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Characterizing Clinical Features and Creating a Gene Expression Profile Associated With Pain Burden in Children With
Victoria Grossi1,2, Jeffrey S Hyams1,2, Nicole C Glidden3
1Division of Digestive Diseases, Hepatology, and Nutrition, Connecticut Children's Medical Center, Hartford, Connecticut, USA.
Insights
Pain in pediatric inflammatory bowel disease (IBD) is not always linked to inflammation. Gene expression of TRPV3, PTGS2, and MAPK14 may contribute to pain burden in children with IBD, offering potential therapeutic targets.
Area of Science:
- Pediatric Gastroenterology
- Molecular Biology
- Pain Research
Background:
- Abdominal pain in pediatric inflammatory bowel disease (IBD) often dissociates from inflammatory activity.
- This suggests non-inflammatory factors contribute to the pain experience in children with IBD.
Purpose of the Study:
- To investigate the relationship between gene expression and pain burden in newly diagnosed pediatric IBD patients.
- To identify potential molecular targets for pain management in IBD.
Main Methods:
- The ALLAY Study enrolled 39 newly diagnosed IBD patients (ages 8-17).
- Rectal biopsies underwent gene expression analysis using a neuropathic and inflammatory pain PCR array.
- Pain burden was assessed using the Pain Burden Interview (PBI) and correlated with gene expression, age, sex, and disease activity.
Main Results:
- Disease activity, but not age or sex, predicted pain burden.
- Gene expression of TRPV3, OPRM1, P2X3, SCN9A, PTGS2, and MAPK14 correlated with PBI scores.
- Differential expression of TRPV3, PTGS2, and MAPK14 was confirmed in patients experiencing pain.
Conclusions:
- Pain burden in pediatric IBD patients is associated with the expression of TRPV3, PTGS2, and MAPK14.
- These genes represent potential therapeutic targets for alleviating pain in IBD.
Background:
There is often dissociation between inflammatory activity and abdominal pain in children with inflammatory bowel disease (IBD), suggesting other factors may play a role in the pain experience.
Methods:
Patients (8 to 17 years) newly diagnosed with IBD were enrolled in the ALLAY Study: Assessing Risk Factors for Abdominal Pain in Children with Inflammatory Bowel Disease (NCT02984059). At diagnostic colonoscopy, 3 rectal biopsies were collected, and gene expression analysis was performed using Qiagen RT2 Profiler Neuropathic and Inflammatory Pain PCR Array. Relative fold difference in gene expression for 84 pain-associated genes was calculated using the 2-ΔΔ Cq method compared with pain-free controls. Factors affecting pain burden (Pain Burden Interview; PBI) were analyzed, including age, sex, rectal inflammation, and gene expression. Data were analyzed using multiple stepwise linear regression and 2-tailed t tests (P ≤ 0.05).
Results:
Thirty-nine newly diagnosed IBD patients were included (65% male, mean age 12.75 years [SD 2.63], 23 Crohn's disease, 16 ulcerative colitis), along with 3 controls. Mean PBI score was 7.73 (SD 6.4, range 0 to 23) for all patients. Age and sex were not predictive of pain burden, but disease activity score was (P = 0.03). Expression of TRPV3, OPRM1, P2X3, SCN9A, PTGS2, and MAPK14 were associated with PBI score. Subsequent 2-tailed t tests comparing patients with no pain (PBI score ≦ 2, N = 11) to those with pain (PBI > 2, N = 28) confirmed differential expression of TRPV3, PTGS2, and MAPK14 was in patients with pain (all P < 0.05).
Conclusion:
Pain burden in newly diagnosed IBD patients may be linked to TRPV3, PTGS2, and MAPK14 expression, suggesting potential therapeutic targets for managing pain in IBD.
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