Gastrointestinal · PANCE / PANRE

Crohn Disease

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Chronic transmural inflammation that can involve any segment of the GI tract; skip lesions and fistulizing disease.

Also known as: Crohn disease, Crohn's disease, CD, regional enteritis

Overview

Chronic, idiopathic, immune-mediated inflammatory bowel disease characterized by transmural inflammation that may involve any segment of the gastrointestinal tract from mouth to anus, with skip lesions and a propensity to form strictures, fistulas, and abscesses.

Epidemiology

Incidence ~5-10 per 100,000/year in North America; prevalence ~250 per 100,000. Bimodal age peaks at 15-30 and 50-70. Female slight predominance. Highest incidence in Ashkenazi Jews, Northern European descent. Smoking doubles risk.

Try two board-style Crohn Disease questions

Real questions from the FirstPassPA bank, with the full explanation. Pick an answer — no signup, no email.

Question 1GastrointestinalMedium
A 28-year-old man with Crohn's disease maintained on vedolizumab presents with three days of fever, chills, and worsening right lower quadrant abdominal pain. Temperature is 38.6°C, blood pressure is 118/74 mm Hg, and pulse is 102/min. The abdomen is tender in the right lower quadrant without rebound or guarding. CT of the abdomen and pelvis with contrast demonstrates a 12-cm intra-abdominal abscess with a fistulous tract to the sigmoid colon. Which of the following is the most appropriate next step in management?
  • AUrgent surgical bowel resection
  • BColonoscopy with mucosal biopsies
  • CCT-guided percutaneous drainage
  • DEscalation of vedolizumab dosing
Reveal answer & full explanation
Correct answer: C — CT-guided percutaneous drainage
  • AUrgent surgical bowel resection
  • BColonoscopy with mucosal biopsies
  • CCT-guided percutaneous drainage✓
  • DEscalation of vedolizumab dosing

Why CT-guided percutaneous drainage is correct

  • CT-guided percutaneous drainage plus broad-spectrum IV antibiotics (e.g., piperacillin-tazobactam or a carbapenem) is first-line for an accessible intra-abdominal abscess larger than 3 cm, per current ACG Crohn's disease guidance
  • Active intra-abdominal infection is a contraindication to continuing biologic therapy because of the risk of overwhelming sepsis — vedolizumab must be held
  • Drainage controls sepsis and often converts an urgent operation into an elective, single-stage resection if surgery is later required
  • Biologic therapy is resumed only after the infection has completely resolved

Why the others are wrong

  • Urgent surgical bowel resection — Reserved for free perforation, peritonitis, collections not amenable to drainage, or failed percutaneous drainage; this hemodynamically stable patient without rebound or guarding should be drained first. The trap is anchoring on the dramatic abscess size and fistula.
  • Colonoscopy with mucosal biopsies — Does not treat the abscess and risks perforation through inflamed, penetrating bowel; it buzzword-matches "Crohn's disease → endoscopic assessment" while ignoring the infectious emergency.
  • Escalation of vedolizumab dosing — Intensifying immunosuppression during active intra-abdominal infection risks overwhelming sepsis; this is premature closure, treating a septic complication as if it were a refractory medical flare.
Question 2GastrointestinalMedium
A 30-year-old man with ileocolonic Crohn's disease has been maintained on adalimumab for 18 months but now reports recurrent abdominal pain and diarrhea. Laboratory testing shows an adalimumab trough level of 3 mcg/mL (therapeutic target ≥7.5 mcg/mL) and positive anti-adalimumab antibodies at 150 AU/mL. Which of the following is the most appropriate next step?
  • AAdd azathioprine to the current regimen
  • BSwitch to vedolizumab or ustekinumab
  • CIncrease the adalimumab dose to weekly
  • DSwitch to an adalimumab biosimilar
Reveal answer & full explanation
Correct answer: B — Switch to vedolizumab or ustekinumab
  • AAdd azathioprine to the current regimen
  • BSwitch to vedolizumab or ustekinumab✓
  • CIncrease the adalimumab dose to weekly
  • DSwitch to an adalimumab biosimilar

Why Switch to vedolizumab or ustekinumab is correct

  • This is loss of response from immunogenicity: a subtherapeutic adalimumab trough (3 mcg/mL, below the ~7.5 mcg/mL target) together with high-titer neutralizing anti-adalimumab antibodies (150 AU/mL).
  • When antidrug antibodies are high and the drug level is low, the antibodies are clearing and neutralizing the drug, so the rational move is to change agents rather than give more of the same drug.
  • Switching to a different mechanism of action—gut-selective vedolizumab (anti-integrin) or ustekinumab (anti-IL-12/23)—sidesteps the established antibody response, consistent with AGA therapeutic drug monitoring guidance.

