Introduction
Chronic abdominal pain (CAP) affects 20-50% of patients with Inflammatory Bowel Disease (IBD) despite clinical remission. CAP in the absence of active inflammation suggests altered pain processing and gut-brain axis (GBA) dysregulation. This study explores psychological, physiological and behavioural contributors to inform integrated GBA targeted care.
Aims & Methods
This cross-sectional analysis of 2525 adults with Crohn’s disease (CD) or Ulcerative colitis (UC) recruited from the UK IBD-Bioresource (December 2022-April 2024). 1445 met remission criteria (Harvey-Bradshaw Index <5 for CD, and Simple Clinical Colitis Activity Index ≤2 for UC). CAP was defined using Rome IV criteria as abdominal pain ≥1 day/week for ≥3 months. Pain severity and interference (Brief Pain Inventory) were correlated with psychological (PHQ-15 [somatization], PHQ-9 [depression], GAD-7 [anxiety]), physiological (PROMIS fatigue/PROMIS sleep disturbance), cognitive-behavioural (CBRQ), sensory sensitivity (HSP-SP), personality (BFQ) and resilience (CD-RISC) measures using Spearman’s rank correlation.
Results
Among 1445 patients in remission (mean age: 53±16 years; 48.3% female), 381 (26.4%) met CAP criteria (mean age: 49±14.63 years; 57% female; 61.7% CD;). Pain severity and interference were most strongly associated with somatic symptom burden (rs=0.47 and rs=0.52; p<0.0001). Fatigue, depression and sleep disturbance were also significant, alongside maladaptive behaviours including fear-avoidance and resting in response to pain (table 1). Somatic symptom burden explained 27% of the variance in pain interference. Pain severity showed modest associations with age (rs=0.15, p=0.004) and BMI (rs=0.15, p=0.006). ). Disease duration was not significantly associated with pain outcomes. Patients with CD reported greater pain interference than those with UC (median =0.432, p=0.016).
Pain interference showed stronger corelations than severity across psychological and behavioural domains, including anxiety (rs=0.34), symptom focusing (rs=0.30), neuroticism (rs=0.28), low sensory threshold (rs=0.20), and resilience (rs=–0.24) (all p<0.0001). These interconnected factors reflect shared biopsychosocial mechanisms underlying CAP in IBD during remission.
Table 1. Key Correlates of Chronic Abdominal Pain: Pain severity and Pain interference in IBD Remission
| Domain | Pain severity (rs) (95% CI) | p-value* | Pain interference (rs) (95% CI) | p-value* |
Somatic symptoms (PHQ-15) | 0.47 (0.38-0.55) | <0.0001 | 0.52 (0.44-0.60) | <0.0001 |
| Depression (PHQ-9) | 0.28 (0.18-0.38) | <0.0001 | 0.48 (0.39-0.55) | <0.0001 |
| Anxiety (GAD-7) | 0.12 (0.01-0.22) | 0.0255 | 0.34 (0.24-0.43) | <0.0001 |
| Fatigue (PROMIS) | 0.34 (0.22-0.44) | <0.0001 | 0.49 (0.40-0.57) | <0.0001 |
| Sleep disturbance (PROMIS) | 0.27 (0.14-0.39) | <0.0001 | 0.21 (0.08-0.34) | 0.0014 |
Fear avoidance (CRBQ) Symptom focusing (CRBQ) All-or-nothing behaviour (CRBQ) Resting behaviour (CRBQ) | 0.29 (0.19-0.39) 0.15 (0.05-0.25) 0.19 (0.09-0.29) 0.21 (0.10-0.31) | <0.0001 0.004 0.0003 <0.0001 | 0.30 (0.19-0.39) 0.30 (0.20-0.40) 0.25 (0.15-0.35) 0.28 (0.18-0.38) | <0.0001 <0.0001 <0.0001 <0.0001 |
| Low sensitivity threshold (HSPS-SF) | 0.15 (0.04-0.25) | 0.2566 | 0.20 (0.10-0.30) | 0.0001 |
| Neuroticism (BFQ) | 0.06 (-0.05-0.17) | 0.252 | 0.28 (0.17-0.37) | <0.001 |
| Resilience (CD-RISC) | -0.06 (-0.17-0.05) | 0.2566 | -0.24 (-0.34- -0.14) | <0.0001 |
*p-value significance level <0.01Abbreviations: PHQ-15: Patient Health Questionnaire-15, PHQ-9: Patient Health Questionnaire-9, GAD-7: Generalized Anxiety Disorder Assessment-7, PROMIS: Patient-Reported Outcomes Measurement Information System, PROMIS: Patient-Reported Outcomes Measurement Information System, HSP-SF: Highly Sensitive Person Scale – Short Form, BFQ: Big Five Personality Questionnaire, CD-RISC: Connor-Davidson Resilience Scale.
Conclusion
CAP in IBD during remission involves complex GBA dysregulation encompassing somatic, emotional and behavioural factors. These findings support a biopsychosocial care model and highlight the need for integrated GBA targeted interventions, including cognitive-behavioural therapy and neuromodulation.