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Overview and Recommendations
Background
- •Recognize IBD as a heterogeneous group of idiopathic inflammatory conditions, primarily and , driven by a complex interplay of genetic susceptibility, environmental triggers, and dysregulated immune responses. While CD is characterized by 'skip lesions' and transmural involvement, UC typically presents with continuous mucosal inflammation starting from the rectum.
- •Identify the global epidemiological shift where IBD prevalence is increasing worldwide, now affecting over 5 million individuals with UC alone. While traditionally a disease of young adults, the 'elderly-onset' population (≥60 years) is the fastest-growing demographic, presenting unique challenges due to comorbidities and increased frailty.
- •Understand the systemic nature of IBD, which extends beyond the gut to include extraintestinal manifestations (EIMs) such as , uveitis, and primary sclerosing cholangitis. IBD is also associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD) and venous thromboembolism (VTE), particularly during active flares.
- •Note the importance of phenotypic variants such as perianal fistulizing Crohn's disease (pfCD) and acute severe ulcerative colitis (ASUC). ASUC is a life-threatening emergency requiring rapid hospitalization and intensive medical rescue to avoid emergency colectomy.
- •Consider the role of genetic drivers like the NOD2 gene, which is found in approximately 40% of Caucasian CD patients and is linked to related multisystem disorders such as Yao syndrome (YAOS) and Blau syndrome.
Evaluation
- •Suspect IBD in patients presenting with chronic diarrhea (especially nocturnal), hematochezia, abdominal pain, weight loss, or unexplained growth failure in pediatric populations. Always ask about a family history of IBD and the presence of extraintestinal symptoms like joint pain or skin rashes.
- •Obtain baseline inflammatory biomarkers, specifically C-reactive protein (CRP) and fecal calprotectin. Fecal calprotectin is highly sensitive for intestinal inflammation and is used to differentiate IBD from functional disorders like (IBS).
- •Order a complete blood count (CBC) and iron studies to screen for anemia, which is the most common systemic complication. Also, check albumin levels as hypoalbuminemia can indicate severe disease and predict poor response to certain biologics like infliximab.
- •Perform a thorough physical examination, including a digital rectal exam and inspection of the perianal area for skin tags, fistulas, or abscesses, which are highly suggestive of Crohn's disease.
- •Utilize (IUS) as a first-line, non-invasive tool to assess bowel wall thickness (BWT). A BWT > 3 mm is a key indicator of active inflammation and can be used for longitudinal monitoring without radiation exposure.
- •Order Magnetic Resonance Enterography (MRE) or CT Enterography (CTE) to evaluate for small bowel involvement, strictures, or penetrating disease (fistulas/abscesses) that cannot be reached by standard endoscopy.
- •Perform a with multiple biopsies from both inflamed and non-inflamed segments. Histological features such as crypt abscesses in UC or non-caseating granulomas in CD are diagnostic hallmarks.
- •Classify the disease using the Montreal Classification for adults or the Paris Classification for pediatric patients to standardize the description of disease location, behavior, and age at onset.
- •Rule out infectious mimics, particularly Clostridioides difficile, which has a high prevalence (up to 28%) in IBD patients on biologics and can trigger or exacerbate flares.
- •Screen for baseline sarcopenia and nutritional deficiencies using EWGSOP2 criteria, as muscle loss is a significant predictor of poor outcomes and incident IBD.
- •Evaluate for perianal disease using pelvic MRI, which is the reference standard for classifying complex branching fistulas, or transperineal ultrasonography (TPUS) as a non-invasive alternative.
- •Assess for psychological comorbidities, including anxiety and depression, which are highly prevalent and closely correlated with disease activity, especially in adolescents.
Management
- •Adopt a 'treat-to-target' strategy aiming for transmural healing (TMH), defined by the normalization of bowel wall thickness on ultrasound, rather than just symptomatic relief. TMH is associated with superior long-term outcomes and lower surgery rates.
- •Induce remission in moderate-to-severe UC using Guselkumab 200 mg or 400 mg IV at weeks 0, 4, and 8, or initiate anti-TNF therapy such as Infliximab 5 mg/kg IV.
- •Manage Acute Severe Ulcerative Colitis (ASUC) with inpatient IV Methylprednisolone 60 mg/day. If no response is seen by day 3 (e.g., PUCAI score > 45 in children), initiate rescue therapy with Infliximab 5 mg/kg or Cyclosporine.
- •Utilize personalized dosing models (e.g., iDose) for Infliximab in ASUC to account for high drug clearance in patients with high inflammatory burdens, aiming to maximize colectomy-free survival.
- •Administer Exclusive Enteral Nutrition (EEN) as first-line induction therapy for pediatric Crohn's disease. Provide 100% of daily caloric requirements via liquid formula for 6 to 8 weeks to induce mucosal healing and avoid steroid toxicity.
