Inflammatory Bowel Disease

Umbrella page for material shared by Ulcerative Colitis and Crohn Disease — epidemiology, classification, clinical features, diagnosis, and medical treatment. Surgical indications/options are disease-specific and live on the individual UC and Crohn’s pages. Content below is from a textbook reference chapter (Sabiston Ch52 - Inflammatory Bowel Disease), not primary literature — no specific trial is backing any individual claim here yet.

Epidemiology and etiology

Largely a disease of the Western world, though incidence is rising elsewhere as diets westernize. US prevalence: IBD in >1 million individuals; UC has the highest reported incidence in Europe (followed by US), Crohn’s the highest in the US (followed by Europe); Europe has the highest overall IBD prevalence.

• Genetic predisposition: >10% of IBD patients have a family history; genome-wide association studies have linked >230 IBD susceptibility loci.
• Smoking is the most-studied environmental factor and has opposite effects: suppresses UC symptoms, exacerbates Crohn’s.
• Early-life antibiotic use and NSAID use have both been proposed as predisposing factors.

Classification

• UC graded by extent: proctitis/proctosigmoiditis (rectum/sigmoid only), left-sided, or pancolitis (entire colon).
• Crohn’s: originally the Vienna Classification, updated to the Montreal Classification — classifies by age of onset, bowel location, and disease behavior (inflammatory, fibrostenotic, or fistulizing), plus a perianal-disease subdivision. Many patients progress inflammatory → fibrostenotic → fistulizing over time (abscess formation when a fibrostenotic segment perforates and drains into an adjacent structure). Top-down medical therapy aims to interrupt this progression before it reaches fibrosis/fistulization.

Clinical presentation

Diarrhea is common to both, but bloody diarrhea/significant hemorrhage is much more common in UC (UC also brings tenesmus, urgency, anemia); abdominal pain tends to predominate in Crohn’s. Stool cultures should be obtained first in any new presentation to exclude infectious causes (Salmonella, Giardia, community-acquired C. difficile).

Perianal Crohn’s (~25% of Crohn’s patients): large anal skin tags (bluish, waxy — not true hemorrhoids, should not be excised due to delayed wound healing), anal fissures (often painless, may be multiple — unlike typical non-Crohn’s fissures), anorectal abscesses/fistulas, anal stenosis. Always perform a DRE.

Extraintestinal manifestations

Up to half of IBD patients have one or more; slightly more prevalent in Crohn’s than UC.

• Joints (most common): arthritis broadly; sacroiliitis is one of the most common single manifestations; ankylosing spondylitis (HLA-B27 positive) can progress to decreased cervical flexion — anesthesia-relevant, may need fiberoptic intubation.
• Skin: erythema nodosum (red, painful, swollen nodules — responds to systemic steroids) and pyoderma gangrenosum (extremely painful ulcerating lesions at sites of trauma, surgical incisions, or stomas). “Pathergy” — pyoderma worsens with surgical manipulation/debridement, so it should be treated nonoperatively (intralesional steroids, topical tacrolimus, biologics), not surgically.
• Eyes: uveitis, iritis, episcleritis — refer to ophthalmology.
• Hepatobiliary — primary sclerosing cholangitis-IBD: affects ~2% of IBD overall (pooled), substantially higher in ulcerative colitis than Crohn’s; conversely, most PSC patients (often

  50–80%) have concurrent IBD. Runs a course largely independent of bowel disease activity, can progress to cirrhosis/liver failure/transplant. PSC-IBD is a distinct phenotype (BSG 2025 - IBD Guidelines (Adults)): pan-colonic or right-sided colitis with relative/absolute rectal sparing, backwash ileitis, and a milder symptomatic course (less corticosteroid use, fewer hospitalisations) that can mask ongoing risk — histologic inflammation is often mild with focal basal plasmacytosis rather than typical UC-pattern changes. Despite the milder symptomatic course, PSC-IBD carries a 3–4x increased colorectal dysplasia/cancer risk versus IBD alone (OR 3.24) and a 4x risk versus non-IBD PSC patients diagnosed under 40 — annual surveillance colonoscopy is recommended from 8 years after IBD symptom onset, or from PSC diagnosis if that comes first, continuing even post-liver-transplant (lifelong high-risk category). Higher pouchitis rates after IPAA in PSC-IBD (14–90% across studies), though pouch failure rates are similar to non-PSC IBD — relevant cross-link to Ulcerative Colitis surveillance and Ileal Pouch-Anal Anastomosis (IPAA).

