Crohn's Disease

Table of Contents

1. What is Crohn’s Disease?
2. What Goes Wrong in the Gut Wall
3. Where It Strikes, and the Three Behaviours
4. Common Symptoms of Crohn’s Disease
5. How It Varies Between People
6. Causes and Risk Factors
7. Diagnosis: The Tests and the Numbers
8. Monitoring: Why Feeling Well Is Not Enough
9. Treatment Options
10. Surgery, and What It Can and Cannot Do
11. Diet and Nutrition: What the Trials Show
12. What the Evidence Does Not Support
13. Prevention and Management Strategies
14. Red Flags: When It Is Urgent
15. Complications of Crohn’s Disease
16. Research Papers
17. Connections
18. Featured Videos

What is Crohn’s Disease?

Crohn’s disease is a chronic inflammatory bowel disease in which the immune system attacks the wall of the digestive tract. It can affect anywhere from the mouth to the anus, and unlike ulcerative colitis it involves the full thickness of the bowel wall rather than just the lining.

That single anatomical fact explains most of what makes Crohn’s difficult. Inflammation confined to the surface causes bleeding and diarrhoea. Inflammation through the whole wall does something else: it can heal with scarring, narrowing the tube into a stricture; or it can burrow all the way through, creating a fistula — an abnormal tunnel to another loop of bowel, the bladder, the vagina or the skin — or an abscess. Those three complications, and not the diarrhoea, are what drive most Crohn’s surgery.

The other characteristic feature is patchiness. Diseased segments alternate with completely normal bowel — “skip lesions” — whereas ulcerative colitis spreads continuously upward from the rectum. This matters diagnostically and it matters surgically: you cannot cure Crohn’s by removing a segment, because the disease is not confined to it.

Incidence has risen sharply worldwide, and Ng and colleagues’ 2017 Lancet systematic review documented the pattern: stabilising at high levels in the West but rising steeply in newly industrialised countries in Asia, Africa and South America. Whatever drives IBD travels with industrialisation.

What Goes Wrong in the Gut Wall

Crohn’s is best understood as a failure of the truce between the gut immune system and the trillions of bacteria it lives alongside. Four elements combine:

1. A genetically susceptible immune system. Over 200 loci are associated with IBD. NOD2 was the first and is the strongest for Crohn’s: it encodes a sensor for a bacterial cell-wall fragment, and loss-of-function variants impair the innate response to bacteria that get through the lining. Genes in autophagy (ATG16L1, IRGM) and the IL-23 pathway are also implicated. Jostins and colleagues’ 2012 Nature analysis showed the same pathways are shared with defences against mycobacterial infection — the immune machinery is not broken so much as mis-tuned.
2. A leaky barrier. The single layer of cells lining the gut, plus its mucus and antimicrobial peptides, keeps bacteria at arm’s length. In Crohn’s that barrier is more permeable, and increased permeability is measurable in unaffected first-degree relatives — suggesting it is a cause rather than only a consequence.
3. An altered microbiome (dysbiosis). Reduced diversity, fewer anti-inflammatory butyrate producers such as Faecalibacterium prausnitzii, and an expansion of adherent-invasive E. coli in ileal disease.
4. An environmental trigger — smoking, an enteric infection, a course of antibiotics, an NSAID.

The result is a self-sustaining inflammatory response driven by TNF-α, IL-12, IL-23 and Th1/Th17 T cells, producing the deep ulceration, granulomas and full-thickness inflammation that define the disease. Every effective drug class in Crohn’s interrupts one of those signals, which is why the mechanism is worth understanding: it is a map of the treatment options.

Where It Strikes, and the Three Behaviours

Clinicians classify Crohn’s by the Montreal classification — age at diagnosis, location, and behaviour — and it is genuinely useful for patients too, because it predicts what is likely to happen.

Location

• Ileal (L1) — the last part of the small intestine, the commonest site. Causes right lower abdominal pain, and specifically impairs vitamin B12 and bile acid absorption.
• Colonic (L2) — harder to distinguish from ulcerative colitis; more likely to cause bleeding.
• Ileocolonic (L3) — the commonest pattern overall.
• Upper gastrointestinal (L4 modifier) — oesophagus, stomach or duodenum; associated with more aggressive disease.
• Perianal (p modifier) — fistulas, fissures, abscesses and skin tags around the anus. Present in a quarter or more, and one of the most distressing and under-discussed aspects of the disease.

