Duodenal gastrin concentration in upper gastrointestinal disorders.

Duodenal gastrin concentration was measured in endoscopic forceps biopsy specimens of the juxta-pyloric duodenal mucosa in patients with various gastrointestinal disorders. Duodenal gastrin concentration was 5.9 +/- 1.2 ng/mg (mean +/- 1 SEM) 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 less than 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.

The effect of the bicarbonate anion on serum ionized calcium concentration in vitro.

The effect of changes in bicarbonate ion concentration on calcium ion concentration was examined in vitro in serum and protein-free solution. The findings in this study support the formation of a calcium-bicarbonate complex (CaHCO3+) that has a KA of 5.20 in protein-free solution. [Ca++] varied inversely with [HCO3-] in both serum and protein-free solution. This variation was independent of the known variation of [Ca++] with pH. In serum [Ca++] varied 0.0036 mM Ca++ per 1 mM change in [HCO3-] compared with a variation of 0.0060 mM Ca++ per 0.01 unit change in pH. Addition of bicarbonate to serum (Pco2 constant) produced a 50% greater decrease in [Ca++] than that produced by a reduction in Pco2 which gave the same pH change. These findings indicate that abnormal bicarbonate concentrations should be considered when ionized calcium concentrations are estimated from total plasma calcium values in acid-base disorders. In metabolic acid-base disorders, the bicarbonate effect adds to the pH effect on calcium ion concentration. In compensated respiratory acid-base disorders, the bicarbonate effect subtracts from the pH effect on calcium ion concentration.

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 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 +/- 1 SE) 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 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 less than 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 less than 0.05).

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.

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 futher 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 patient's serum. The results suggested that gastrin antibody acutely inhibited basal but not betazole-stimulated secretion.