Why the others are wrong

  • Add azathioprine to the current regimen — adding an immunomodulator can blunt antibody formation early, but once high-titer antidrug antibodies are established it rarely recaptures response during active disease; right idea, wrong timing.
  • Increase the adalimumab dose to weekly — dose escalation overcomes low levels from pharmacokinetic failure (low drug, no antibodies), not antibody-mediated neutralization, so it fails in this setting.
  • Switch to an adalimumab biosimilar — a biosimilar shares the originator's epitopes, so existing anti-adalimumab antibodies cross-react and neutralize it as well; changing the product without changing the mechanism does not escape immunogenicity.
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Risk factors

  • Family history (NOD2/CARD15, ATG16L1, IL23R polymorphisms)
  • Smoking (DOUBLES risk and worsens course — opposite of UC)
  • Western diet (high fat/processed, low fiber)
  • Antibiotic exposure in childhood
  • Appendectomy (modest)
  • Urban residence, northern latitudes
  • NSAID use can trigger flares

Pathophysiology

Dysregulated mucosal immune response to commensal gut microbiota in genetically susceptible individuals. Innate immune defects (NOD2) impair bacterial clearance; Th1/Th17 responses drive transmural inflammation. Granulomas (non-caseating) in ~30% of biopsies. Transmural extension produces strictures, fistulas, and abscesses.

Clinical presentation

Symptoms

  • Chronic diarrhea (often non-bloody but can be bloody if colonic)
  • Crampy abdominal pain, especially RLQ (ileocecal disease)
  • Weight loss, fatigue, low-grade fever
  • Perianal disease: fistulas, fissures, abscesses, skin tags
  • Aphthous oral ulcers
  • Symptoms of stricture: postprandial pain, bloating, vomiting, obstruction
  • Extraintestinal: arthritis, episcleritis/uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis (less than UC), kidney stones (oxalate), gallstones

Signs / physical exam

  • RLQ tenderness, palpable mass (inflammatory phlegmon)
  • Perianal fistulas, skin tags, fissures, abscesses
  • Aphthous ulcers, glossitis
  • Pallor (anemia), cachexia
  • Clubbing (chronic disease)
  • Skin: erythema nodosum, pyoderma gangrenosum
  • Eye: scleritis, uveitis
  • Joints: peripheral arthritis, sacroiliitis

Classic findings

Young adult with months of crampy RLQ pain, intermittent diarrhea, weight loss, and perianal fistula or abscess.

Differential diagnosis

  • Ulcerative colitis — Continuous rectal involvement, mucosal-only inflammation, no skip lesions or fistulas, bloody diarrhea
  • Intestinal tuberculosis — Ileocecal stricturing, caseating granulomas, TB risk factors; QuantiFERON, AFB stain/culture
  • Behçet disease — Oral and genital ulcers, uveitis, ileocecal ulcers
  • Infectious colitis (Yersinia, Salmonella, Campylobacter, C. diff, CMV) — Acute onset, exposure history, positive stool studies
  • NSAID enteropathy — NSAID use; mid-small bowel ulcers and diaphragm-like strictures
  • Lymphoma / small bowel adenocarcinoma — Refractory stricture or mass on imaging; biopsy
  • Ischemic colitis — Older patient, watershed areas (splenic flexure), atherosclerotic risk factors
  • Diverticulitis — Older patient, sigmoid predominant, fever, leukocytosis, CT findings

Diagnostic workup

Diagnostic criteria

Composite of clinical, endoscopic, radiologic, and histologic features. Hallmarks: discontinuous inflammation, skip lesions, transmural disease, terminal ileal involvement, non-caseating granulomas (when present), fistulizing or stricturing behavior.

Labs

  • CBC (microcytic anemia from iron deficiency or anemia of chronic disease)
  • CRP, ESR (inflammatory markers; correlate with activity)
  • BMP, LFTs, albumin (nutritional status, PSC)
  • Iron studies, B12, folate, vitamin D
  • Fecal calprotectin (>250 mcg/g supports active inflammation)
  • Stool studies: C. diff, culture, ova/parasites — exclude infection at diagnosis and flares
  • Serology: ASCA+/pANCA- pattern supports Crohn over UC (limited sensitivity; not for primary diagnosis)
  • QuantiFERON, hepatitis B/C, HIV, varicella titers, TB skin test — before biologic therapy

Imaging

  • Ileocolonoscopy with biopsy of terminal ileum and each colonic segment — establishes diagnosis; aphthous → linear/serpiginous ulcers, cobblestoning, skip lesions, ileal involvement
  • CT or MR enterography — small bowel disease, fistulas, abscess, stricture; MRE preferred in young patients to limit radiation
  • Pelvic MRI for perianal fistula assessment
  • Capsule endoscopy if proximal small bowel disease suspected and no stricture
  • Upper endoscopy if upper GI symptoms (more common in pediatric Crohn)

Diagnostic algorithm

FeatureCrohn DiseaseUlcerative Colitis
LocationMouth to anus; terminal ileum most commonColon only; starts at rectum
DistributionSkip lesionsContinuous
DepthTransmuralMucosa/submucosa only
Rectal involvementVariable; may be sparedAlways involved
GranulomasNon-caseating in ~30%Absent
Fistulas/stricturesCommonRare
SmokingWorsensProtective (paradoxically)
SurgeryNot curativeCurative (colectomy)
SerologyASCA+/pANCA-pANCA+/ASCA-
Bloody diarrheaSometimesHallmark
Crohn disease vs ulcerative colitis — clinical and pathologic distinctions.