• Joints — spondyloarthropathy, drug-specific guidance (BSG 2025 - IBD Guidelines (Adults)): anti-TNF is first-line for concurrent axial/peripheral spondyloarthropathy (SpA) and IBD. Ustekinumab and risankizumab are licensed for IBD + psoriatic arthritis/psoriasis but not for axial SpA specifically; tofacitinib and upadacitinib have UK licences spanning UC/Crohn’s and PsA/axial SpA to varying degrees (tofacitinib not licensed for Crohn’s). Etanercept, abatacept, secukinumab, ixekizumab, and brodalumab should be avoided in IBD patients with concurrent SpA — they lack IBD efficacy and carry a risk of causing IBD exacerbation (etanercept specifically linked to IBD relapse when used for SpA). Separately, anti-TNF therapy itself can paradoxically induce psoriasis/psoriasiform rash in 2–5% of treated IBD patients (risk factors: smoking, ileocolonic Crohn’s, female sex, younger age at initiation) — this doesn’t automatically warrant anti-TNF discontinuation; options include topical management, in-class drug switch, or biologic class change depending on severity.

Diagnosis

Endoscopy is the primary diagnostic method — colonoscopy to assess extent and examine the terminal ileum.

• UC: inflammation begins at the dentate line and extends proximally, continuously (no skip lesions). Endoscopic severity is commonly graded with the Mayo Clinic Scoring System (grade 1 normal-ish → grade 4 significant bleeding/friability).
• Crohn’s: patchy/discontinuous (“skip”) inflammation; deeper, punched-out ulcerations covered with fibrin; longer serpiginous ulcers described as “bear claw” ulcerations, often worse on the mesenteric side. Ileocolic distribution in nearly half of patients, followed by colonic-only involvement; can also affect small bowel or upper GI tract. Terminal ileum intubation is important when Crohn’s is suspected.

Histology:

• UC: neutrophils in the lamina propria, goblet-cell mucin depletion, crypt abscesses (nonspecific), inflammation restricted to the mucosa (superficial), continuous — no transmural sinus tracts, deep fissuring ulcers, or granulomas in an area that isn’t deeply ulcerated.
• Crohn’s: transmural inflammation (seen on resected specimens); noncaseating granulomas in roughly a third of patients; transmural lymphoid aggregates in non-deeply-ulcerated areas; “skip”/patchy involvement, sometimes called “focal active enteritis” on biopsy.
• Differential for both: infectious colitis, drug-induced colitis.

IBD undetermined / indeterminate colitis: up to 10–15% of patients have overlapping UC/Crohn’s features on biopsy. “Indeterminate colitis” is specifically the diagnosis made on a colectomy specimen when features of both are present — more common in fulminant disease where heavy inflammation obscures precise classification.

Medical treatment

Treatment philosophy has shifted over the last two decades from “bottom-up” (safest/cheapest medications first, escalate on failure) to “top-down” (more potent medications used earlier) — aiming to suppress disease before structural damage (fibrosis, fistulas) accumulates. Note: many of these drugs are associated with higher postoperative complication rates and with reactivation of latent infections — relevant to preop planning.

Drug class	Examples	Indication	Route
Biologics	Infliximab, adalimumab	UC, CD	IV / SC
	Golimumab	UC	IV
	Natalizumab	CD	IV
	Vedolizumab	UC, CD	IV
	Ustekinumab	UC, CD	IV, SC
Aminosalicylates	Sulfasalazine	UC, CD	PO
	Mesalamine	UC, CD	PO, enema, suppository
Immunosuppressives	Conventional steroids	UC, CD	PO, IV, suppository
	Budesonide	UC, CD	PO, rectal foam
	Antimetabolites	UC, CD	PO
	Tofacitinib	UC	PO
Probiotics	Lactobacillus, Bifidobacterium	UC, CD	Food/tablets/capsules/powders
Antibiotics	Ciprofloxacin, metronidazole	UC, CD	PO, IV
	Rifaximin	Off-label	PO

Aminosalicylates — sulfasalazine’s sulfapyridine ring limits use in sulfa allergy and requires folic acid supplementation; active moiety is 5-ASA. Mesalamine formulations target different GI segments by design (Pentasa dissolves in the stomach and releases throughout the GI tract; Asacol uses a pH-dependent release beginning in the terminal ileum, coating the whole colon; “MMX” formulations are once-daily, releasing throughout the colon for better compliance). Topical suppository (Canasa) or enema (Rowasa) forms, given at bedtime, are most effective for mild-to- moderate distal disease.