- •Transition to maintenance therapy with Subcutaneous (SC) Infliximab 120 mg every 2 weeks, which often achieves higher colonic tissue concentrations than IV administration.
- •Consider Ustekinumab for Crohn's disease, induced with a weight-tiered IV dose (e.g., 6 mg/kg for patients ≥40 kg) and maintained with 90 mg SC every 8 weeks, especially in patients with symptomatic ileal strictures.
- •Employ small molecule JAK inhibitors like Upadacitinib 15-30 mg daily or Filgotinib 200 mg daily for refractory UC cases that have failed biologic therapy.
- •Monitor therapy using Therapeutic Drug Monitoring (TDM) to assess drug trough levels and the development of anti-drug antibodies (ADAs), particularly when clinical response is lost.
- •Address iron deficiency anemia with IV Iron (e.g., Ferric Carboxymaltose 1000 mg) rather than oral iron during active flares to ensure better absorption and avoid GI irritation.
- •Implement bone protection for patients on prolonged corticosteroids, including Calcium 1000–1200 mg/day and Vitamin D 800–1000 IU/day, to mitigate the risk of osteoporosis and fractures.
- •Refer for surgical consultation early in cases of uncomplicated ileocaecal CD; laparoscopic ileocaecal resection is a valid alternative to Infliximab with high rates of long-term therapy-free remission.
- •Manage fibrostenotic strictures with Endoscopic Balloon Dilation (EBD) or Endoscopic Stricturotomy (ESt) for short (< 5 cm) accessible lesions before considering surgical resection.
- •Maintain maintenance therapy throughout pregnancy to prevent flares, as active disease is the greatest risk to the fetus. Anti-TNFs, Vedolizumab, and Ustekinumab are generally considered safe during gestation.
- •Avoid live vaccines in patients on biologics or immunosuppressants. Ensure all age-appropriate vaccinations and screenings (e.g., TB, Hepatitis B/C) are completed prior to starting advanced therapies.
Board Review — High Yield
- •ASCA vs pANCA — Anti-Saccharomyces cerevisiae antibodies (ASCA) are associated with Crohn's; pANCA is more common in Ulcerative Colitis.
- •Transmural vs Mucosal — Crohn's involves the full thickness of the bowel wall (transmural); UC is limited to the mucosa and submucosa.
- •Skip Lesions — Characteristic of Crohn's disease, where areas of inflammation are separated by normal-appearing mucosa.
- •Crypt Abscesses — A classic histological finding in Ulcerative Colitis representing neutrophils within the colonic crypts.
- •Toxic Megacolon — A surgical emergency defined by colonic dilation > 6 cm associated with systemic toxicity.
- •Exclusive Enteral Nutrition (EEN) — The preferred first-line induction therapy for pediatric Crohn's disease, superior to steroids for mucosal healing.
- •Rutgeerts Score — Used to assess the risk of endoscopic recurrence in Crohn's disease after ileocaecal resection.
- •NOD2/CARD15 — The first gene associated with Crohn's disease susceptibility, particularly ileal involvement.
Deep Dive — Evidence Details
Definition, Synonyms, and Classification
- ▸IBD principally comprises ulcerative colitis and Crohn’s disease. [162]
- ▸IBD unclassified is used when IBD is established but UC and CD cannot be reliably distinguished. [168]
- ▸UC classification includes anatomic extent and objective inflammatory activity. [163][164][176]
- ▸CD classification includes disease location, activity, behavior, complications, and postoperative status. [165][166][167][178]
- ▸Microbiome, molecular, artificial-intelligence, and quantitative histologic findings may support phenotyping but do not independently replace integrated clinical classification. [162][164][166][173]
Definition
Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory disorder of the gastrointestinal tract. In contemporary clinical usage, the term principally encompasses ulcerative colitis (UC) and Crohn’s disease (CD), which are the two major, clinically established IBD entities. [162] The term is also used for patients with chronic intestinal inflammation whose clinical, endoscopic, radiologic, and histopathologic findings do not permit a reliable distinction between UC and CD; these patients may be classified as IBD unclassified (IBD-U). [168]C
IBD is a clinicopathologic diagnosis rather than a single symptom-based condition. Its classification integrates disease distribution, inflammatory pattern, endoscopic appearance, histology, clinical behavior, and longitudinal evolution. [163][164][166][178]D The disease may also be accompanied by extraintestinal manifestations (EIMs), including articular, dermatologic, ocular, and other systemic involvement; therefore, EIMs are clinically relevant components of the IBD phenotype rather than separate synonyms for intestinal disease. [170][174]
Synonyms and related terminology
Common umbrella terms include “inflammatory bowel disease,” “chronic inflammatory bowel disease,” and the abbreviation IBD. The principal disease-specific names are ulcerative colitis, abbreviated UC, and Crohn’s disease, abbreviated CD. [162] “IBD-U” is the preferred descriptive term when available evidence supports IBD but does not adequately establish UC or CD. [168]C