Behaviour

• Inflammatory / non-stricturing, non-penetrating (B1) — how most people begin.
• Stricturing (B2) — narrowing causing obstruction, with cramping pain after meals, bloating, and vomiting. Strictures may be inflammatory (drug-responsive) or fibrotic (needing dilation or surgery); distinguishing them on MRI matters.
• Penetrating (B3) — fistula and abscess formation.

Behaviour tends to progress over time from B1 towards B2 or B3, which is the central argument for treating early and effectively rather than waiting: you are trying to prevent a transition, not just settle symptoms.

Common Symptoms of Crohn’s Disease

• Chronic diarrhoea, often without blood in small-bowel disease — a point that causes delay, because people expect blood.
• Abdominal pain, classically cramping and in the right lower abdomen with ileal disease; pain shortly after eating suggests a stricture.
• Weight loss and reduced appetite, from inflammation, malabsorption, and eating less to avoid symptoms.
• Fatigue, driven by inflammation, anaemia and poor sleep. Consistently rated by patients as one of the worst symptoms.
• Fever, low-grade in active disease; a swinging fever suggests an abscess.
• Perianal symptoms — pain, discharge, a lump, or a persistent split. Ask and be asked about these; they are treatable and are often silently endured.
• Mouth ulcers, sometimes preceding bowel symptoms.
• Growth failure and delayed puberty in children, sometimes the presenting feature before any gut symptom.
• Extra-intestinal features — joint pain and arthritis, erythema nodosum (tender red shin nodules), pyoderma gangrenosum, uveitis and episcleritis, and primary sclerosing cholangitis. Some track disease activity, some do not.

How It Varies Between People

• Diagnostic delay is the norm. Median time from first symptom to diagnosis is often years, longest in small-bowel disease with no bleeding. Symptoms are frequently attributed to irritable bowel syndrome. A faecal calprotectin test at that point is cheap and would resolve most of these delays.
• Poor-prognosis features at diagnosis — young age, extensive small-bowel disease, deep ulcers on endoscopy, perianal involvement, a need for steroids at diagnosis, and smoking — argue for early effective treatment rather than a step-up approach.
• Smoking behaves oppositely in the two forms of IBD. It roughly doubles the risk of Crohn’s and clearly worsens its course, while being associated with lower risk of ulcerative colitis. This has occasionally been misread as a reason for Crohn’s patients to smoke. It is not. Stopping smoking is one of the most effective single interventions in Crohn’s — comparable in effect to some drugs.
• Symptoms and inflammation are poorly correlated. Some people feel dreadful with mild inflammation; others have deep ulcers and feel fine. This is the central reason objective monitoring exists.
• Overlapping IBS is common. After inflammation is controlled, a substantial minority still have pain and altered bowel habit from visceral hypersensitivity. Recognising this prevents endless escalation of immunosuppression that cannot help.
• Perianal disease is a distinct phenotype with its own treatment pathway — combined medical and surgical, usually anti-TNF plus drainage — and much better outcomes when managed jointly from the start.

Causes and Risk Factors

• Family history — the strongest single risk factor; roughly 5–20% have an affected relative, and concordance in identical twins is around 30–35%.
• Smoking — increases risk, severity, surgery rate and post-operative recurrence.
• Age — peak onset 15–30, with a smaller second peak after 60.
• Living in or moving to an industrialised country; second-generation migrants acquire the risk of their new country, which points squarely at environment.
• Early-life antibiotic exposure, associated in several cohorts.
• A preceding gastroenteritis, which can precipitate onset.
• NSAIDs, which can trigger flares.
• Diet — higher intake of ultra-processed food and emulsifiers, and lower fibre and fruit intake, are associated with higher risk in prospective cohorts. These are associations, not proven causes.
• Appendicectomy, associated with slightly increased Crohn’s risk (and decreased ulcerative colitis risk).
• Not a cause: stress, personality and diet do not cause Crohn’s. Stress can worsen symptoms and trigger flares in established disease, which is a different claim, and patients are still too often told the disease is their own doing.