Corticosteroids — still prominent for severe disease: inexpensive, fast-acting, no insurance preauthorization needed. Side effects: cushingoid appearance, aseptic hip necrosis, hypertension, mood changes (up to psychiatric presentations), hyperglycemia, increased postoperative infectious complications, cataracts, striae, growth retardation in children. Outpatient pulse dosing: prednisone 40–60 mg/day tapering 5–10 mg every 2 weeks down to 10 mg/day, then 5 mg every 2 weeks to discontinuation. Inpatient: IV hydrocortisone 100 mg q6–8h depending on severity.

Immunomodulators — thiopurines (azathioprine, 6-mercaptopurine) are steroid-sparing, typically started after 1–2 failed steroid-wean attempts; TPMT genotyping is recommended before starting (poor metabolizers are at higher risk of leukopenia/pancreatitis); oral, once-daily, weight-based; 3–4 month lag to effect, so not useful for acute flares; long-term use raises non-Hodgkin lymphoma risk. Methotrexate is an alternative steroid-sparing option (IM or oral — IM particularly useful if diarrhea/absorption is a concern), with LFT elevation and pulmonary fibrosis as key side effects; also requires folic acid supplementation.

Biologics — anti-TNF-α therapy began with infliximab (FDA approval for Crohn’s, 1998), followed by adalimumab (2007), certolizumab pegol and natalizumab (2008), golimumab for UC (2013), vedolizumab (anti-α4β7 integrin, 2014), ustekinumab (anti-IL-12/23, 2016), and tofacitinib (JAK inhibitor, UC, 2018). Side effects include reactivation of latent infections (TB, histoplasmosis, actinomycosis, hepatitis) — screen with TB skin test or QuantiFERON gold plus a hepatitis panel before starting (no reliable test exists for histoplasmosis exposure). Combination thiopurine + anti-TNF therapy carries a low but notable risk of hepatosplenic T-cell lymphoma, particularly in young men.

Symptom severity assessment: Truelove and Witts classification (diarrhea frequency, blood in stool, fever, tachycardia, anemia, ESR); fecal calprotectin/lactoferrin as inflammatory markers; for Crohn’s specifically, the Crohn’s Disease Activity Index (CDAI — 8 variables including bowel movements/day, abdominal pain, hematocrit, weight loss; requires a 7-day diary; <150 = remission,

450 = severe) and the simplified, clinical-data-only Harvey-Bradshaw Index.

Therapeutic drug monitoring (BSG 2025 guideline)

Applies across both diseases; adds concrete numbers to what was previously only qualitative mentions of TPMT testing above. Full detail on BSG 2025 - IBD Guidelines (Adults).

• Purine analogue metabolites: target 6-TGN 235–450 pmol/8×10⁸ RBCs, MMP <5700 pmol/8×10⁸ RBCs (or MMP:6-TGN ratio >11 suggests hypermethylation — consider low-dose purine analogue + allopurinol 100mg/day instead). TPMT genotyping/phenotyping before starting (as above); NUDT15 variant testing also relevant, especially in patients of East/South Asian ancestry (higher myelosuppression risk), though not yet widely available in the UK.
• Anti-TNF trough levels: reactive TDM (checking levels + antidrug antibodies on secondary loss of response) is well-supported; the PANTS study suggests later-time-point (week 14+) optimal trough targets of 6.1–10.0 mg/L for infliximab and 10.1–12.0 mg/L for adalimumab, though evidence is insufficient to formally recommend routinely targeting such high levels. Combination with an immunomodulator reduces anti-drug antibody formation.
• Vedolizumab/ustekinumab exposure-efficacy data are less consistent; dose escalation (shortening the interval) may help in partial responders, but routine trough-level testing isn’t yet evidence-supported for these agents.

Pregnancy (BSG 2025 guideline)

A topic essentially absent from this wiki before this ingest — full detail on BSG 2025 - IBD Guidelines (Adults).