“IBD-like disease” should not automatically be treated as synonymous with conventional IBD. It may describe an intestinal inflammatory phenotype occurring in the context of an inborn error of immunity or another defined systemic disorder; for example, SOCS1 haploinsufficiency has been reported with an IBD-like disease phenotype. [177]C Similarly, immunomodulator-responsive enteropathy in dogs is a veterinary inflammatory intestinal condition and should not be conflated with human IBD. [181]D
Principal classification
Ulcerative colitis
UC is one of the two principal forms of IBD. [162] In the supplied evidence, UC is further described by anatomic extent, including proctitis, left-sided disease, and extensive colitis or pancolitis; pediatric imaging observations also used the Paris-style extent labels E1/E2 for more limited disease and E3/E4 for extensive disease. [176] UC classification may additionally incorporate inflammatory activity assessed endoscopically, including the Mayo Endoscopic Score, and histologic evaluation of mucosal biopsies. [164][163] UC-associated neoplasia is a disease-related complication category that may be classified according to whether a lesion arises in a colitis-affected or colitis-unaffected area and according to endoscopic, morphologic, and immunohistochemical features. [169]
Crohn’s disease
CD is the second principal form of IBD and is characterized by substantial heterogeneity in disease location, tissue involvement, behavior, and treatment response. [162][165] Location-based classification includes ileal Crohn’s disease, colonic disease, and disease involving other gastrointestinal segments or multiple locations; the available systematic review specifically demonstrated distinct microbiome and metabolome patterns across CD locations. [165] CD assessment may also distinguish inflammatory activity from complications such as stricturing, penetrating disease, postoperative recurrence, and the need for intestinal resection, although the supplied studies address these categories in different clinical settings. [166][167]C[171][178]D
CD classification incorporates objective endoscopic and histopathologic findings. Endoscopic assessment is used to evaluate active disease and postoperative recurrence, while biopsy assessment may quantify cryptitis, crypt architectural abnormalities, and inflammatory-cell infiltration. [166][178]D Surgical history is not itself a defining requirement for CD, but ileocecal resection and subsequent endoscopic recurrence are important longitudinal disease states in patients with ileocecal CD. [167]C[171][178]D
IBD unclassified
IBD-U applies when a patient has convincing evidence of IBD but the available information does not allow a stable assignment to UC or CD. [168]C IBD-U is a provisional or evolving classification in many patients: longitudinal follow-up may result in reclassification, although some patients remain unclassified over time. [168]C Treatment patterns and disease course should therefore be documented separately from the initial label, rather than assuming that IBD-U represents a mild or biologically uniform subtype. [168]C
Classification principles and boundaries
Microbiome alterations, particularly reduced microbial diversity, are consistently associated with IBD but are not currently sufficient by themselves to define UC, CD, or IBD-U. [162] Likewise, serum-based molecular signatures, artificial-intelligence image analysis, or quantitative histopathology may support diagnosis and phenotyping, but the supplied studies evaluate these approaches as investigational or validation tools rather than replacements for integrated clinical classification. [164][166][173]C Genetic, immune, metabolic, and extraintestinal features may refine phenotyping, but they should be interpreted within the established UC–CD–IBD-U framework. [165][170][175][177]C[180]D
The key diagnostic threshold is evidence of chronic intestinal inflammatory disease; the key classification threshold is whether the total clinical, endoscopic, radiologic, and histologic pattern supports UC, CD, or neither with sufficient confidence. [163][166][168]C
| Category | Defining classification concept | Examples or supporting domains |
|---|---|---|
| Ulcerative colitis (UC) | Principal IBD form classified mainly by colonic extent and inflammatory activity | Proctitis, left-sided disease, extensive colitis/pancolitis; endoscopic and histologic activity [163][164][176] |
| Crohn’s disease (CD) | Principal IBD form characterized by heterogeneous location, activity, behavior, and complications | Ileal or other-location disease, stricturing or penetrating complications, postoperative recurrence [165][166][167]C[178]D |
| IBD unclassified (IBD-U) | IBD is supported, but evidence is insufficient for confident UC or CD assignment | Longitudinal reassessment may confirm a stable category or lead to reclassification [168]C |
| IBD-like disease | An inflammatory intestinal phenotype associated with another defined disorder | Inborn errors of immunity, including SOCS1 haploinsufficiency [177]C |
Epidemiology and Risk Factors
- ▸UC incidence is increasing in Asia, and paediatric-onset IBD remains a major treatment and healthcare-planning subgroup. [122,124,126]
- ▸Risk assessment should account for geography, respiratory disease, prenatal medication exposure, metabolic syndrome, anemia, frailty, cancer, and endemic infections. [117,127-129,132,133,135]
- ▸Postoperative complications in CD surgery occur in approximately **20%–50%** of reported cases. [118]