Diagnosis: The Tests and the Numbers

There is no single test. Diagnosis combines symptoms, blood and stool markers, endoscopy with biopsy, and cross-sectional imaging.

Stool and blood tests

• Faecal calprotectin — the most useful single test, and under-used. It measures a neutrophil protein in stool and distinguishes inflammatory bowel disease from irritable bowel syndrome. Broadly: under 50 µg/g makes IBD unlikely; over 250 µg/g indicates active inflammation; 50–250 µg/g is a grey zone needing repeat or further investigation. NSAIDs, PPIs and infection can raise it.
• CRP — useful but imperfect; roughly a fifth of people with active Crohn’s never mount a CRP response, particularly with isolated ileal disease.
• Full blood count — anaemia, raised platelets as an inflammatory marker.
• Iron studies, B12, folate, vitamin D — deficiency is common, and ileal disease or ileal resection specifically causes B12 malabsorption.
• Albumin — low in severe disease.
• Stool culture and C. difficile toxin — always, before assuming a flare. Infection mimics and precipitates flares, and steroids into untreated C. difficile are harmful.

Endoscopy

• Ileocolonoscopy with biopsies is the reference test. Typical findings: patchy inflammation, aphthous then deep linear ulcers, a cobblestone appearance, and skip lesions. Biopsies may show non-caseating granulomas — characteristic but present in fewer than half.
• Upper endoscopy where upper GI involvement is suspected, and routinely in children.
• Capsule endoscopy for small-bowel disease not reached by other means — but a patency capsule should be used first if a stricture is possible, as the capsule can lodge.

Imaging

• MR enterography — the preferred cross-sectional test. Shows disease extent, wall thickening, and distinguishes inflammatory from fibrotic strictures, with no radiation, which matters in a young population facing decades of imaging.
• Intestinal ultrasound — increasingly used, quick, radiation-free and repeatable in clinic; excellent for terminal ileal disease in experienced hands.
• CT — reserved for acute presentations where speed matters, such as suspected perforation or abscess.
• Pelvic MRI — the standard for mapping perianal fistulas before treatment.

What else it might be

Intestinal tuberculosis (which looks strikingly similar and is made much worse by anti-TNF drugs), Yersinia and Campylobacter infection, NSAID enteropathy, coeliac disease, Behçet’s disease, lymphoma, and ulcerative colitis. Tuberculosis screening before starting biologics is mandatory, not optional.

Monitoring: Why Feeling Well Is Not Enough

The single biggest change in Crohn’s care over the past decade is the shift from treating symptoms to treating inflammation. Symptoms respond to steroids while ulcers persist, and persistent ulcers go on causing strictures and fistulas regardless of how someone feels.

The current goal, usually called treat to target, is stepwise: first symptom relief, then normalisation of CRP and faecal calprotectin, and ultimately endoscopic healing — the absence of ulcers on colonoscopy. Achieving endoscopic healing is associated with fewer hospitalisations, less surgery and better long-term outcomes.

Practically, this means periodic calprotectin measurement even when well, and a colonoscopy or MR enterography at intervals rather than only when things go wrong. It also means that if calprotectin is high while you feel fine, that is a reason to change treatment — a conversation that surprises many patients and is worth understanding in advance.

Therapeutic drug monitoring is the other under-used tool: measuring the blood level of infliximab or adalimumab and testing for anti-drug antibodies when a biologic seems to stop working. Losing response is often a dose problem or an antibody problem, not a drug-failure problem, and the fix differs completely.

Treatment Options

Inducing remission

• Corticosteroids — prednisolone, or budesonide for ileal and right-colonic disease (budesonide is largely metabolised on first pass through the liver, so it has far fewer systemic effects). Effective for induction, useless for maintenance, and harmful cumulatively. Needing two or more steroid courses a year, or being unable to come off steroids, is a clear indication to escalate maintenance treatment — not to prescribe more steroids.
• Exclusive enteral nutrition — a liquid formula diet as the sole source of nutrition for 6–8 weeks. In children it is as effective as steroids for inducing remission and superior for mucosal healing and growth, and it is first-line paediatric treatment in Europe. It is hard to sustain and less effective in adults, largely because adherence is lower.
• Antibiotics — metronidazole and ciprofloxacin have a role in perianal disease and in abscess, not in luminal Crohn’s generally.

