Inflammatory Bowel Disease — Symptoms, Causes & Treatment | MyMedicPlus

Inflammatory bowel disease (IBD) is a chronic, relapsing-remitting autoimmune condition of the gastrointestinal tract, comprising two main forms: Crohn's disease (CD) and ulcerative colitis (UC). CD can affect any part of the GI tract from mouth to anus (most commonly the terminal ileum and colon) with transmural inflammation; UC affects the colon continuously from the rectum upward with mucosal inflammation only. IBD affects over 6.8 million people globally, with rising incidence in newly industrialized nations — suggesting an important role of the 'Western' microbiome and lifestyle in pathogenesis. Approximately 25–40% of IBD patients have at least one extraintestinal manifestation — peripheral arthropathy (most common), sacroiliitis, primary sclerosing cholangitis (PSC — strongly associated with UC, increases colorectal cancer risk 5-fold), erythema nodosum, pyoderma gangrenosum, anterior uveitis, and aphthous stomatitis. PSC complicates UC in approximately 5% of cases and is independently associated with biliary cirrhosis, cholangiocarcinoma, and colorectal cancer even after colectomy. The incidence of IBD has increased dramatically over the past 50 years, particularly in newly industrialized countries adopting a Western diet and lifestyle.

IBD results from a dysregulated immune response to intestinal microbiota in genetically susceptible individuals, with over 200 IBD-associated genetic loci identified (NOD2, IL23R among the strongest). Risk factors include family history (15–20% of IBD patients have an affected first-degree relative), previous enteric infection (Campylobacter, Salmonella), NSAIDs and antibiotic use, vitamin D deficiency, urban residence, high-fat/low-fiber Western diet, childhood hygiene hypothesis (reduced microbial exposure), and appendectomy (protective for UC). Cigarette smoking paradoxically worsens Crohn's disease but is mildly protective in UC. The 'old friends' hypothesis and hygiene hypothesis propose that loss of microbial diversity and parasitic exposure in Westernized environments fails to adequately train regulatory T-cells, predisposing to excessive inflammatory responses. Appendectomy before age 20 is associated with 70% reduced risk of subsequent UC, supporting the role of the appendix in intestinal immune regulation. Dietary emulsifiers (carboxymethylcellulose, polysorbate 80) in processed foods disrupt the intestinal mucus layer and alter microbiome composition, promoting gut inflammation in animal models.

UC presents with bloody diarrhea (the hallmark), rectal urgency, tenesmus, mucus in stools, abdominal cramping, and weight loss. Disease severity ranges from proctitis (rectum only) to pancolitis. Crohn's disease presents with non-bloody diarrhea, right iliac fossa abdominal pain in ileocolic disease, weight loss, fever, fatigue, and perianal disease (fistulae, abscesses) in up to 40% of patients. IBD is associated with extraintestinal manifestations in 25–40% of patients: peripheral arthritis, sacroiliitis, primary sclerosing cholangitis (strongly associated with UC), erythema nodosum, pyoderma gangrenosum, anterior uveitis, and aphthous mouth ulcers. Disease activity in UC is graded using the Mayo Clinic Score or Simple Clinical Colitis Activity Index (SCCAI): mild UC (less than 4 bloody stools/day, CRP below 30 mg/L), moderate (4–6 stools/day with systemic upset, CRP 30–50 mg/L), and severe (more than 6 bloody stools/day with systemic toxicity — Truelove and Witts criteria — requiring immediate hospital admission for IV steroids and surgical review). Crohn's disease activity is assessed using the Harvey-Bradshaw Index or Crohn's Disease Activity Index (CDAI).