• Pre-conception: aim for ≥3 months of corticosteroid-free clinical remission before conception — active disease at conception roughly doubles the risk of disease activity/relapse during pregnancy and is independently associated with adverse foetal outcomes (low birth weight, preterm birth, small-for-gestational-age, spontaneous abortion). Stop methotrexate ≥3 months pre-conception (both sexes — teratogenic); stop JAK inhibitors and S1P modulators ≥3 months pre-conception.
• During pregnancy: continue anti-TNF therapy throughout pregnancy — reduces relapse risk with no increased adverse-pregnancy-outcome signal versus non-pregnant IBD patients (some retrospective data link continuation beyond 24 weeks to higher maternal infection/complication rates, but not to worse foetal outcomes). Vedolizumab and ustekinumab appear low-risk with less extensive data. JAK inhibitors (tofacitinib, upadacitinib, filgotinib) and S1P modulators (ozanimod, etrasimod) are contraindicated during conception, pregnancy, and lactation. 5-ASAs and purine analogues are considered low-risk and should be continued if needed for disease control. Corticosteroids: moderate risk, likely lower with budesonide than prednisolone given reduced placental transfer — active disease requiring steroids is itself the bigger foetal risk, so undertreatment is not the safer choice.
• Delivery and postpartum: caesarean section generally preferred for active perianal disease or in patients with an ileal pouch-anal or ileorectal anastomosis; otherwise delivery mode is obstetric/patient-preference-driven. VTE prophylaxis is important postpartum, especially after caesarean section in active IBD. Breastfeeding is considered low-risk/should continue for essentially all standard IBD medications (5-ASA, purine analogues, corticosteroids, anti-TNF, vedolizumab, ustekinumab) — except JAK inhibitors and S1P modulators, which are not recommended during lactation.
• Infant vaccination: live vaccines (including BCG) should be withheld until 12 months of age in infants with in-utero exposure to biologics — several fatal disseminated BCG infections have been reported in infants vaccinated before 1 month of age after infliximab/adalimumab exposure. Standard inactivated-vaccine schedules proceed normally; exposed infants mount appropriate antibody responses to them.

Perioperative management and superadded infection (BSG 2025 guideline)

• VTE prophylaxis: IBD carries ~2x baseline VTE risk versus non-IBD, further elevated with active inflammation (HR 8.4) and hospitalisation for any reason (~1.5x). Pharmacological VTE prophylaxis is recommended for essentially all IBD patients admitted for acute illness or surgery unless contraindicated — including ASUC patients (does not worsen colonic bleeding). Elevated risk persists 60–90 days post-discharge; UK practice extends prophylaxis post-discharge after major abdominal surgery.
• Perioperative drug management: corticosteroids should be stopped/minimised preoperatively where possible (equivalent IV hydrocortisone if steroid-dependent and NPO). Immunosuppressive agents (purine analogues, methotrexate) and biologics (anti-TNF, vedolizumab, ustekinumab) can be continued perioperatively — large observational studies (PUCCINI, French REMIND) found no significant postoperative infection increase with anti-TNF exposure. JAK inhibitor perioperative safety data are limited (one series: 13.2% VTE rate after tofacitinib exposure before colectomy in ulcerative colitis) — prolonged VTE prophylaxis suggested in these patients.
• CMV and C. difficile superinfection: CMV present in up to 10–30% of steroid-refractory IBD; best diagnosed via colonic tissue immunohistochemistry/PCR (serum tests correlate poorly); treated with IV ganciclovir then oral valganciclovir to complete a 2–3 week course, continuing background immunosuppression unless disseminated disease. C. difficile — see Infectious Colitis for full detail; IBD is an independent CDI risk factor regardless of antibiotic/PPI exposure, and CDI in IBD carries higher colectomy, complication, and mortality rates than in non-IBD patients.

Open items / gaps

• Both UC and Crohn’s now have primary-guideline-sourced medical management — see Ulcerative Colitis (from ACG 2025 - Ulcerative Colitis Guideline and AGA 2024 - Moderate-to-Severe UC Pharmacotherapy Guideline) and Crohn Disease’s new “Advanced therapy, monitoring, and post-surgical management” section (from BSG 2025 - IBD Guidelines (Adults)). The wiki’s IBD medical-management asymmetry flagged earlier in this ingest session is now closed.
• The shared drug-class table above is still textbook-level (mechanism/route only) — UC-specific positioning lives on Ulcerative Colitis, Crohn’s-specific positioning lives on Crohn Disease, and genuinely cross-cutting content (TDM, pregnancy, perioperative management, PSC-IBD, spondyloarthropathy) now lives here.
• BSG’s UC-specific recommendations were not exhaustively transcribed to Ulcerative Colitis during this ingest (see BSG 2025 - IBD Guidelines (Adults)‘s Limitations) — UC ground was already well covered by the other two guidelines, so BSG content prioritized Crohn’s and cross-cutting topics. Flag if a specific BSG UC recommendation is needed and missing.
• Fecal calprotectin/lactoferrin use in practice: UC-specific cutoffs and monitoring guidance is on Ulcerative Colitis; Crohn’s-specific cutoffs still not separately detailed.
• See Ulcerative Colitis and Crohn Disease for disease-specific surgical open items.