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Characterizing clinical features and location-specific gene expression profiles associated with pain burden in
Jasmeet S Mokha1, Jeffrey S Hyams1, Nicole C Glidden2
11Connecticut Children's Medical Center, Digestive diseases, Hartford, CT, US.
Insights
Genes linked to pain modulation may be differentially expressed in children with functional dyspepsia (FD). Specific genes in the antrum and duodenum show potential links to pain burden in pediatric FD patients.
Area of Science:
- Gastroenterology
- Genetics
- Pediatric Medicine
Background:
- Functional dyspepsia (FD) is a common condition in children characterized by chronic abdominal pain.
- The underlying mechanisms of pain in pediatric FD are not fully understood.
- Genetic factors influencing pain modulation may play a role in the development of chronic pain in FD.
Purpose of the Study:
- To investigate the differential gene expression in children with functional dyspepsia (FD).
- To identify specific genes associated with pain burden in pediatric FD.
- To explore potential genetic therapeutic targets for managing pain in FD.
Main Methods:
- Children with suspected FD and controls underwent esophagogastroduodenoscopy.
- Rome IV questionnaires assessed diagnostic criteria, pain burden, and symptom severity.
- Gene expression analysis of 84 pain-associated genes was performed on antral and duodenal biopsies.
Main Results:
- No significant differences in eosinophilic counts were found between FD patients and controls.
- Five candidate genes (antral EDN1, PTGES3; duodenal HTR1A, P2Y1, SCN3A) were associated with pain burden (p < 0.01).
- Antral PTGES3 and duodenal SCN3A were identified as high-priority genes linked to pain in FD (p < 0.001).
Conclusions:
- Differential gene expression in pediatric FD, particularly PTGES3 and SCN3A, may contribute to pain.
- These genes are involved in pain conduction, modulation, and neurotransmission.
- Identifying these genes offers potential therapeutic targets for pain management in functional dyspepsia.
Background:
In children with functional dyspepsia (FD), genes involved in pain modulation may be differentially expressed contributing to chronic pain.
Methods:
Children with suspected FD (cases) and known eosinophilic esophagitis (controls) undergoing esophagogastroduodenoscopy completed the Rome IV Diagnostic, Pain Burden and Frequency Severity-Duration questionnaires. Two antral and two duodenal biopsies were collected and relative fold differences in gene expression for 84 pain-associated genes compared to pain-free controls were calculated.
Results:
Sixty-six subjects with FD (postprandial distress syndrome = 34, epigastric pain syndrome = 7, both = 25; 65% female; mean age 13.7 years) and 13 pain-free controls (8% female; mean age 12.7) were studied. There were no significant differences in antral and duodenal eosinophilic counts or distribution between the pain and pain-free groups. Pain severity and burden did not differ significantly between FD subgroups and neither measure significantly correlated with eosinophil counts in the antrum or duodenum. Analysis of 47 antral and 39 duodenal biospecimens revealed 5 candidate genes significantly associated with pain burden: antral EDN1, PTGES3 and duodenal HTR1A, P2Y1, SCN3A (p < 0.01). Subsequent stringent statistical analysis comparing those with significant pain versus no pain revealed antral PTGES3 and duodenal SCN3A were the highest priority candidate genes (p < 0.001).
Conclusions:
Pain burden in pediatric FD may be linked to antral EDN1, PTGES3 and duodenal HTR1A, P2Y1, SCN3A differential expression. These genes are known to be involved in pain conduction, modulation, and neurotransmission, suggesting potential therapeutic targets for managing pain in FD.
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