Colonoscopy with biopsy is the gold standard for IBD diagnosis, characterizing mucosal inflammation pattern, extent, and severity. CRP and fecal calprotectin (stool marker) assess inflammatory activity — fecal calprotectin above 200 µg/g predicts mucosal inflammation with 80% sensitivity and is used for non-invasive monitoring. MR enterography (MRE) is essential for assessing small bowel Crohn's extent, strictures, and perianal disease. Stool cultures exclude infective causes. Capsule endoscopy evaluates small bowel mucosa when MRE is inconclusive. Biochemistry: CBC (anemia, leukocytosis), albumin, CRP, and iron studies. Magnetic resonance enterography (MRE) is the gold standard for assessing small bowel Crohn's extent, activity (mural enhancement, wall thickening, mucosal ulceration), and complications (fistulae, abscesses, strictures) — superior to CT in avoiding radiation and providing soft tissue characterisation. Wireless capsule endoscopy visualises the entire small bowel mucosa and is used when MRE and conventional endoscopy are inconclusive for small bowel Crohn's (contraindicated if intestinal stricture suspected).

Treatment goals are mucosal healing and sustained remission. UC: aminosalicylates (mesalazine/5-ASA) for mild-moderate disease; corticosteroids for acute flares (not maintenance); thiopurines (azathioprine) for maintenance; biologics for moderate-severe disease. Crohn's disease: early introduction of biologics for moderate-severe disease is now recommended. Biologic agents: anti-TNF (infliximab, adalimumab, certolizumab); anti-integrin (vedolizumab — gut-selective); IL-12/23 inhibitor (ustekinumab); IL-23 inhibitor (risankizumab). Small molecules: JAK inhibitors (tofacitinib, upadacitinib) for UC. Surgery (colectomy) is curative in UC; in CD it treats complications but does not cure the underlying condition. Therapeutic drug monitoring (TDM) of biologics — measuring serum trough drug levels and anti-drug antibodies — is now standard practice for optimising infliximab and adalimumab therapy. Target infliximab trough level above 3–7 mg/L for luminal disease; above 10 mg/L for fistulating or perianal disease. Low trough levels with high anti-drug antibodies indicate immunogenic failure — switch to a different biologic class; low trough without antibodies suggests pharmacokinetic failure — increase dose or frequency.

Stricturing Crohn's disease causes intestinal obstruction. Penetrating disease causes fistulae and abscesses requiring drainage and anti-TNF therapy or surgery. Toxic megacolon — colonic dilatation above 6 cm with systemic toxicity — is a life-threatening complication of UC flares requiring emergency colectomy. Colorectal cancer risk is elevated in long-standing extensive colitis — surveillance colonoscopy every 1–5 years after 8 years of extensive colitis is recommended. Primary sclerosing cholangitis complicates UC in 5% and leads to biliary cirrhosis and biliary tract cancer. Short bowel syndrome from repeated surgical resections causes malabsorption requiring parenteral nutrition.

IBD cannot currently be prevented, but lifestyle modifications may reduce flare frequency and progression. Quit smoking absolutely for Crohn's disease — smoking doubles disease severity, flare frequency, and surgical rates. Exercise and stress management reduce flare frequency. Optimize nutritional status: iron deficiency anemia is common and requires supplementation or IV iron infusion; vitamin D and B12 supplementation are often required in Crohn's. Ensure all vaccinations are up to date before starting immunosuppressive therapy — live vaccines are contraindicated on biologics. Colonoscopic cancer surveillance every 1–5 years after 8 years of extensive colitis is essential.

Seek emergency care for: severe abdominal pain, distension, or rebound tenderness (possible toxic megacolon or perforation — surgical emergency), high fever with bloody diarrhoea above 6 times per day (severe IBD flare requiring IV steroids), or significant rectal bleeding causing haemodynamic instability. See your gastroenterologist urgently for: an IBD flare not improving with oral steroids after 3-5 days, fever during a flare (excludes infection before immunosuppressant escalation), new severe abdominal pain in established IBD (exclude perforation, abscess, or stricture). See a doctor promptly for: rectal bleeding, mucus in stool, urgency or tenesmus (particularly with weight loss or anaemia in adults over 40 — red flags for colorectal cancer). IBD patients should have annual colorectal cancer surveillance colonoscopy from 8-10 years after diagnosis.