Gastric somatostatin content and binding in children with hypertrophic pyloric stenosis: a long-term follow-up study.

Because somatostatin (SS) inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric SS concentration may be one of the factors responsible for hypergastrinemia found in patients formerly operated on for hypertrophic pyloric stenosis (HPS). To investigate this issue, the SS-like immunoreactivity (SLI) concentration was estimated in antral and fundic mucosal samples from control and HPS children. In addition, SS binding to cytosol from gastric mucosa (fundus and antrum), fasting serum gastrin levels, and serum gastrin response to a standard breakfast were studied. The mean fundic and antral SLI concentrations were significantly lower in HPS children than in controls. The depletion of fundic and antral SLI content was associated with an increase in the number of gastric SS binding sites. The fasting serum gastrin levels and serum gastrin responses to the standard breakfast (after 60 minutes) of HPS children were significantly higher than those of controls. Since, together with the increase of SS binding to gastric mucosa, there is an increase in the gastrin serum levels, despite the inhibitor effect of SS on gastrin release, the binding capacity cannot be the main factor determining the response to SS in children with HPS. The present results suggest that both SS and gastrin have a role in the pathogenesis of HPS.