- ▸Frailty is defined as **≥3** Fried-derived criteria in the cited cohort. [135]
- ▸Advanced therapies may reduce paediatric resection rates but can be associated with infection, psychiatric, and immunogenicity risks. [123,124,126,130]
Global and temporal epidemiology
Inflammatory bowel disease (IBD) comprises Crohn disease (CD) and ulcerative colitis (UC), both chronic inflammatory disorders whose epidemiology varies by age, geography, and calendar period. Recent evidence indicates that UC incidence is increasing in Asia; a Korean multicentre inception cohort enrolled 353 patients with newly diagnosed moderate-to-severe UC between 2014 and 2017 and followed them for a median of 4.9 years. [122]C The available references do not provide a pooled global prevalence or incidence estimate, but they document IBD across Europe, the Middle East, East Asia, and the United Kingdom, supporting its worldwide distribution. [123][124][126][128][129][133]C
Paediatric-onset disease is an important epidemiological subgroup. A UK population-based cohort included children aged ≤17 years diagnosed with IBD between 2007 and 2024 and evaluated changing anti-TNF exposure and abdominal surgery rates over an 18-year period. [124] A nationwide US claims study evaluated children and adolescents aged 6–17 years who newly initiated infliximab or adalimumab, illustrating the substantial paediatric population requiring advanced therapy. [126] Pediatric treatment patterns are also evolving, with systematic-review evidence addressing combined biologic and/or small-molecule therapy in children through January 2026. [119]
Demographic and geographic factors
Disease burden and treatment-related outcomes differ across populations. In a Middle Eastern cohort from the United Arab Emirates, anti-TNF immunogenicity was evaluated across 314 treatment courses in 248 patients, comprising infliximab and adalimumab exposure. [123] The study highlights the importance of regional data because immunogenicity rates and drug-level thresholds may vary according to population and clinical context. [123] A Spanish population-based study from the Valencian Community examined symptomatic leishmaniasis among patients with IBD receiving biologic therapy in a Mediterranean endemic region, emphasizing that local infectious exposures modify risk in immunosuppressed populations. [133]C
Age is also relevant to comorbidity. A Danish nationwide cohort included 53,591 patients with IBD and 267,955 age- and sex-matched controls to assess interstitial lung disease (ILD), while a separate Danish study included 59,494 patients with IBD, of whom 20,551 had CD and 38,943 had UC, to evaluate IBD management in the setting of cancer. [128][132] These studies reflect the growing clinical importance of multimorbidity as IBD populations age. [128][132]
Environmental and early-life risk factors
Prenatal exposure to acid-suppressive medication has been investigated as a potential early-life risk factor. A nationwide South Korean mother–child cohort assessed proton-pump inhibitor and H2-receptor antagonist exposure during pregnancy and subsequent incident IBD, including CD and UC, in offspring followed through 2023. [129] Because the cited study is observational, any association should not be interpreted as proof of causation, and confounding by maternal illness or healthcare utilisation remains relevant. [129]
Respiratory disease may share epidemiological or biological links with IBD. A systematic review and meta-analysis of observational studies evaluated the bidirectional association between IBD and obstructive lung diseases, including chronic obstructive pulmonary disease, asthma, and bronchiectasis. [117] A Danish nationwide cohort additionally assessed incident ILD and mortality among patients with IBD. [128] Together, these studies support consideration of chronic respiratory disease as an important associated condition, although the references do not establish a single causal pathway. [117][128]
Comorbidity and disease-related risk factors
Metabolic syndrome (MetS) is an increasingly relevant comorbidity. A real-world cohort of adults with CD or UC followed from 2010 to 2024 evaluated temporal trends in cardiometabolic disease and compared outcomes among patients with IBD and MetS, IBD without MetS, and MetS without IBD. [127] The study specifically examined cardiovascular, hepatic, renal, and IBD-related outcomes, indicating that cardiometabolic risk should be incorporated into long-term assessment. [127]
Anemia is particularly frequent in CD compared with UC. A systematic review identified chronic inflammation, impaired iron absorption, intestinal blood loss, and microbiome-related mechanisms as contributors; CD-associated dysbiosis may include increased siderophore-producing Enterobacteriaceae that compete with host iron acquisition. [120] Frailty is another clinically important phenotype. In a prospective single-centre cohort of adults hospitalised with active IBD who required biologic or small-molecule initiation, frailty was defined using a modified Fried index, with ≥3 criteria indicating frailty and 1–2 criteria indicating an intermediate state. [135]C
Risk factors for adverse outcomes
