William S. Hughes

Antral Gastrin Concentration in Patients With Vagotomy and Pyloroplasty

Antral gastrin concentration was measured in endoscopic forceps biopsy specimens and prepyloric mucosa in patients with vagotomy and pyloroplasty, duodenal ulcer patients and nonulcer patients. Antral gastrin concentration in vagotomy and pyloroplasty patients, 35.5 +/- 4.1 ng of gastrin per mg of tissue (mean +/- SEM), was significantly greater (P less than 0.01) than antral gastrin concentration in duodenal ulcer patients, 13.0 +/- 2.4 ng per mg, and antral gastrin concentration in controls, 14.8 +/- 3.1 ng per mg. Basal and meal-stimulated serum gastrin levels in vagotomy and pyloroplasty patients were also significantly greater (P less than 0.05) than gastrin levels in either duodenal ulcer patients or controls. Acid secretion rates were not significantly correlated with serum or antral gastrin concentrations in the patients groups.

Hypergastrinemia in Familial Multiple Endocrine Adenomatosis

Abstract Fasting serum gastrin levels of 46 members of 5 families with familial multiple endocrine adenomatosis were measured; 14 patients had hypergastrinemia (a serum gastrin level greater than 2...

The Effect of the Alkaline Tide on Serum-Ionized Calcium Concentration in Man

The effect of the gastric alkaline tide on serum-ionized calcium levels was determined in human subjects. Gastric acid seretion was stimulated by a standard steak meal, human synthetic gastrin, and betazole hydrochloride. Ionized calcium levels fell to a similar extent after each stimulus. The mean decrease in calcium ion concentration in all experiments was 5.4% of the basal concentration. The fall in serum calcium ion concentration was highly correlated with the rise in serum pH. We speculate that increased formation of calcium bicarbonate complex in the serum as well as increased binding of ionized calcium by serum protein accounts for the surprisingly large effect of the alkaline tide on serumionized calcium levels.

Antral gastrin concentration in upper-gastrointestinal disease

Antral gastrin concentration (AGC) was measured in prepyloric mucosa specimens obtained by forceps biopsy during endoscopic examination of 174 clinic and hospital patients. AGC in 32 patients who had normal endoscopic findings, the control group, varied widely from 2 to 38.6 ng gastrin/mg tissue. The mean AGC of the control patients was 14.2±1.4 (mean ±1se) ng gastrin/mg tissue. AGC was similar to control values in 18 patients with duodenal ulcer, 14.7±2.1; 12 patients with a pyloric channel or antral ulcer, 16.4±3.5; and 48 patients with miscellaneous diagnoses, 14.3±1.5 AGC was significantly less than control values in 13 patients with a ulcer in the body or fundus of the stomach, 5.9±1.5, and 4 patients with the Zollinger-Ellison syndrome, 4.9±2.4. AGC was significantly greater than in control values in 16 patients with gastritis, 25.8±4.3; 22 patients with esophagitis, 23.2±3.0; and 9 patients with gastric atrophy and fasting serum hypergastrinemia 44.6±12.3. In a group of 77 of these patients with heterogeneous diagnoses, meal-stimulated 3-hr integrated gastrin output was directly related to AGC (r=0.47,P<0.001). In a group of 106 patients AGC was inversely related to histalogstimulated maximum acid output. The correlation was very weak (r=−0.20) but significant (P<0.05).

Basal and Calcium-Stimulated Gastroesophageal Sphincter Pressure in Patients with Zollinger-Ellison Syndrome

Basal lower esophageal sphincter (LES) pressure was measured in 6 patients with the Zollinger-Ellison syndrome (ZES) and hypergastrinemia, and in 6 patients with duodenal ulcer and normogastrinemia. Basal LES pressure in ZES patients, 17.0 +/- 3.7 (mean +/- SE) mm Hg was similar to basal LES pressure in duodenal ulcer patients, 18.3 +/- 3.5 mm Hg (P greater than 0.10). LES pressure and serum gastrin concentration were not related in the ZES patients, r = 0.03, or in the duodenal ulcer patients, r = 0.20. Intravenous infusion of calcium gluconate in ZES patients produced a marked rise in serum gastrin concentration, delta = 1580 +/- 1110 pg per ml (P less than 0.001), and a moderate but significant rise in LES pressure, delta = 5.9 +/- 0.9 mm Hg (P less than 0.05). In duodenal ulcer patients calcium infusion produced only slight rises in gastrin concentration, delta = 10 +/- 12 pg per ml, and LES pressure, delta = 2.1 +/- 0.5 mm Hg, which were not significant (P greater than 0.10). This study suggests that basal LES pressure is not regulated by blood gastrin levels in the ZES. We interpret the calcium infusion study to show that the LES pressure in patients with ZES may respond to acute changes in endogenous gastrin levels.

The interrelations of gastrin release, antral gastrin concentration and acid secretion rate.

