endoscopy decision (excellent test to distinguish IBD from IBS). Colonoscopy with multiple biopsies: gold standard — UC shows continuous mucosal inflammation from rectum proximally; Crohn's shows skip lesions, cobblestone pattern, aphthous ulcers, transmural inflammation, and non-caseating granulomas on histology. MRI enterography (MRE): modality of choice for small bowel Crohn's, identifying active inflammation, strictures, and fistulae without radiation. CT abdomen: for acute presentations (toxic megacolon, perforation, abscess). Ileocolonoscopy and biopsy essential for initial diagnosis.

Treatment Options

Ulcerative colitis — induction and maintenance of remission: Mild-moderate UC: topical (rectal) and/or oral 5-aminosalicylates (mesalazine/mesalamine) are first-line for induction and maintenance; oral prednisolone for acute flares not responding to 5-ASA. Moderate-severe UC: systemic corticosteroids (IV hydrocortisone for hospitalised severe colitis), azathioprine or mercaptopurine (thiopurines) for steroid-sparing maintenance, anti-TNF biologics (infliximab — IV infusion; adalimumab — subcutaneous injection; golimumab), vedolizumab (gut-selective anti-integrin biologic), tofacitinib (JAK inhibitor — oral). Colectomy for medically refractory disease or colorectal cancer risk. Crohn's disease: induction — budesonide (ileal/ileocolonic CD), prednisolone, exclusive enteral nutrition (particularly in children); maintenance — azathioprine, methotrexate, anti-TNF agents (infliximab, adalimumab, certolizumab), vedolizumab, ustekinumab (anti-IL-12/23). Perianal fistulising Crohn's: infliximab, setons (surgical drains). Surgery for strictures, abscesses, or medically refractory disease. Therapeutic drug monitoring (TDM) — measuring anti-TNF drug trough concentrations and anti-drug antibody levels — is now standard practice to optimise anti-TNF therapy; dose adjustment to achieve therapeutic target drug levels improves clinical outcomes and reduces the risk of secondary treatment failure from immunogenicity.

Complications of IBD

IBD carries significant risk of both intestinal and extra-intestinal complications. Intestinal complications include fibrous strictures causing bowel obstruction (most common in Crohn's disease); fistulas (abnormal connections between bowel and adjacent organs — bladder, vagina, or skin); abscess formation; acute severe colitis (medical emergency requiring IV hydrocortisone, ciclosporin, or infliximab — 25-30% require emergency colectomy); toxic megacolon (life-threatening colonic dilatation above 6 cm requiring urgent surgery); haemorrhage; and perforation. Colitis-associated colorectal cancer: UC and Crohn's colitis increase colorectal cancer risk 2-3 fold after 8-10 years of extensive colitis — annual or biennial surveillance colonoscopy is mandatory. Extra-intestinal manifestations affect 25-40% of patients: peripheral arthropathy, sacroiliitis, uveitis, episcleritis, erythema nodosum, pyoderma gangrenosum, and primary sclerosing cholangitis (PSC — associated with UC, may progress to cirrhosis and liver failure). Nutritional deficiencies include iron, B12, folate, vitamin D, zinc, and calcium. Immunosuppressants and biologics increase risk of serious infections, lymphoma (thiopurines — 4x increased risk), and non-melanoma skin cancer.

Prevention & Flare Management

IBD cannot currently be prevented, but flare triggers can be managed. Maintain medication adherence — stopping 5-ASA maintenance therapy causes UC relapse in 80% within 1 year. Avoid NSAIDs (ibuprofen, aspirin — exacerbate IBD; use paracetamol instead). Smoking cessation for Crohn's disease (smoking worsens Crohn's significantly — increases flare rate and surgical requirement). Low-residue diet during flares; reintroduce fibre gradually. Stress management — stress is a common flare trigger. Engage with an IBD nurse specialist for early flare detection and treatment escalation. Annual colorectal cancer surveillance colonoscopy from 8-10 years after IBD diagnosis (UC and Crohn's colitis carry increased colorectal cancer risk). Vitamin D and calcium supplementation for corticosteroid-associated bone loss. Psychological support for anxiety and depression (common in IBD).

