# Inflammatory Bowel Disease: Crohn's Disease & Ulcerative Colitis

Inflammatory bowel disease (IBD) is a group of chronic immune-mediated GI conditions comprising Crohn's disease (CD) and ulcerative colitis (UC). Over 7 million people worldwide have IBD, with peak onset at 15–35 years. Prevalence is steadily rising, particularly in developing countries, linked to 'westernization' of lifestyle. IBD is a lifelong disease with periods of flares and remissions, requiring long-term, often lifelong therapy.

Ulcerative colitis: affects only the colon (from rectum proximally). Inflammation is continuous and limited to the mucosa. Typical symptoms: bloody diarrhea, tenesmus, urgency. Subtypes by extent: proctitis (rectum), left-sided colitis, pancolitis.

Crohn's disease: can affect any GI segment from mouth to anus (most commonly terminal ileum and colon). Inflammation is 'patchy' (skip lesions) and transmural (through entire wall). Typical symptoms: abdominal pain, diarrhea (often non-bloody), weight loss, fever. Complications: strictures, fistulas (perianal, interenteric), abscesses.

IBD-unclassified (IBD-U): 10–15% of cases — cannot distinguish CD from UC with available data.

IBD results from four interacting factors: Genetics: >200 susceptibility loci (NOD2/CARD15 — main for CD). Concordance in monozygotic twins: 50% for CD, 16% for UC. Microbiome: dysbiosis — reduced diversity (especially Firmicutes, Bacteroidetes), increased Enterobacteriaceae. Immune dysregulation: inappropriate immune response to commensal flora. In CD — Th1/Th17 predominance (IL-12, IL-23, TNF-α). In UC — Th2 and NKT cells (IL-5, IL-13). Environmental factors: smoking (doubles CD risk but protects against UC!), childhood antibiotics, Western diet (high fat, low fiber), NSAIDs, stress.

Clinical + laboratory markers + endoscopy + histology + imaging — comprehensive approach. Laboratory markers: CRP and ESR (inflammation), fecal calprotectin (>250 mcg/g — high sensitivity for IBD; used for monitoring), CBC (anemia, leukocytosis), albumin (nutritional status), ferritin + TSAT (iron deficiency). pANCA (more UC) and ASCA (more CD) — serological markers.

Endoscopy: ileocolonoscopy with biopsy — gold standard. UC: continuous inflammation from rectum, contact bleeding, pseudopolyps. CD: aphthous ulcers, cobblestoning, skip lesions, strictures. Upper endoscopy — when suspecting upper GI involvement (CD). Video capsule endoscopy — for suspected small bowel CD.

Imaging: MR enterography (MRE) — gold standard for small bowel assessment (wall thickening, strictures, fistulas, abscesses). CT enterography — in acute settings. Pelvic MRI — for perianal CD.

Modern 'treat-to-target' strategy: Short-term: symptom relief (clinical remission). Medium-term: biomarker normalization (CRP, calprotectin <250). Long-term: endoscopic remission (mucosal healing) — the key endpoint associated with preventing complications, hospitalizations, and surgeries. Ultimate goal: histological remission (in UC).

[Mesalazine](/search?q=mesalazine) (mesalamine, Salofalk®, Pentasa®, Asacol®) — the cornerstone of mild-to-moderate UC therapy. Local anti-inflammatory action in intestinal mucosa. Proctitis: rectal suppositories 1 g/d. Left-sided colitis: enemas 2–4 g/d + oral mesalazine. Pancolitis: oral 4–4.8 g/d + topical. Combination of oral + rectal is more effective than monotherapy. Maintenance: lifelong mesalazine (reduces relapses and colorectal cancer). [Sulfasalazine](/search?q=sulfasalazine) — alternative (cheaper but more side effects: headache, nausea, oligospermia).

[Prednisolone](/search?q=prednisolone) 40–60 mg/d with gradual taper over 8–12 weeks — for moderate-to-severe flares. Do not use for maintenance — side effects (osteoporosis, diabetes, infections, adrenal insufficiency) with prolonged use. [Budesonide](/search?q=budesonide) MMX (Cortiment®) 9 mg/d — topical corticosteroid with 10–15% systemic bioavailability. Alternative to prednisolone for mild-to-moderate UC flares. IV hydrocortisone/methylprednisolone — for severe flares (hospitalization).

[Azathioprine](/search?q=azathioprine) 2–2.5 mg/kg/d — the main immunomodulator for UC. Steroid-sparing agent: enables GCS discontinuation in steroid dependence. Onset: 8–12 weeks (not for induction!). Monitoring: TPMT genotyping before starting (enzyme deficiency → severe myelosuppression); CBC every 2 weeks × 2 months, then every 3 months; liver enzymes. Side effects: myelosuppression, hepatotoxicity, pancreatitis, slightly increased lymphoma risk. 6-mercaptopurine — active metabolite, alternative if intolerant.

