Circulating gastrointestinal hormone abnormalities in patients with severe idiopathic constipation.

OBJECTIVE

This study aimed to determine if there is an abnormality of circulating gastrointestinal hormones in patients with severe idiopathic constipation.

METHODS

Twelve patients, all female (median age 34 yr) and 12 healthy controls (eight female, median age 32 yr) were studied. A radioisotope-labeled solid/liquid meal was ingested, and the serum hormone response, as well as the relationship between serum hormones and rates of gastric emptying and small intestinal transit, were studied for 180 min postprandially.

RESULTS

Somatostatin levels were higher in patients with constipation (basal level, controls vs patients, 31 vs 57 pmol/L, p < 0.05, median values; peak level, 48 vs 60, p < 0.05). Patients showed a significantly lower somatostatin integrated incremental meal response (2182 vs 104, p < 0.05). No correlation was found between the somatostatin levels and rates of upper gastrointestinal transit in patients. Pancreatic glucagon was significantly decreased (p=0.04). Enteroglucagon levels were significantly lower (p > 0.05) in patients between 30 and 60 min after the meal. The peak found after the meal in normal subjects was absent. Basal levels of pancreatic glucagon correlated with small bowel transit by two different measures: head of meal (r=0.69, p=0.03) and cecal filling at the time of 50% gastric emptying (r=0.84, p=0.002). No significant differences between the two groups could be found for basal and peak levels at different times and integrated incremental response to the meal for insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK), gastrin, pancreatic polypeptide (PP), motilin, neurotensin, and peptide tyrosine tyrosine (PYY).

CONCLUSION

Patients with severe idiopathic constipation have specific abnormalities of circulating gut hormones that most likely play a role in gastrointestinal motility and that may be of pathophysiological significance.