Maintaining remission

• Thiopurines — azathioprine, mercaptopurine. Slow to work (8–12 weeks), requiring TPMT or NUDT15 testing before starting and regular blood monitoring. Modest efficacy alone; genuinely useful combined with an anti-TNF, where they reduce antibody formation.
• Methotrexate — an alternative, particularly where joint disease coexists.
• Anti-TNF antibodies — infliximab (infusion) and adalimumab (subcutaneous). ACCENT I (Hanauer et al., Lancet 2002) established that scheduled maintenance infliximab kept patients in remission far better than episodic dosing. SONIC (Colombel et al., NEJM 2010) then compared infliximab, azathioprine and the combination in patients naive to both: corticosteroid-free clinical remission at 26 weeks was achieved by 56.8% on combination therapy, 44.4% on infliximab alone and 30.0% on azathioprine alone. That trial is the reason combination therapy became standard for moderate-to-severe disease.
• Vedolizumab — blocks α4β7 integrin, preventing lymphocytes homing to the gut. Because the action is gut-selective, systemic infection risk is low, which makes it attractive in older patients and those with prior malignancy. GEMINI 2 (Sandborn et al., NEJM 2013) established its efficacy; onset is slower than anti-TNF.
• Ustekinumab — blocks the shared p40 subunit of IL-12 and IL-23. In the UNITI programme (Feagan et al., NEJM 2016) it induced and maintained remission including in patients who had failed anti-TNF drugs, with a favourable safety profile.
• Risankizumab — a selective IL-23 (p19) inhibitor. The ADVANCE and MOTIVATE induction trials and the FORTIFY maintenance trial (D’Haens and Ferrante et al., Lancet 2022) showed benefit for both clinical remission and endoscopic response. Selective IL-23 blockade is now a leading option.
• JAK inhibitors — upadacitinib is effective in Crohn’s, taken orally, and carries the class boxed warning for serious infection, thrombosis, major cardiovascular events and malignancy.

Supportive treatment that matters

• Iron — intravenous iron is often better tolerated and better absorbed than oral in active disease, and oral iron can worsen symptoms.
• Vitamin B12 — injections are needed after ileal resection or with extensive ileal disease; oral supplements will not work if the absorption site is gone.
• Bile acid sequestrants — colestyramine or colesevelam for the watery diarrhoea of bile acid malabsorption after ileal resection. This is a very common, very treatable and frequently missed cause of persistent diarrhoea in someone whose Crohn’s is otherwise in remission.
• Vitamin D and calcium, plus bone density monitoring given steroid exposure.
• Vaccination before immunosuppression; live vaccines are contraindicated once it has started.
• Skin cancer surveillance and sun protection, particularly on thiopurines.

Surgery, and What It Can and Cannot Do

Around half of people with Crohn’s need surgery within ten years of diagnosis, though the figure is falling with better medical treatment. Surgery is not a failure of treatment; sometimes it is the right treatment.

• What it does well — removes a fibrotic stricture, drains an abscess, resects a short segment of refractory ileal disease. For limited ileocaecal disease, early resection compares favourably with starting a biologic in trial data, and should be presented as a genuine option rather than a last resort.
• What it cannot do — cure. Endoscopic recurrence at the join occurs in the majority within a year without preventive treatment, and clinical recurrence follows.
• Strictureplasty — widening a stricture without removing bowel. Preserves length, which matters over a lifetime of possible operations.
• Post-operative prophylaxis — starting a drug within weeks of surgery, and a colonoscopy at 6–12 months to look for recurrence before symptoms appear, substantially reduces later relapse. Smoking cessation matters more here than almost anywhere else.
• Perianal fistula — managed jointly: drainage with a seton first, then anti-TNF, then definitive repair. Attempting to close a fistula without controlling the inflammation reliably fails.
• Short bowel syndrome is the reason surgeons preserve every centimetre they can; repeated resections eventually compromise absorption permanently.