In CD surgery, postoperative complication rates are reported at approximately 20%–50%, including surgical-site infection, intra-abdominal abscess, and anastomotic leakage. [118] A systematic review identified clinical and perioperative predictors and evaluated predictive biomarkers, although accurate individual risk stratification remains difficult. [118] Postoperative endoscopic recurrence after ileocolic resection may also be influenced by retained mesenteric tissue: a multicentre study examined residual ileocolic artery length as a surrogate for residual mesenteric burden. [125]
Treatment exposure modifies risk but may also reduce disease complications. An 18-year paediatric cohort associated increasing anti-TNF use with reductions in abdominal resection rates, although this was observational evidence. [124] Conversely, advanced therapy was associated with higher risks of tuberculosis and depression/anxiety than conventional therapy in a 13-hospital common-data-model analysis, with reported hazard ratios of 2.86 and 1.58, respectively. [130] In children, comparative infection risk between infliximab and adalimumab was assessed using nationwide claims data, but the cited abstract does not provide the effect estimate. [126] Anti-TNF immunogenicity occurred in 28.3% (89/314) of treatment courses in the Middle Eastern cohort and was evaluated as a contributor to loss of response. [123]
Finally, IBD patients with prior or coexisting cancer represent a growing subgroup requiring individualised treatment and surgical-risk assessment. [132] Rare intestinal ulceration with pancytopenia and concurrent myelodysplastic syndrome or aplastic anaemia has been associated with high mortality in pooled case-based evidence, although this represents an uncommon, highly selected complication rather than a population-level risk factor. [121]
| Domain | Evidence | Reference |
|---|---|---|
| Asian epidemiology | Increasing UC incidence reported in Asia; Korean cohort of 353 newly diagnosed moderate-to-severe patients | [122]C |
| Paediatric IBD | UK cohort included patients aged ≤17 years over 2007–2024; US claims cohort included ages 6–17 years | [124][126] |
| Anti-TNF immunogenicity | 28.3% (89/314) of treatment courses in a Middle Eastern cohort | [123] |
| CD surgical morbidity | Reported postoperative complication rates of 20%–50% | [118] |
| Frailty | ≥3 modified Fried criteria classified patients as frail | [135]C |
| Advanced-therapy risks | Tuberculosis HR 2.86; depression/anxiety HR 1.58 versus conventional therapy | [130] |
Management of Inflammatory Bowel Disease
- ▸Targeting transmural healing (TMH) via intestinal ultrasound is superior to targeting clinical symptoms alone for preventing long-term complications.
- ▸Subcutaneous Infliximab provides higher colonic tissue concentrations than IV administration and may overcome low-titer anti-drug antibodies.
The of Inflammatory Bowel Disease (IBD) has evolved from symptom-based control to a "treat-to-target" paradigm focusing on objective markers of inflammation. This approach aims to prevent structural bowel damage and reduce the long-term need for surgery [54]. Management strategies differ significantly between (CD) and (UC), though both rely on a tiered approach of induction and maintenance therapy using biologics and small molecules.
Supportive Care and Complication Management
- ▸Use structured long-term monitoring that includes disease activity, nutrition, growth, anemia, bone health, treatment toxicity, and complications. [182]
- ▸EEN is an established pediatric induction strategy; adult evidence suggests a pooled real-world remission rate of 66%, but study heterogeneity remains important. [140,144]
- ▸CDED may be used alone or with PEN; available pediatric studies do not establish uniform superiority of PEN or EEN combinations. [136,137,183]
- ▸Investigate anemia systematically and treat pancytopenia with intestinal ulceration as an urgent gastroenterology–hematology problem. [120,121]
- ▸Assess strictures for inflammatory versus fixed components and select medical, endoscopic, or surgical therapy according to anatomy and obstruction risk. [56,142,146]
- ▸Screen for tuberculosis and mental-health complications during advanced therapy; observed hazard ratios were 2.86 and 1.58, respectively. [130]
Scope and monitoring
Supportive care in inflammatory bowel disease (IBD) should be integrated with disease control, nutritional assessment, surveillance for treatment toxicity, and proactive management of intestinal and extraintestinal complications. The 2026 ECCO–ESPGHAN update provides an evidence-based framework for management, monitoring, and long-term care of pediatric Crohn’s disease (CD), based on a systematic review through 2024 with targeted updates through June 2025. [182] Management should be individualized according to age, disease location and behavior, inflammatory burden, nutritional status, growth, complications, and treatment-related risks. [182]
Nutrition and dietary therapy
Exclusive enteral nutrition (EEN) remains an established induction option in children with active CD. [140] In a comparison of pediatric small-bowel CD cohorts, EEN and corticosteroids were evaluated for sustained steroid-free remission at 1 year, growth, time to biologic therapy, and time to luminal resection; these outcomes support considering induction choice within a strategy that prioritizes steroid avoidance and long-term disease control. [140] EEN has also been evaluated in adults: a 2026 systematic review of 40 studies involving 2,459 patients reported a pooled clinical-remission rate of 66% in real-world cohorts, although the evidence included both randomized and non-randomized studies and should be interpreted in light of heterogeneity and risk of bias. [144]
