Gastric emptying and disease activity in inflammatory bowel disease

Jutta Keller, Ulrich Binnewies, Marie Rösch, Jens Juul Holst, Christoph Beglinger, Viola Andresen, Peter Layer

    24 Citationer (Scopus)

    Abstract

    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 13C-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 (T1/2 > 150 min) (P = 0·028 vs. HC). Moreover, T1/2 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 T1/2 (P = 0·05). Following therapy clinical activity indices and T1/2 were decreased in IBD (P ≤ 0·01 vs. baseline), and T1/2 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.

    OriginalsprogEngelsk
    TidsskriftEuropean Journal of Clinical Investigation
    Vol/bind45
    Udgave nummer12
    Sider (fra-til)1234-42
    Antal sider9
    ISSN0014-2972
    DOI
    StatusUdgivet - 1 dec. 2015

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