Diet and Nutrition: What the Trials Show

Diet is where patients get the most advice and the least evidence. Here is what is actually established.

• Exclusive enteral nutrition works. This is the strongest dietary evidence in Crohn’s: a formula-only diet for 6–8 weeks induces remission in children as effectively as steroids, with better mucosal healing.
• The Crohn’s Disease Exclusion Diet plus partial enteral nutrition works in children. Levine and colleagues (Gastroenterology 2019) randomised children with mild-to-moderate disease and found the exclusion diet with partial enteral nutrition was better tolerated than exclusive enteral nutrition and produced sustained corticosteroid-free remission in a higher proportion at week 12. It restricts specific components — including emulsifiers, processed meats and certain fats — while keeping real food.
• During a stricture or obstruction, a low-fibre or low-residue diet reduces symptoms. This is mechanical, temporary, and should not become permanent.
• In remission, eat a full and varied diet. Long-term restriction causes deficiency and, in children, growth failure. Build meals around vegetables, fruit, olive oil, fish, eggs, poultry, meat, legumes as tolerated, nuts and whole grains such as brown rice, oats and barley — adjusting texture rather than eliminating whole food groups.
• Nutritional deficiencies to test for and correct — iron, B12 (especially with ileal disease or resection), folate (particularly on methotrexate or sulfasalazine), vitamin D, zinc, magnesium, and the fat-soluble vitamins A, D, E and K where fat absorption is impaired.
• Ultra-processed foods and emulsifiers such as polysorbate-80 and carboxymethylcellulose are associated with higher IBD incidence in cohort studies and disrupt the mucus layer in animal models. The human trial evidence is early. Reducing them is a low-cost, low-risk change with a plausible mechanism, and should be described that honestly rather than as established treatment.

What the Evidence Does Not Support

• Steroids for maintenance. They do not maintain remission and cause cumulative harm — osteoporosis, diabetes, cataract, adrenal suppression, infection. Steroid dependence is a signal to escalate, not to continue.
• 5-ASA drugs (mesalazine) for Crohn’s. Effective in ulcerative colitis, but the evidence in Crohn’s is weak to absent for both induction and maintenance. They are still widely prescribed out of habit.
• Antibiotics for luminal Crohn’s generally. Useful for perianal disease and abscess; not established for uncomplicated luminal inflammation. Anti-mycobacterial regimens aimed at Mycobacterium avium subspecies paratuberculosis have not shown convincing sustained benefit in randomised trials.
• Probiotics for Crohn’s. Unlike pouchitis and some ulcerative colitis settings, probiotics have not been shown to induce or maintain remission in Crohn’s.
• Faecal microbiota transplantation as established therapy. Biologically appealing, still experimental in Crohn’s, and should be done in a trial rather than privately.
• Permanent restrictive diets in remission — specific carbohydrate, gluten-free, paleo and similar. None has good randomised evidence for altering the disease, and all carry a real nutritional cost in a population already at risk of deficiency.
• Smoking as protective. True for ulcerative colitis risk; the opposite in Crohn’s.
• Cannabis as a disease-modifying treatment. It can improve symptoms and appetite in trials; it has not been shown to reduce inflammation or improve endoscopic outcomes. Symptom relief without inflammation control is precisely the trap that leads to strictures.

Prevention and Management Strategies

• Stop smoking. The most effective single lifestyle intervention in Crohn’s, reducing flares, surgery and post-operative recurrence.
• Take maintenance treatment consistently, including when well. Non-adherence is the commonest cause of relapse.
• Avoid NSAIDs where possible; use paracetamol for routine pain and discuss alternatives for arthritis.
• Get faecal calprotectin checked periodically, not only when symptomatic.
• Keep vaccinations up to date ahead of immunosuppression, including annual influenza, pneumococcal, and HPV where indicated. Live vaccines are contraindicated on immunosuppression.
• Protect your skin — sun protection and skin checks, particularly on thiopurines.
• Colonoscopic surveillance for colorectal cancer where colonic disease has been present for eight years or more; risk rises with extent and duration of colonic inflammation.
• Look after bones — vitamin D, calcium, weight-bearing exercise, and DEXA scanning after significant steroid exposure.
• Address mental health. Anxiety and depression are common, worsen symptom perception, and are associated with worse disease outcomes. Treating them is part of treating the disease.
• Plan pregnancy in remission. Active disease at conception is the main risk to pregnancy; most Crohn’s drugs (except methotrexate, which is absolutely contraindicated) can be continued. Stopping treatment on discovering pregnancy is a common and harmful mistake.
• Ask about an IBD nurse specialist and a written flare plan — the fastest route to early treatment.