The Crohn’s disease exclusion diet (CDED), used alone or with partial enteral nutrition (PEN), is supported by a contemporary meta-analysis assessing induction response, remission, and maintenance of remission. [183] In children with mild-to-moderate CD, a prospective randomized study directly compared CDED alone with CDED plus PEN, addressing whether supplemental enteral nutrition adds benefit to dietary exclusion. [137] A separate pediatric randomized cohort comparing modified CDED plus PEN with CDED plus EEN found no significant difference in primary or clinical outcomes between groups; oral-microbiome sampling was performed at baseline and during follow-up, although the COVID-19 pandemic limited later sampling. [136] Metabolomic analyses of children receiving a reverse-engineered, whole-food blended EEN formula demonstrated treatment-associated remodeling of stool, urine, serum, and plasma metabolites, with exploratory associations between metabolite changes and remission. [186] These findings support dietitian-supervised nutritional therapy but do not establish that microbiome or metabolomic testing should routinely guide treatment; a pediatric multi-omics machine-learning model intended to predict EEN response remains an emerging, investigational approach. [141]
Anemia and cytopenias
Anemia is a common systemic complication of IBD and is reported more frequently in CD than in ulcerative colitis. [120] Contributing mechanisms include chronic inflammation, impaired iron absorption, intestinal blood loss, and potentially microbiome-mediated competition for iron involving siderophore-producing bacteria, particularly Enterobacteriaceae. [120] Evaluation should therefore distinguish iron deficiency, inflammation-associated iron restriction, nutritional deficiencies, ongoing blood loss, and medication- or marrow-related cytopenias. [120]
Intestinal ulceration accompanied by pancytopenia is an uncommon but potentially life-threatening presentation reported in IBD and intestinal Behçet disease, particularly when myelodysplastic syndrome or aplastic anemia coexists. [121] Pancytopenia with ulceration warrants urgent hematologic assessment, evaluation for marrow failure or hematologic malignancy, infection assessment, and coordinated gastroenterology–hematology management because the pooled literature specifically addresses substantial mortality and prognostic factors in this setting. [121]
Bone health and fracture prevention
IBD is associated with osteoporosis and fracture risk, particularly in patients exposed to glucocorticoids. [184][185] DXA-based research has examined abdominal and femoral fat distribution, bone mineral density, body composition, and fracture history; regional adiposity remained a potential fracture-risk marker after adjustment for body mass index, hip lean mass, bone density, comorbidities, and glucocorticoid exposure. [184] Bone-health care should therefore include assessment of disease activity, steroid exposure, nutritional adequacy, and individualized fracture risk, with DXA when clinically indicated. [184] In patients undergoing shoulder arthroplasty, an insurance-claims matched cohort specifically evaluated revision arthroplasty, rotator-cuff repair, and other complications in adults with IBD, underscoring the importance of communicating IBD and immunosuppressive exposure during orthopedic planning. [185]
Strictures, obstruction, and fistulizing complications
Symptomatic strictures require assessment of inflammatory activity, fixed fibrosis, length, severity, and obstructive complications. [142]C MRI research has evaluated T2* and diffusion-weighted intravoxel incoherent-motion parameters against location-matched surgical histopathology to distinguish inflammatory from noninflammatory small-bowel strictures; this remains a specialized imaging approach rather than a replacement for multidisciplinary assessment. [142]C In ileal stricturing CD, ustekinumab has been studied in an international multicenter retrospective cohort of 57 adults treated within 6 months of imaging-confirmed symptomatic disease, with outcomes including endoscopic balloon dilation, surgery, recurrent obstruction, and treatment persistence. [56]
Endoscopic balloon dilation (EBD), endoscopic stent placement, and endoscopic stricturotomy have been compared indirectly in a systematic review of 39 studies comprising 1,614 patients. [146] The review assessed technical and clinical success, adverse events, repeat procedures, and surgery; treatment selection should therefore account for stricture anatomy, endoscopic accessibility, suspected fibrosis, recurrence risk, and surgical suitability. [146] Obstruction, abscess, perforation, sepsis, or failure of endoscopic or medical management requires urgent surgical and multidisciplinary review. [56][146]
Perianal and upper-gastrointestinal disease