When to See a Doctor

Contact your IBD team urgently or go to A&E for: severe abdominal pain; bloody diarrhoea more than 8 times in 24 hours; fever above 38.5°C with IBD; signs of dehydration; rectal bleeding requiring hospitalisation; and suspected bowel obstruction (absolute constipation, vomiting, abdominal distension). Contact your IBD nurse or GP within 24-48 hours for any increase in bowel frequency, blood in stool, abdominal pain, or systemic symptoms such as fever or significant weight loss. New perianal symptoms (abscess, fistula, painful swelling) need prompt assessment. If newly diagnosed with bloody diarrhoea, see a GP urgently — early colonoscopy is needed to establish diagnosis and exclude infection.

Frequently Asked Questions

Both Crohn's disease and ulcerative colitis (UC) are forms of inflammatory bowel disease, but they differ in location, pattern of inflammation, and behaviour. UC is restricted to the colon and rectum, always involves the rectum, and causes continuous mucosal (surface-layer) inflammation — characteristically presenting with bloody diarrhoea. Crohn's disease can affect any part of the GI tract from mouth to anus, has skip lesions (areas of normal bowel between inflamed segments), causes transmural (full-thickness) inflammation, and typically presents with diarrhoea (often non-bloody), right lower quadrant pain, and weight loss. Perianal complications (fistulae, abscesses) are specific to Crohn's. Treatment approaches differ, though both conditions share many therapies.
Yes, both UC and Crohn's colitis increase the risk of colorectal cancer (CRC), related to chronic bowel inflammation. The risk increases with disease duration, extent (total colitis has higher risk than limited proctitis), severity of inflammation, primary sclerosing cholangitis (PSC) co-existing with UC (highest risk group — 5-fold CRC risk), and family history of CRC. Annual or biennial surveillance colonoscopy is recommended from 8-10 years after IBD diagnosis, or immediately at diagnosis if PSC is present. Chronic bowel inflammation detected at surveillance is treated with intensified therapy or surgery before it progresses to cancer. Good long-term inflammation control reduces cancer risk.
Diet does not cause IBD, but certain foods can trigger flares or worsen symptoms in susceptible individuals. Common problem foods during flares include high-residue foods (raw vegetables, nuts, seeds, fruit skins), spicy food, alcohol, fizzy drinks, and dairy products in some patients (secondary lactose intolerance is common during active disease). Exclusive enteral nutrition (liquid formula diet) is a first-line treatment for Crohn's disease in children, inducing remission comparably to steroids in some studies. During remission, a balanced diet rich in vegetables, fruits, and whole grains is recommended. Specific carbohydrate diets, low-FODMAP, and Mediterranean-style diets have been investigated with some positive results, but no single diet is universally recommended for all IBD patients.
Anti-TNF biologics (infliximab, adalimumab) and newer agents (vedolizumab, ustekinumab) have extensive safety data over 15-20 years of use in IBD. Key risks include: increased susceptibility to infections (particularly tuberculosis with anti-TNFs — mandatory TB screening before starting); opportunistic infections; possible increased lymphoma risk with thiopurines (azathioprine); and rarely, demyelinating conditions or worsening heart failure with anti-TNF agents. Vedolizumab is gut-selective with lower systemic immunosuppression risk — preferred for older patients or those with multiple co-morbidities. The benefit of achieving and maintaining mucosal healing (reducing cancer risk, preventing hospitalisation, preserving bowel) generally substantially outweighs biologic therapy risks in most patients.

References

  1. NICE Guideline NG129 — Crohn's Disease: Management, 2019 (updated 2023)
  2. NICE Guideline NG130 — Ulcerative Colitis: Management, 2019 (updated 2023)
  3. Ungaro R et al. — Ulcerative Colitis, The Lancet, 2017
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Last updated: 2026-07-06

Important: This information is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider for diagnosis and treatment.

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