Red Flags: When It Is Urgent

• Severe abdominal pain with vomiting and no passage of stool or wind — bowel obstruction. Go to hospital.
• High fever with severe localised pain and tenderness — suspect an abscess, which needs imaging and drainage, not more steroids.
• Sudden severe generalised abdominal pain with a rigid abdomen — possible perforation; a surgical emergency.
• Significant rectal bleeding, dizziness or fainting.
• New perianal pain and swelling — a perianal abscess needs drainage within days, not weeks.
• Marked abdominal distension with diarrhoea and systemic illness — toxic megacolon, rare in Crohn’s colitis but life-threatening.
• Fever or infection while on immunosuppression — seek advice promptly and name the drugs.
• Leg swelling or pleuritic chest pain — active IBD roughly triples the risk of venous thromboembolism, and this is under-appreciated by patients and clinicians alike.

Complications of Crohn’s Disease

• Strictures and bowel obstruction.
• Fistulas — between bowel loops, or to bladder, vagina or skin — and abscesses.
• Perianal disease, including complex fistulas and incontinence.
• Malnutrition and micronutrient deficiency, and growth failure in children.
• Anaemia, from iron deficiency, B12 deficiency, and chronic inflammation.
• Osteoporosis, from inflammation, steroids, low vitamin D and low body weight.
• Colorectal and small-bowel cancer, with risk related to duration and extent of inflammation.
• Venous thromboembolism during active disease and hospital admission.
• Short bowel syndrome after repeated resections, occasionally requiring parenteral nutrition.
• Gallstones and kidney stones — both specifically increased after ileal disease or resection, through bile acid loss and increased oxalate absorption respectively.
• Primary sclerosing cholangitis, less common than in ulcerative colitis but important, with its own cancer surveillance requirements.
• Treatment complications — infection and reactivation of latent tuberculosis or hepatitis B with anti-TNF drugs, lymphoma risk with thiopurines (small in absolute terms and highest in young men), and steroid toxicity.
• Fatigue, anxiety and depression, which persist for many even in remission and deserve treatment in their own right.

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Research Papers

Historical background

Burrill Crohn, Leon Ginzburg and Gordon Oppenheimer described “regional ileitis” in JAMA in 1932, from fourteen patients at Mount Sinai Hospital in New York. Earlier descriptions exist — the Scottish surgeon Kennedy Dalziel published a strikingly similar series in 1913 — and the paper’s alphabetical author order is why the disease carries Crohn’s name rather than Ginzburg’s or Oppenheimer’s. Treatment was surgical for decades. Corticosteroids arrived in the 1950s, thiopurines in the 1960s, and the decisive change came in 1998 with infliximab, the first anti-TNF antibody, which showed that blocking a single cytokine could heal the bowel.

Key research papers

Each citation below was checked against its PubMed record; the linked DOI resolves to the paper named.

