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Gastric emptying and disease activity in inflammatory bowel disease
Author(s) -
Keller Jutta,
Binnewies Ulrich,
Rösch Marie,
Juul Holst Jens,
Beglinger Christoph,
Andresen Viola,
Layer Peter
Publication year - 2015
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12542
Subject(s) - inflammatory bowel disease , gastric emptying , medicine , disease , gastroenterology , stomach
Background Gastric emptying ( GE ) is delayed in a subset of patients with inflammatory bowel disease ( IBD ). We have shown before that altered release of gastrointestinal hormones may contribute to GE disturbances, but overall effects of disease activity remain unclear. Thus, we aimed to evaluate GE in patients with IBD during active disease and following therapy. Design A total of 20 healthy subjects ( HC ) and 26 patients with IBD hospitalized because of an acute episode of their disease (Crohn's disease ( CD ) n = 13, ulcerative colitis ( UC ) n = 13) underwent a standardized 13 C‐octanoic acid GE breath test (baseline test). Plasma glucose, cholecystokinin ( CCK ), peptide YY ( PYY ) and glucagon‐like peptide‐1 ( GLP ‐1) were measured periodically throughout the test. A total of 16 patients underwent a second GE test after 3–4 months of therapy. Results At baseline, nine patients with IBD had pathologically delayed GE half‐time (T½ > 150 min) ( P = 0·028 vs. HC ). Moreover, T½ was significantly longer in the total group of patients with IBD than in HC (129 ± 12 min vs. 96 ± 7, P = 0·030). Postprandial GLP ‐1 responses were elevated in IBD ( P = 0·002 vs. HC ) and correlated with T½ ( P = 0·05). Following therapy clinical activity indices and T½ were decreased in IBD ( P ≤ 0·01 vs. baseline), and T½ no longer differed from HC ( P > 0·5). Moreover, GLP ‐1 plasma levels decreased significantly ( P = 0·031). Conclusions Higher disease activity in IBD is associated with prolonged GE and increased release of GLP ‐1. Following effective therapy, GE is accelerated and GLP ‐1 release decreases significantly. Thus, increased release of GLP ‐1 from the inflamed mucosa might contribute to GE disturbances in IBD .