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Case-control study assesses food-triggered epigastric pain in adults, suggesting new syndrome characteristics.
Postprandial epigastric pain syndrome was recently suggested as a disorder of gut-brain interaction. We assessed gastroduodenal motility and histology in patients with acute epigastric pain triggered by specific foods. In this case-control, exploratory study, patients with epigastric pain and matched controls underwent upper endoscopy to exclude organic disease and gastroduodenal biopsies for histology. All participants underwent a dynamic gastroduodenal MRI, with a baseline acquisition followed by a food-trigger intake and three MRI acquisitions at 15-minute intervals. We studied seven pairs of participants (57% women, 33.3 ± 10.7 years old), all with unrevealing endoscopy. During the MRI, epigastric pain patients had pain crises that scored 6.6 ± 2.4 of a maximum of 10 points, triggered by caipirinha, red wine, banana, and coffee. No control subject had a pain crisis. Epigastric pain patients and controls did not differ in gastric motor parameters (P > 0.05), including accommodation, wall motion, and gastric emptying. Epigastric pain patients showed a negative correlation between pain score and wall motion time to peak (r = -0.81, P = 0.027). The duodenal mast cell count was higher in epigastric pain patients than in controls [median 140 (interquartile 25–75%: 117–153) vs. 86 (76–117); P = 0.020]. In patients presenting with acute epigastric pain following specific food intake, pain intensity might correlate with gastric wall motion parameters and duodenal mast cell infiltration. After confirmatory studies, such a postprandial epigastric pain syndrome might be recognized as a painful gastric glitch.
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Ambrós et al. (2026) studied this question.
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