1. Crohn BB, Ginzburg L, Oppenheimer GD. Regional ileitis: a pathologic and clinical entity. JAMA. 1932;99(16):1323–1329.
2. Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn’s disease. Lancet. 2017;389(10080):1741–1755. (PMID 27914655)
3. Ng SC, Shi HY, Hamidi N, et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: a systematic review of population-based studies. Lancet. 2017;390(10114):2769–2778. (PMID 29050646)
4. Jostins L, Ripke S, Weersma RK, et al. Host–microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature. 2012;491(7422):119–124. (PMID 23128233)
5. Ananthakrishnan AN, Bernstein CN, Iliopoulos D, et al. Environmental triggers in IBD: a review of progress and evidence. Nat Rev Gastroenterol Hepatol. 2018;15(1):39–49. (PMID 29018271)
6. Hanauer SB, Feagan BG, Lichtenstein GR, et al. Maintenance infliximab for Crohn’s disease: the ACCENT I randomised trial. Lancet. 2002;359(9317):1541–1549. (PMID 12047962)
7. Colombel JF, Sandborn WJ, Reinisch W, et al. Infliximab, azathioprine, or combination therapy for Crohn’s disease (SONIC). N Engl J Med. 2010;362(15):1383–1395. (PMID 20393175)
8. Sandborn WJ, Feagan BG, Rutgeerts P, et al. Vedolizumab as induction and maintenance therapy for Crohn’s disease (GEMINI 2). N Engl J Med. 2013;369(8):711–721. (PMID 23964933)
9. Feagan BG, Sandborn WJ, Gasink C, et al. Ustekinumab as induction and maintenance therapy for Crohn’s disease (UNITI). N Engl J Med. 2016;375(20):1946–1960. (PMID 27959607)
10. D’Haens G, Panaccione R, Baert F, et al. Risankizumab as induction therapy for Crohn’s disease: results from the phase 3 ADVANCE and MOTIVATE induction trials. Lancet. 2022;399(10340):2015–2030. (PMID 35644154)
11. Ferrante M, Panaccione R, Baert F, et al. Risankizumab as maintenance therapy for moderately to severely active Crohn’s disease (FORTIFY). Lancet. 2022;399(10340):2031–2046. (PMID 35644155)
12. Lichtenstein GR, Loftus EV, Isaacs KL, et al. ACG clinical guideline: management of Crohn’s disease in adults. Am J Gastroenterol. 2018;113(4):481–517. (PMID 29610508)
13. Torres J, Bonovas S, Doherty G, et al. ECCO guidelines on therapeutics in Crohn’s disease: medical treatment. J Crohns Colitis. 2020;14(1):4–22. (PMID 31711158)
14. Levine A, Wine E, Assa A, et al. Crohn’s disease exclusion diet plus partial enteral nutrition induces sustained remission in a randomized controlled trial. Gastroenterology. 2019;157(2):440–450.e8. (PMID 31170412)

Live PubMed searches

The following PubMed topic searches surface the current peer-reviewed literature on Crohn’s disease. Each link opens a live query; results update as new papers are indexed.

1. PubMed search: Crohn disease
2. PubMed search: Crohn disease treat to target
3. PubMed search: faecal calprotectin inflammatory bowel disease
4. PubMed search: anti-TNF therapeutic drug monitoring IBD
5. PubMed search: perianal fistulizing Crohn disease
6. PubMed search: exclusive enteral nutrition Crohn
7. PubMed search: Crohn disease exclusion diet
8. PubMed search: postoperative recurrence Crohn disease prophylaxis
9. PubMed search: MR enterography Crohn stricture
10. PubMed search: intestinal ultrasound inflammatory bowel disease
11. PubMed search: NOD2 Crohn disease
12. PubMed search: bile acid malabsorption ileal resection
13. PubMed search: IBD pregnancy biologic safety
14. PubMed search: inflammatory bowel disease venous thromboembolism

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Connections

• Gastroenterology
• The Gut Barrier & Your Microbiome — interactive animation
• Ulcerative Colitis
• Inflammatory Bowel Disease Overview
• Celiac Disease
• Irritable Bowel Syndrome
• SIBO
• Crohn's vs Ulcerative Colitis: Key Differences
• Biologics: TNF, IL-23, and Integrin Inhibitors
• JAK Inhibitors and S1P Modulators
• Diet for IBD: SCD and Mediterranean
• Extraintestinal Manifestations: Joints, Skin, Eyes
• Chronic Diarrhea
• AS and IBD Overlap
• Ankylosing Spondylitis
• Gut Healing Protocol
• Elimination Diet
• Vitamin D3
• Zinc
• Diverticulitis
• Colorectal Cancer
• Herbs covered on this site that discuss this condition: Cat's Claw (Uncaria tomentosa) · Wormwood · Andrographis (Andrographis paniculata) · Boswellia · Aloe Vera · Chamomile (Matricaria chamomilla)

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