Crohn’s disease is a chronic, episodic, inflammatory bowel disease (IBD) that affects the entire wall of the bowel or intestines. Crohn’s disease can affect any part of the gastrointestinal tract from mouth to anus; as a result, the symptoms of Crohn’s disease vary among afflicted individuals. The disease is characterized by areas of inflammation with areas of normal lining between in a symptom known as skip lesions. The cardinal symptoms are chronic diarrhea, abdominal pain, and fatigue; weight loss, fever, anemia, and perianal or extraintestinal findings may also be presenting features. Chronic diarrhea is the most common symptom, though some patients do not experience it. Constipation is not typical and, when present, usually reflects an obstructing stricture.^[1][2] Treatment for Crohn’s disease depends on the location and severity of disease, complications, and the person’s response to previous medical treatments when treated for recurring symptoms. ^[3]

Descriptions consistent with Crohn’s disease appear in the medical literature from the 18th century onward, including reports by Giovanni Battista Morgagni (1769), Samuel Wilks (1859), Antoni Leśniowski (1903), and Thomas Kennedy Dalziel (1913).^[4][5] The disease was established as a distinct clinicopathologic entity in 1932, when Burrill Bernard Crohn, Leon Ginzburg, and Gordon Oppenheimer described 14 patients with inflammation of the terminal ileum under the title “Regional ileitis: a pathologic and clinical entity.”^[4][6] Over the following decades the concept expanded from an ileal disease to a pan-enteric, transmural inflammatory bowel disease (IBD). It was then stratified by location and behavior, which was later formalized in the Montreal classification. Its etiology has been reframed as a dysregulated mucosal immune response to the gut microbiota in a genetically susceptible host.^[7][8]

Crohn’s disease is classified using the Montreal classification (2005), which replaced the 1998 Vienna classification and stratifies patients by three axes: age at diagnosis (A), disease location (L), and disease behavior (B), with modifiers for upper gastrointestinal involvement (L4) and perianal disease (p).^[9][10] Disease location is relatively stable over time, whereas disease behavior commonly progresses from inflammatory to stricturing or penetrating phenotypes.^[11] The Paris classification (2011) adapts the Montreal system for pediatric patients.^[12]

Crohn’s disease (CD) arises when environmental triggers and gut microbial dysbiosis provoke a poorly regulated mucosal immune response across an impaired epithelial barrier in a genetically susceptible host.^[13][14] No single gene, microbe, or environmental factor is sufficient on its own. The result is a self-perpetuating cycle of barrier breakdown, microbial translocation, and Th1/Th17-skewed transmural inflammation, which current therapies interrupt at specific points.^[15][14] More than 200 susceptibility loci have been identified. They converge on four processes: innate microbial sensing (NOD2), autophagy (ATG16L1), epithelial barrier integrity, and IL-23/Th17 signaling.^[16][17] The hallmark pathologic features are:

• Transmural inflammation
• Skip lesions
• Non-caseating granulomas
• A propensity for stricture and fistula formation

Crohn’s disease (CD) has no single identifiable cause. The best-supported model is a dysregulated mucosal immune response to the gut microbiota in a genetically susceptible host, triggered and modified by environmental exposures, resulting in impaired epithelial barrier function and chronic transmural inflammation.^[13][2] Genetic susceptibility, environmental exposure, and the microbiome each appear necessary but not individually sufficient.^[15] More than 200 susceptibility loci have been identified, with NOD2 the strongest single-gene risk factor in populations of European ancestry. Defective innate handling of intestinal bacteria (NOD2 and autophagy pathways) and a Th1/Th17–IL-23–driven effector response are central mechanisms.^[16] Established environmental contributors include cigarette smoking and early-life antibiotic exposure. No single infectious agent has been proven causal; the role of Mycobacterium avium subspecies paratuberculosis (MAP) remains unproven and controversial.

The most common disease that mimics the symptoms of Crohn’s disease is ulcerative colitis, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases, since the course of the diseases and treatments may be different. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis.

CD is no longer confined to high-income Western populations. In early-industrialized regions (North America, Europe, Oceania), adult incidence has plateaued or declined, while prevalence keeps rising (“compounding prevalence”). The steepest incidence increases are now in newly industrialized regions of Asia, Latin America, and Africa.^[18][19] Peak age at diagnosis is roughly 15–35 years, with a smaller later peak. Pediatric and very-early-onset disease continue to rise even where adult incidence has stabilized.^[13] There is no consistent sex predominance in adults. Prevalence in the United States is highest in White Americans, but CD occurs in all racial and ethnic groups.^[20]

Crohn’s disease (CD) develops in genetically susceptible individuals through the interaction of inherited risk, environmental exposures, and gut microbial dysbiosis. No single factor is necessary or sufficient to cause disease.^[13][15][21] The strongest risk factor is a first-degree relative with CD. The most important modifiable risk factor is cigarette smoking.^[13][2] Other established risk factors include childhood antibiotic exposure, appendectomy, urban residence, and an industrialized (“Western”) lifestyle and diet. Breastfeeding and physical activity are associated with lower risk.^[22] Most environmental associations come from observational data, and causality has not been established for most of them.^[22]

No professional society recommends screening asymptomatic members of the general population for Crohn’s disease. In practice, “screening” covers three separate activities. The first is case finding in symptomatic patients, where fecal calprotectin (FC) is the guideline-endorsed first-line, non-invasive test for deciding who needs endoscopy.^[23] The second is risk stratification of asymptomatic first-degree relatives (FDRs), which is still investigational and confined to research and prevention-trial settings.^[24] The third is colorectal cancer (CRC) surveillance in established Crohn’s colitis, a formal, guideline-mandated program whose start time and intervals differ between societies.^[25][26]