The interrelations of meal stimulated gastrin release, antral gastrin concentration (AGC) and acid secretion rate were examined in a heterogenous group of 72 patients, Gastrin release calculated as the integrated gastrin output was directly related to AGC, r = 0.50 (p less than 0.001) and inversely related to maximum acid output (MAO), r = -0.31 (p less than 0.01). The relation between integrated gastrin output and AGC was significant in 21 patients with low acid secretion rates (MAO: less than 10 mEq/h), r = 0.66 (p less than 0.01) and in 27 patients with normal acid secretion rates (MAO: 10-25 mEq/h), r = 0.56 (p less than 0.05), but not in 24 patients with high acid secretion rates (MAO: greater than 25 mEq/h), r= 0.35 (p greater than 0.05). A weak inverse relation between AGC and MAO may exist in patients with low acid secretion rates, r = -0.40 (p less than 0.10). Considered together using multiple regression procedures AGC and MAO explained less than one-half of the variability in meal stimulated gastrin release.

Antral gastrin concentration in gastric ulcer disease. The finding of high concentrations in a few patients.

Antral gastrin concentration (AGC) was measured in forceps biopsy specimens of prepyloric mucosa obtained at endoscopy in 65 patients with various kinds of gastric ulcer and in 31 nonulcer control patients. AGC in 32 patients with a lesser curvature gastric ulcer, 10.0±2.0 (mean ±1se) ng gastrin/mg tissue was significantly less (P<0.01) than AGC in 31 nonulcer control patients, 14.4±1.4. AGC was similar to the control values in 23 patients with a pyloric channel ulcer, 15.2±1.7; 5 patients with a greater curvature ulcer, 15.0±4.8; and 3 patients with both duodenal and gastric ulcers, 15.8±0.7. AGC was significantly greater (P<0.01) than the control values in 3 patients with a vagotomy and pyloroplasty and a gastric ulcer, 29.8±5.0. In contrast with most lesser curvature gastric ulcer patients who had low AGC, 3 gastric ulcer patients had antral gastrin values which were about three times the mean AGC of the controls. Two of these patients had fasting serum gastrin values which were more than twice the mean control fasting serum gastrin. Meal-stimulated integrated gastrin responses in these 3 patients ranged from three to nine times the mean control response. These findings suggest that a high AGC may account for a few instances of increased serum gastrin concentrations in gastric ulcer patients.

Therapy with gastrin antibody in the Zollinger-Ellison syndrome

The therapeutic effectiveness of parenterally administered rabbit antigastrin antibody was evaluated in a patient with the Zollinger-Ellison syndrome who had a fasting serum gastrin level of 3020 pg/ml and a basal gastric acid secretion of 48.9 mEq/hr. Control globulin reduced gastric secretion to 32 mEq/hr. Gastrin antibody reduced it further to 8.7 mEq/hr. Betazole hydrochloride which was given 75 min after administration of gastrin antibody stimulated acid secretion to 57.2 mEq/hr. One day later basal acid secretion was uninhibited although some antibody activity was present in the patients serum. The results suggested that gastrin antibody acutely inhibited basal but not betazole-stimulated secretion.

Duodenal gastrin concentration in upper gastrointestinal disorders.

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxtapyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9±1.2 ng/mg (mean ±1sem) in control patients. Duodenal gastrin concentration was similar to control values in patients with duodenal ulcer, pyloric channel ulcer, vagotomy and pyloroplasty, and gastric atrophy and hypergastrinemia. In gastric ulcer patients, duodenal gastrin concentration, 2.8±0.6 ng/mg, was significantly less than the control value (P<0.05). Duodenal gastrin concentration was approximately one third of antral gastrin concentration in control, duodenal ulcer, and gastric ulcer patients and was approximately one fifth of antral gastrin concentration in vagotomy and pyloroplasty patients and gastric atrophy patients. Duodenal and antral gastrin concentrations were significantly correlated in normal controls and in gastric ulcer patients. The finding of normal duodenal gastrin concentration in patients with vagotomy and pyloroplasty and patients with gastric atrophy suggests that, unlike antral gastrin concentration, duodenal gastrin concentration is unaffected by a decrease in acid secretion rate. The low duodenal gastrin concentration in gastric ulcer patients indicates that the duodenum may be involved in the pathophysiology of gastric ulcer disease.

Dose Dependance of Insulin-Stimulated Gastrin Release in the Dog

The relations among insulin dose, gastric acid secretion and serum gastrin levels were examined in dogs with chronic gastric fistulae. Intravenous insulin doses of 0.125, 0.25, 0.50, and 1.0 U/kg were studied. Although the fall in glucose measured at 30 min was similar after all doses, gastrin levels rose significantly only after the two highest doses. In spite of the difference in gastrin levels there was no significant difference in peak acid outputs after the four doses.