Inflammatory bowel disease in paediatrics: Navigating the old challenges and emerging frontiers

Table 1 Global vs Arabian Gulf pediatric inflammatory bowel disease epidemiology

Feature	Global	Arabian Gulf region
Overall trend	Rising incidence worldwide, particularly in newly industrialized and urbanizing regions	Significant and consistent increase in incidence and recognition, especially over the past two decades
Incidence change (1990-2019)	Increase 22.8% globally in children/adolescents (Global Burden of Disease data)	Increasing across Gulf countries (e.g., Saudi Arabia, Qatar, Bahrain) with documented annual case growth
Proportion diagnosed before age 20	Approximately 25%-30% of total IBD cases	Similar or higher in some regional cohorts, with peak onset between ages 10-16
VEO-IBD (age < 6)	Rising; accounts for approximately 15% of pediatric IBD in some registries; often severe or monogenic	Presumed to be rising; more common in consanguineous populations; monogenic IBD increasingly reported
High-incidence regions	Canada, Northern Europe (Sweden, United Kingdom), Oceania (NZ, Australia): ≥ 10-20/100000/year	Transitioning from low to moderate incidence; still lower than North America/Europe but rapidly increasing
Recent pediatric incidence (per 100000/year)	Canada: 15-20 +; Sweden: 10-12; Japan: 3-4.5; South Korea: 2.5-4.0; Brazil: Approximately 5.5	Bahrain: CD 1.0, UC 2.5; Saudi Arabia: Regional estimates 3-4; Jordan (all ages): 6.9
Prevalence (per 100000 pediatric population)	Canada: CD 50-60, UC 30; United States (2016): Approximately 77 total; Europe: CD 8.2-60, UC 8.3-30	Bahrain: CD 9.3, UC 16.3; Saudi Arabia: CD 4.1, UC 2.76; Kuwait: CD 1.53, UC 0.6; Egypt: CD 2.0, UC 1.5
Highest incidence	Canada: Up to 23 per 100000/year (Nova Scotia, Alberta); among the highest globally	Jordan: 6.9 per 100000/year (all ages); Bahrain: Pediatric incidence of approximately 3.5 per 100000/year
Genetic role	About 20% have a family history; monogenic IBD is common in VEO-IBD	Consanguinity increases familial clustering and monogenic IBD risk in early-onset cases
Environmental risk factors	Westernization, hygiene hypothesis, antibiotic exposure, sedentary lifestyle	Similar environmental changes linked to rising IBD (urbanization, western diets, reduced microbial exposure)
Common pediatric phenotype	CD more common than UC; aggressive disease in younger children (CD)	CD predominates; ileocolonic involvement, more extensive disease, frequent growth failure, severe onset in many cohorts
IBD-U	Approximately 10%-15% at initial diagnosis; requires further subclassification	Common at presentation due to overlapping features and limited access to advanced diagnostics
Data gaps	Better registry coverage in North America/Europe; underreported in parts of Asia, South America	Hospital-based data dominate; lack of national registries in many MENA states

CD: Crohn’s disease; UC: Ulcerative colitis; VEO-IBD: Very early-onset inflammatory bowel disease; IBD-U: Inflammatory bowel disease-unclassified; IBD: Inflammatory bowel disease; MENA: Middle East and North Africa.

Table 2 Key differentiating factors between Crohn’s disease and ulcerative colitis

Feature	CD	UC	IBD-U
Location	Any part of the GI tract (mouth to anus)	Limited to the colon and rectum	Colon only
Inflammation pattern	Discontinuous (skip lesions)	Continuous	Colonic, but with features unclear for CD/UC
Depth of involvement	Transmural (full thickness)	Mucosal and submucosal (superficial)	Overlapping or ambiguous features
Rectal involvement	Often spared (rectal sparing)	Always involved (proctitis)	Variable, can be involved
Microscopic features	Non-caseating granulomas (characteristic)	Crypt abscesses (common), no granulomas	Ambiguous; may have some transmural features but no granulomas
Fistulas/strictures	Common	Rare (unless long-standing, severe disease)	Rare, but can develop features over time
Perianal disease	Common	Rare	Rare
Cobble stoning	Characteristic endoscopic appearance (CD)	Absent	Absent (classic UC)
Surgical cure	Not curative (disease can recur)	Curative for GI manifestations	Variable, depends on evolving phenotype

CD: Crohn’s disease; UC: Ulcerative colitis; IBD-U: Inflammatory bowel disease-unclassified; GI: Gastrointestinal.

Table 3 Comparison of paediatric vs adult-onset inflammatory bowel disease

Feature	Pediatric-onset IBD	Adult-onset IBD
Disease extent	More extensive disease (e.g., pancolitis in UC, panenteric CD)	More localized (e.g., left-sided colitis in UC)
Severity at onset	Often more severe with rapid progression	Variable; may have a milder course at onset
Growth and development	Commonly affected (growth failure, delayed puberty, bone density loss)	Growth is not an issue
Perianal disease	More common in pediatric Crohn’s disease	Less frequent
Extraintestinal manifestations	More frequent and severe	Present, but generally less common
Disease behavior over time	More aggressive with higher risk of complications (stricturing, penetrating)	Slower progression in many cases
Response to therapy	Often good response, but long-term therapy and toxicity concerns	Shorter treatment duration; toxicity concerns more manageable
Psychosocial impact	High impact on quality of life, schooling, and emotional development	Significant, but generally with better coping mechanisms
Treatment adherence	More challenging, especially during adolescence	Usually, better self-management and adherence

CD: Crohn’s disease; UC: Ulcerative colitis; IBD: Inflammatory bowel disease.