Society: AGA

Introduction: Patients with upper gastrointestinal (UGI) symptoms of abdominal pain, nausea, vomiting, and bloating often complain within the postprandial period. These symptoms overlap in gastroparesis (GP) and functional dyspepsia (FD), with the only distinction of gastric emptying delay being the main facet in clinical evaluation that separates the two entities. The small bowel postprandial response, an increase in contractile activity following meal intake, is known to be blunted in GP compared to healthy volunteers (HV) as measured by wireless motility capsule (WMC). This neuro-mediated reflex has not been evaluated in those with FD. The primary aim of the study was to assess the small bowel postprandial response in FD compared to GP and HV.
Methods: WMC data of HV and subjects with UGI symptoms suggestive of GP from prior clinical trials were analyzed. A gastric emptying time (GET) cut-off of 5 hours was used to classify symptomatic subjects as GP or FD. All subjects ingested a 250 cc standardized Ensure® meal after a 6-hour fast post-WMC ingestion. Area under the pressure curve (AUC), a measure of both contractile frequency and amplitude, data was extracted from a 20 minutes pre-prandial baseline and three consecutive 20-minute postprandial time periods to allow for granular assessment of contractility during the first 60-minute postprandial period. Comparison of postprandial windows to baseline and comparison of respective windows between subject groups was performed using a paired and unpaired t-tests, respectively. Significance level was defined as p< 0.05.
Key Results: 107 HV, 18 FD and 24 GP subjects were analyzed. All subjects showed a significant postprandial increase in AUC in all periods compared to baseline (p < 0.05). HV showed a robust meal response from meal ingestion to 40 minutes which expectedly decreases from 40 to 60 minutes postprandially (Figure 1). GP had a blunted meal response in all post-prandial time periods compared to HV (Figure 1). FD had a postprandial response pattern distinct from HV and GP, showing some intermediate blunting immediately after the meal but with distinctly increased contractile activity later compared to GP (Figure 1).
Conclusion: FD subjects have small bowel motor component abnormalities during the meal response without delayed gastric emptying. The patterns appear to be intermediate blunting (within the first 20-minutes postprandially) of the small bowel meal response in between a healthy and gastroparetic pattern. These motility abnormalities in the small bowel could be contributing to symptoms in FD or be a consequence of neuro-enteric dysfunction in FD patients.

Figure 1. Comparison of the area under the curve (AUC) of the small bowel pressure profile before and after a standardized meal intake between healthy, functional dyspepsia (FD), and gastroparesis (GP) subjects.

Brian Surjanhata

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