A surgically drained perianal abscess in a child may precede a later CD diagnosis. [67]D In a tertiary-center cohort of 204 children aged 3–18 years without previously diagnosed IBD or an established fistula at presentation, clinical, laboratory, operative, and follow-up features were analyzed, including age-adjusted anemia and hypoalbuminemia defined as serum albumin <3.5 g/dL. [67]D Persistent drainage, recurrent abscess, fistula formation, anemia, hypoalbuminemia, or other intestinal symptoms should prompt evaluation for underlying CD. [67]D
Esophageal CD is rare and nonspecific in presentation, which may delay diagnosis. [139] A systematic review of 90 studies involving 100 adults characterized symptoms, diagnostic pathways, and treatment approaches; evaluation generally requires endoscopy with biopsy and exclusion of infectious, reflux-related, malignant, and other inflammatory causes. [139]
Treatment safety and imaging
Advanced IBD therapies were associated with higher observed risks of tuberculosis and depression/anxiety than non-advanced therapy in a 13-hospital common-data-model analysis; reported hazard ratios were 2.86 for tuberculosis and 1.58 for depression/anxiety. [130] Pretreatment infection-risk assessment, ongoing vigilance for tuberculosis, and mental-health screening should therefore be incorporated into longitudinal care. [130] Abbreviated MR enterography protocols that omit contrast and antiperistaltic agents have been prospectively compared with conventional contrast-enhanced MRE for activity and complication detection; abbreviated imaging may improve efficiency and compliance, but protocol selection should reflect the diagnostic question and local validation. [147]
| Clinical issue | Evidence-informed priorities |
|---|---|
| Nutritional compromise or active CD | Consider dietitian-supervised EEN, CDED, PEN, or combination strategies according to age, disease severity, feasibility, and treatment goals. [136][137][140][144][183] |
| Anemia | Evaluate inflammation, iron deficiency, blood loss, malabsorption, and nutritional deficiency; account for microbiome-mediated iron competition as an emerging mechanism. [120] |
| Ulceration with pancytopenia | Urgent hematology assessment for marrow failure or hematologic malignancy, alongside evaluation of IBD activity and infection. [121] |
| Bone or fracture risk | Review glucocorticoid exposure, nutrition, disease activity, and individualized need for DXA and fracture prevention. [184][185] |
| Symptomatic stricture | Characterize inflammatory versus noninflammatory disease; consider medical therapy, EBD, other endoscopic approaches, or surgery. [56][142]C[146] |
| Perianal abscess in a child | Ensure follow-up for recurrent disease, fistula, anemia, hypoalbuminemia, and possible subsequent CD. [67]D |
| Advanced therapy | Incorporate tuberculosis prevention/surveillance and depression/anxiety monitoring. [130] |
Special Populations
- ▸Preconception and pregnancy care should prioritize objective disease control and coordinated individualized management. [150][151][152][153][154][155]
- ▸In CD, disease activity and ileal disease—not previous abdominal surgery—were associated with preterm birth in a prospective cohort. [156]
- ▸Pregnancy safety evidence is strongest for anti-TNF therapy; evidence for vedolizumab, ustekinumab, and JAK inhibitors is less mature. [22]
- ▸Vedolizumab pregnancy data include a prospective registry of 275 pregnancies and updated systematic-review evidence. [102][158]
- ▸Paediatric UC with acute severe colitis requires proactive monitoring and timely medical or surgical escalation. [98]
Pregnancy and preconception
Pregnancy in inflammatory bowel disease (IBD) requires coordinated, individualized care because disease activity, medication concerns, limited pregnancy-specific evidence, and inconsistent clinical practice can affect conception, adherence, and maternal–fetal outcomes. The 2025–2026 Global Consensus Statement was developed by 39 IBD and content experts and 7 patient advocates from 6 continents to address these knowledge and practice gaps. [150][151][152][153][154][155] Preconception counselling should therefore include assessment of disease activity, current and previous therapies, nutritional status, pregnancy intentions, and obstetric and surgical history, with treatment decisions balancing the risks of uncontrolled IBD against medication exposure. [150][151][152][153][154][155]
Disease control is a central determinant of pregnancy outcome. In a prospective cohort of 1,046 women with Crohn’s disease (CD), previous CD-related surgery was not associated with adverse pregnancy, delivery, or neonatal outcomes after adjustment; increased disease activity and ileal disease were associated with preterm birth, with odds ratios of 1.14 (95% CI 1.06–1.22) and 2.19 (95% CI 1.26–3.83), respectively. [156] The cohort also found that women with previous surgery had more active disease, emphasizing that observed pregnancy risk may reflect disease activity rather than surgical history itself. [156]
Medication safety and infant considerations
