Abstract

Introduction: Inflammatory Bowel Disease (IBD) involves chronic inflammation of the gastrointestinal (GI) tract characterized by TNF-a release. Gastrointestinal Electrical Stimulator (GES), used to treat upper GI motility symptoms (UGI sx), has been shown to exert an anti-inflammatory effect via TNF-a suppression. We hypothesize that patients with Crohn's Disease (CD) and UGI sx may respond to GES via its immune modulating effect. Methods: We examined 284 patients with gastroparesis (Gp) sx who underwent GES placement. Patients with Gp sx were evaluated by a standardized upper and lower GI PRO (Dig Dis Sci 2016;61(1):176-180). Scores were obtained at baseline (B), after temporary GES placement (T), and post-permanent GES placement (P) > one year (range 12-15 months). The 11 Crohn's disease (CD) patients were analyzed for improvement in their CD activity using the Harvey Bradshaw Index (HBI). For data analysis, a 3 point decrease in the HBI was stated to be a clinical response to GES and an HBI of Analysis of data was done using an unadjusted repeated measures analysis. Results are reported as mean ± SD, and by percent improvement in symptoms. A statistically significant outcome was defined as p≤0.05.2827_A Figure 1. PRO for Gp with Crohn's2827_B Figure 2. PRO for Gp without IBD2827_C Figure 3. Harvey Bradshaw Index seen in CD patients at baseline and after permanent GES placementResults: Our cohort prevalence of CD was found to be 4%, with the following demographics: 2 M & 9 F, mean age 49.8 yrs. Within the CD +Gp subgroup (Table1), statistically significant improvements in symptom scores occurred after both temporary and permanent GES placement for all UGI sx. Overall, effects were notable for long term improvement in all UGI sx with no change seen in lower GI sx, after GES placement. The PRO for UGI sx decreased by 50-75% after temporary GES and 15-50% after permanent GES placement. Within the CD subgroup, when comparing HBI at baseline to HBI after permanent pacemaker placement, 64% patients showed a clinical response by a 3 point reduction in their HBI, and one patient achieved clinical remission with an HBI of <5, as is shown in Table 3. Conclusion: A 4% incidence of CD was seen in our Gp cohort. Gp patients with CD responded well to GES for UGI sx. We also found a strong effect on HBI, suggesting that the neuromodulatory effect of GES seen in Gp can also improve CD sx. The interaction of gastroparesis and CD should be further evaluated as a potential reason for UGI sx in CD patients, while the beneficial effects that electrical stimulation imparted upon CD sx also warrant additional investigation.

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