Treatment

First-line

  • Smoking cessation — single most impactful intervention
  • Nutritional optimization; supplement iron, B12, vitamin D
  • Induction: corticosteroids (prednisone, budesonide ileal-release for ileocecal disease) for acute flares — NOT for maintenance
  • Biologic anti-TNF — infliximab, adalimumab, certolizumab — induction and maintenance; combine with thiopurine (azathioprine) for synergistic effect (SONIC trial)
  • Anti-integrin — vedolizumab (gut-selective α4β7) — maintenance
  • Anti-IL-12/23 — ustekinumab — induction and maintenance
  • Anti-IL-23 — risankizumab — induction and maintenance
  • JAK inhibitor — upadacitinib — induction and maintenance for moderate-severe Crohn

Second-line / adjunct

  • Immunomodulators — azathioprine, 6-mercaptopurine, methotrexate — for steroid-sparing maintenance and combination with biologics
  • Antibiotics — ciprofloxacin, metronidazole — for perianal/fistulizing disease, abscess
  • 5-ASA agents (mesalamine) — limited efficacy in Crohn; not first-line
  • Surgery — for stricture, fistula refractory to medical therapy, abscess (drainage), perforation, dysplasia, or medically refractory disease; NOT CURATIVE — recurrence at anastomosis common

Complications

  • Strictures with bowel obstruction
  • Fistulas (enteroenteric, enterocutaneous, enterovesical, enterovaginal, perianal)
  • Abscesses (intra-abdominal, perianal)
  • Perforation
  • GI bleeding
  • Malabsorption (B12 — terminal ileum, fat-soluble vitamins, bile salts → diarrhea and oxalate kidney stones)
  • Colorectal cancer (especially with colonic disease >8-10 yr or PSC)
  • Small bowel adenocarcinoma (in chronically inflamed segments)
  • Extraintestinal manifestations and treatment side effects (infection, lymphoma with thiopurines/anti-TNF, demyelinating disease)

PANCE pearls

  • Skip lesions, transmural inflammation, terminal ileal involvement, and granulomas distinguish Crohn from UC.
  • Smoking DOUBLES Crohn risk and worsens course — paradoxically protective in UC. Always counsel cessation.
  • Top-down therapy (early biologic + immunomodulator) is superior to step-up in moderate-severe disease (SONIC trial showed infliximab + azathioprine > either alone).
  • Check TPMT or NUDT15 before starting thiopurines to avoid severe myelosuppression.
  • Vaccinate before biologics: hepatitis B, pneumococcal, influenza, HPV; AVOID live vaccines (MMR, varicella, yellow fever) once on biologic therapy.
  • Perianal Crohn requires combined medical (anti-TNF + antibiotics) and surgical (seton placement, drainage) management; pelvic MRI maps fistula anatomy.
  • Surgery is NOT curative in Crohn — bowel-sparing approach (stricturoplasty, limited resection); endoscopic recurrence rates 70% at 1 year without postoperative prophylaxis.
  • Colorectal cancer surveillance: colonoscopy every 1-3 yr starting 8-10 yr after disease onset for colonic involvement.

References

  • ACG 2018 — Lichtenstein GR et al. ACG Clinical Guideline: Management of Crohn's Disease in Adults. Am J Gastroenterol 2018;113:481-517
  • AGA 2021 — Feuerstein JD et al. AGA Clinical Practice Guidelines on the Medical Management of Moderate to Severe Luminal and Perianal Fistulizing Crohn's Disease. Gastroenterology 2021;160:2496-2508
  • SONIC Trial — Colombel JF et al. Infliximab, Azathioprine, or Combination Therapy for Crohn's Disease. NEJM 2010;362:1383-1395
  • ECCO 2020 — Torres J et al. ECCO Guidelines on Therapeutics in Crohn's Disease: Medical Treatment. J Crohns Colitis 2020;14:4-22

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Commonly confused with

vs Ulcerative Colitis

Related Gastrointestinal diagnoses

Gastroesophageal Reflux Disease (GERD)Peptic Ulcer Disease (PUD)Helicobacter pylori InfectionEosinophilic Esophagitis (EoE)Esophageal VaricesAchalasiaEsophageal CancerGastric CancerIrritable Bowel Syndrome (IBS)Ulcerative Colitis (UC)Diverticulitis and DiverticulosisColorectal Cancer (CRC)HemorrhoidsAcute Appendicitis

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