Crohn’s disease is a chronic, relapsing–remitting, transmural inflammatory bowel disease that tends to progress over time from purely inflammatory disease to stricturing or penetrating complications.^[16][23] Disease location is usually stable, but up to half of patients develop a stricture, internal fistula, or perianal complication within 20 years of diagnosis, and contemporary population-based cohorts show that roughly 1 in 5 patients with uncomplicated disease progress and about 1 in 4 require resection within 10 years.^[23][27] Major complications include bowel obstruction from strictures, fistulae, intra-abdominal and perianal abscesses, extraintestinal manifestations, nutritional deficiencies, treatment-related toxicity, and an increased risk of small bowel and colorectal adenocarcinoma.^[16][28] There is no cure. Long-term mortality is modestly higher than in the background population, and patients with Crohn’s colitis need risk-stratified colonoscopic surveillance for colorectal cancer.^[29][26]

Many people with Crohn’s disease have symptoms for years prior to the diagnosis. The usual onset is between 15 and 30 years of age but can occur at any age. Abdominal pain may be the initial symptom of Crohn’s disease. Crohn’s disease, like many other chronic, inflammatory diseases, can cause a variety of systemic symptoms. In addition to systemic and gastrointestinal involvement, Crohn’s disease can affect many other organ systems

Physical examination findings in crohn’s disease include fever, fatigue, weakness, bloody diarrhea, abdominal pain, hypotension and tachycardia.

The laboratory findings in a patient with Crohn’s disease include anemia, low albumin, elevated ESR, elevated serum alkaline phosphatase, deranged LFTs and electrolyte abnormalities.

Xray of the abdomen is not required for the diagnosis of Crohn’s disease. Xray may sometimes be one in case colitis is suspected. Xray is normal in mild to moderate disease and can show dilation and/or “thumb printing sign” in fulminant cases.

CT enterography (CTE) and MR enterography (MRE) are the standard cross-sectional modalities for evaluating the small bowel.^[1] Findings include skip lesions, bowel wall thickening, surrounding inflammation, abscess, and fistulae.

Magnetic resonance imaging (MRI) is another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available.

The diagnosis of Crohn’s disease can sometimes be challenging, and a number of tests are often required to assist the physician in making the diagnosis. Ileocolonoscopy with biopsy is the diagnostic gold standard; over 80% of patients with IBD have mucosal involvement within reach of the colonoscope, and the terminal ileum is successfully intubated in 80–97% of cases when the cecum is reached. More proximal small-bowel disease beyond the reach of the colonoscope is evaluated with CT or MR enterography, and small-bowel capsule endoscopy is reserved for high clinical suspicion despite negative ileocolonoscopy and cross-sectional imaging.^[1][16]

Other imaging findings for Crohn’s disease can be seen by the help of barium enema. Barium enema may show ulcerations and skip lesions. Barium enema must be avoided in severe cases as it can lead to the manifestation of toxic megacolon.

Pharmacologic management of luminal Crohn’s disease in adults is stratified by disease severity (mild-to-moderate, moderate-to-severe, severe/fulminant), risk of progression, and prior exposure to advanced therapy. Treatment has two phases: induction of remission and maintenance of remission. Current guidelines have moved away from the historical “step-up” sequence (aminosalicylates → corticosteroids → immunomodulators → biologics) toward early advanced therapy in moderate-to-severe or high-risk disease, with a treat-to-target goal of steroid-free clinical and endoscopic remission rather than symptom control alone.^[1][30][31] Controlled ileal-release budesonide 9 mg once daily is first-line induction therapy for mild-to-moderate ileocecal disease and should not be continued beyond approximately 3 months or used for maintenance; oral mesalamine is not recommended for induction or maintenance.^[1][31] Corticosteroids induce but do not maintain remission. Hospitalized patients with severe disease receive intravenous corticosteroids, with early consideration of infliximab and surgical consultation. Before starting a biologic or JAK inhibitor, screen for latent tuberculosis and hepatitis B, review and update vaccinations (pneumococcus, influenza, COVID-19, herpes zoster, RSV, HPV), and obtain baseline laboratory studies. Anti-TNF agents are cautioned in advanced heart failure and demyelinating disease, and JAK inhibitors carry venous thromboembolic and cardiovascular warnings.^[30]

Surgery is a core but non-curative treatment in Crohn’s disease (CD). Up to approximately 70% of patients require at least one intestinal resection during their disease course. Recurrence at or proximal to the anastomosis is expected rather than exceptional.^[32] Endoscopic recurrence develops in 70–90% of patients within the first postoperative year.^[33] The principal indications for surgery are:

• Medically refractory disease.
• Fibrostenotic obstruction.
• Penetrating disease.
• Free perforation.
• Hemorrhage.
• Neoplasia.^[32]

In selected patients with limited ileocecal disease, early laparoscopic ileocecal resection is now a reasonable first-line alternative to anti-TNF therapy rather than a salvage procedure.^[1][34] Contemporary management emphasizes:

• A minimally invasive, bowel-sparing operation.
• Preoperative optimization to avoid emergency surgery.
• Risk-stratified, endoscopy-guided postoperative prophylaxis.^[32][35]

Smoking cessation is the best-established modifiable intervention affecting disease course and recurrence; former smokers have a flare risk similar to never-smokers, whereas continued smoking is associated with more flares, stricturing and perianal complications, and postoperative recurrence.^[1][36]