Anti-TNF: [Infliximab](/search?q=infliximab) (Remicade®) IV 5 mg/kg (weeks 0, 2, 6, then every 8 weeks) and [Adalimumab](/search?q=adalimumab) (Humira®) SC (160→80→40 mg every 2 weeks). Induction and maintenance for moderate-to-severe UC refractory to GCS/immunomodulators. Golimumab (Simponi®) — alternative.

[Vedolizumab](/search?q=vedolizumab) (Entyvio®) — anti-α4β7 integrin antibody. Gut-selective: blocks lymphocyte migration specifically to the gut. Fewer systemic immunosuppressive side effects. IV 300 mg (weeks 0, 2, 6, then every 8 weeks). Particularly effective in UC.

[Ustekinumab](/search?q=ustekinumab) (Stelara®) — anti-p40 subunit of IL-12/IL-23 antibody. Approved for UC (2023). IV induction → SC every 8–12 weeks.

JAK inhibitors: tofacitinib (Xeljanz®) 10 mg × 2/d (induction) → 5 mg × 2/d (maintenance); upadacitinib (Rinvoq®) — more selective JAK1 inhibitor. Oral! Rapid onset. Side effects: herpes zoster, increased thrombosis risk (tofacitinib at high doses), hyperlipidemia.

[Budesonide](/search?q=budesonide) (Budenofalk®) 9 mg/d — for mild-to-moderate ileocecal CD (first line). Systemic GCS — for moderate-severe flares. 5-ASA in CD: low efficacy, not recommended (unlike UC). [Methotrexate](/search?q=methotrexate) 25 mg/week SC (induction) → 15 mg/week (maintenance) — azathioprine alternative if intolerant. Folic acid 5 mg 24 hours after MTX.

Biologic therapy for CD: anti-TNF (infliximab, adalimumab) — first-line biologics. Vedolizumab — gut-selective, good when anti-TNF intolerant. Ustekinumab — IL-12/23 blockade, excellent option after anti-TNF loss of response. Risankizumab (Skyrizi®) — selective anti-IL-23 (p19), approved for CD (2023), high efficacy. Early aggressive therapy (top-down): in young patients with poor prognosis factors (perianal disease, strictures, extensive involvement) — immediate biologic therapy ± immunomodulator.

UC: colectomy — 'curative' surgery. Indications: refractory severe colitis, toxic megacolon, perforation, dysplasia/cancer. Ileal pouch-anal anastomosis (J-pouch) — standard reconstruction. 15–30% of UC patients require surgery in their lifetime.

CD: surgery does NOT cure — recurrence after resection 50–70% at 10 years. Indications: strictures (stricturoplasty for short ones), fistulas, abscesses, treatment refractoriness. Principle: minimal resections (bowel preservation). Postoperative prophylaxis: azathioprine or anti-TNF started 2–4 weeks after surgery.

Perianal fistulas occur in 30–50% of CD patients. Pelvic MRI — diagnostic standard. Treatment: antibiotics (metronidazole + ciprofloxacin 3–6 months), seton drainage (surgical), anti-TNF (infliximab — most studied). Ustekinumab and vedolizumab — alternatives. Combined surgery + biologic therapy — optimal approach.

Calprotectin — the key monitoring marker. Target: <250 mcg/g (optimally <150). Elevation → endoscopy for assessment. Therapeutic drug monitoring (TDM): measuring biologic drug levels and antibodies → dose optimization or switching. For infliximab: target trough >5 mcg/mL. Colorectal cancer screening: chromoendoscopy starting 8 years after UC/Crohn's colitis onset, every 1–3 years (depending on risk factors). UC CRC risk: 2% at 10 years, 8% at 20 years, 18% at 30 years.

Pregnancy with IBD is safe in remission. Flares during pregnancy are worse for the fetus than most medications. Safe: mesalazine, thiopurines (azathioprine), anti-TNF (infliximab, adalimumab — can continue through 3rd trimester), vedolizumab, ustekinumab. Contraindicated: methotrexate (teratogen! Discontinue 3–6 months prior), tofacitinib, mycophenolate. Planning pregnancy during remission is key to success.

No single 'IBD diet' exists. Crohn's Disease Exclusion Diet (CDED) — promising for inducing remission in mild pediatric CD (GCS alternative). Mediterranean diet — associated with reduced inflammation. Avoid: excess sugar, ultra-processed foods. For strictures — low-fiber diet. Nutritional support for malnutrition (common in small bowel CD). Deficiencies: iron, B12 (after terminal ileum resection), vitamin D, zinc. Smoking cessation — MANDATORY in CD (halves recurrence rates).

*This article is for informational purposes only and does not replace gastroenterologist consultation. IBD treatment should be managed by a specialist.*