Available pregnancy evidence is strongest for established therapies, whereas data for newer agents remain limited. A 2026 systematic review and meta-analysis included 67 observational studies and 17,441 pregnancies exposed to advanced therapies and evaluated early pregnancy loss, preterm birth, congenital malformations, small-for-gestational-age birth, and other adverse outcomes. The pooled prevalence of early pregnancy loss was 8.2% (95% CI 6.2–10.8); the abstract also reported an overall preterm-birth estimate of 8.9% (95% CI 7.9–...), although the supplied reference does not provide the complete interval or class-specific results. [22] Anti-TNF therapy was described as having a well-established safety evidence base, while evidence for vedolizumab, ustekinumab, and Janus kinase inhibitors was characterized as more limited. [22]
Vedolizumab-specific evidence is expanding. A prospective registry followed 275 pregnancies from the United States and Canada: 99 vedolizumab-exposed pregnancies, 76 disease-matched pregnancies exposed to another biologic, and 100 pregnancies without chronic health conditions. Maternal and infant follow-up continued to 1 year postpartum, and the registry assessed major pregnancy, birth, and infant outcomes. [158] A separate updated systematic review and meta-analysis synthesized cohort studies and randomized trials through June 26, 2025, examining live birth, preterm birth, early pregnancy loss, caesarean delivery, congenital malformations, small-for-gestational-age birth, and composite perinatal complications after vedolizumab exposure. [102]
International guidance generally supports continuing indicated immunomodulating treatment during pregnancy rather than exposing the mother and fetus to active disease or relapse risk. [159] In a prospective cohort of women with IBD and their infants, maternal immunomodulating therapy and maternal Tdap vaccination were evaluated for effects on transplacental antibody transfer. [159] Another study used detailed flow cytometry and cytokine assays during pregnancy, at delivery, postpartum, and at 6 weeks of age to examine maternal and infant immune phenotypes after in-utero exposure to IBD therapies. [160]C
Monitoring and diagnostic evaluation
The ECCO–ESGAR–ESP–IBUS diagnostic and monitoring guideline provides recommendations for initial diagnosis, complication detection, treatment monitoring, pregnancy-related diagnostics, postoperative assessment, and cancer surveillance. [97] Monitoring during pregnancy should be proactive and adapted to symptoms, objective inflammatory assessment, nutritional needs, and fetal and obstetric circumstances, while avoiding unnecessary diagnostic delay. [97][150][151][152][153][154][155]
Delivery and perineal considerations
Delivery planning should be individualized according to disease phenotype, obstetric indications, prior surgery, and the presence or absence of active perianal disease. [150][151][152][153][154][155] A study of primiparous women with singleton, cephalic, term vaginal births specifically examined perineal injury in IBD without active perianal disease; women with active perianal disease were excluded according to institutional guidance. [161] A population-based Ontario matched cohort evaluated severe maternal morbidity from 20 weeks’ gestation through 42 days postpartum and assessed whether delivery method altered risk among individuals with CD or ulcerative colitis (UC). [66]D
Children and adolescents
Acute severe colitis (ASC) is a relatively frequent and potentially emergency presentation of paediatric UC. Updated ESPGHAN–ECCO guidance recommends a standardized, proactive approach based on close monitoring and timely medical and surgical intervention to improve outcomes. [98]
Environmental and medication exposures
A systematic review and meta-analysis evaluated passive-smoking exposure in relation to IBD incidence and disease outcomes for CD and UC using PRISMA and MOOSE methods and searches through May 2025. [99] The supplied abstract describes the research question and methodology but does not provide the pooled effect estimates; passive-smoking counselling should therefore be incorporated into preventive care without attributing a specific magnitude of risk from this reference alone. [99]
A nationwide South Korean mother–child cohort examined whether prenatal exposure to proton-pump inhibitors or H2-receptor antagonists was associated with incident IBD, CD, or UC in offspring, with follow-up through December 31, 2023. [129] The supplied abstract establishes the cohort design and outcome question but does not provide the study’s effect estimates; these medications should not be stopped or continued solely on the basis of an unreported association. [129]
| Population or issue | Evidence-based priority |
|---|---|
| Pregnancy | Maintain disease control and individualize medication and delivery decisions. [150][151][152][153][154][155] |
| Crohn’s disease surgery history | Previous surgery alone was not associated with adverse pregnancy or neonatal outcomes. [156] |
| Advanced therapies | Interpret newer-agent pregnancy data cautiously; anti-TNF evidence is comparatively established. [22] |
| Vedolizumab exposure | Use registry and systematic-review data when counselling, recognizing that evidence remains observational and evolving. [102][158] |
| Paediatric ASC | Use standardized close monitoring with timely medical and surgical intervention. [98] |
| Passive smoking or prenatal acid suppression | Counsel and interpret associations using the reported study results; the supplied abstracts do not provide effect estimates. [99][129] |
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