Gastric acid and
pepsin secretion and serum
gastrin concentrations were measured in nine patients with uncomplicated
duodenal ulcer (DU) and 10 normal controls in the fasting state and in response to graded doses of
bombesin, a tetradecapeptide
gastrin releaser, and, for reference, synthetic
gastrin G-17. Serum
gastrin with
bombesin stimulation was significantly greater in
duodenal ulcer (maximum 467 pg/ml) than in controls (153 pg/ml), while in seven of the DU group tested
gastrin levels after a meal were not different from that seen in five of the normal controls. Gastric acid concentrations and outputs were greater in
duodenal ulcer with both stimuli. Secretory responses were then related to serum
gastrin levels; despite increasing
gastrin levels with
bombesin stimulation, peak outputs achieved with
bombesin were only 50% of G-17 maximum in normals and up to 90% of maximum in
duodenal ulcer. Up to the point of peak response to
bombesin,
acid and
pepsin outputs were the same with exogenous and endogenous
gastrin, ie,
bombesin acted only via G-17. Furthermore, in direct comparison of
duodenal ulcer and normals with G-17 infusion,
acid and
pepsin outputs related to serum
gastrin were congruent up to 75% of
duodenal ulcer maximum, at which point normals reached their maximum level. These data have shown that
duodenal ulcer patients are not more sensitive to either exogenous or endogenous
gastrin; we have also shown regulatory defects in
duodenal ulcer patients not previously described: an exaggerated release of
gastrin with
bombesin stimulation, and a defective inhibition of
acid and
pepsin secretion with higher doses of
bombesin.