Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome - PubMed (original) (raw)
Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome
S Fukudo et al. Gut. 1998 Jun.
Abstract
Background: Corticotropin-releasing hormone (CRH) plays a key role in modulating intestinal motility in stressed animals.
Aims: To evaluate the effect of CRH on intestinal motility in humans and to determine whether patients with irritable bowel syndrome (IBS) have an exaggerated response to CRH.
Subjects: Ten IBS patients diagnosed by Rome criteria and 10 healthy controls.
Methods: CRH (2 micrograms/kg) was intravenously administered during duodenal and colonic manometry and plasma adrenocorticotropic hormone (ACTH) was measured by radioimmunoassay.
Results: CRH induced motility of the descending colon in both groups (p < 0.001) and induced greater motility indexes in IBS patients than in controls (p < 0.05). CRH produced duodenal phase III motor activity in 80% of the subjects and duodenal dysmotility in 40% of IBS patients. Abdominal symptoms evoked by CRH in IBS patients lasted significantly longer than those in controls (p < 0.05). CRH induced significant increases in plasma ACTH levels in both groups (p < 0.001) and produced significantly higher plasma ACTH levels in IBS patients than in controls (p < 0.001).
Conclusion: Human intestinal motility is probably modulated by exogenous CRH. The brain-gut in IBS patients may have an exaggerated response to CRH.
Figures
Figure 1
Manometric recordings of a normal control subject. R, respiration; D1, duodenal bulb/antrum; D2, proximal second portion of the duodenum; D3, distal second portion of the duodenum; DC, descending colon; SC1, proximal sigmoid colon; SC2, mid sigmoid colon; pH, duodenal pH. Note the fine colonic contractions after intravenous CRH. Even though CRH was injected during duodenal phase I immediately after phase III at the end of baseline, administration of CRH evoked duodenal phase III.
Figure 2
Manometric findings of a patient with IBS. Abbreviations as for fig 1_. Administration of CRH stimulated the colon, particularly the descending colon, and evoked duodenal phase III which was followed by phase II contractions. This patient complained of abdominal pain during the period expressed by a solid bar._
Figure 3
Changes in motility indexes of the descending colon induced by CRH. *p<0.05 versus controls by Mann-Whitney U test.
Figure 4
Effects of CRH on plasma ACTH. *p<0.05 versus controls by Scheffe F test and Mann-Whitney U test.
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