Gastric Acid Secretory Response inHelicobacter pylori-Positive Patients with Duodenal Ulcer Disease

BACKGROUND: Patients with duodenal ulcer (DU) have an increased parietal cell mass and sensitivity to secretagogues, with increased acid output.AIM: To determine the effect ofHelicobacter pylorieradication on parietal cell sensitivity and gastric acid secretion.SUBJECTS AND METHODS: Twenty-fiveH pylori-positive DU patients and 18H pylori-negative healthy volunteers were studied. SerumH pyloriimmunoglobulin G, basal acid output and acid secretory response to graded doses of pentagastrin were determined before and after treatment, at six months and at one year. Subjects were randomly assigned to ranitidine or sucralfate treatment for six weeks, and all DU patients received bismuth subsalicylate, metronidazole and tetracycline for the first two weeks.RESULTS:H pyloriwas eradicated in 66% of patients receiving sucralfate and 92% receiving ranitidine. Compared with healthy volunteers, DU patients demonstrated a 2.7-fold greater basal acid output, a 1.3-fold greater peak acid output, significantly higher acid output for each dose of pentagastrin and a 1.38-fold increase in the area under the pentagastrin dose acid response curve. Cure ofH pylori, irrespective of ulcer healing regimen, resulted in a gradual decrease in acid secretory capacity with basal acid output, peak acid output and area under the pentagastrin dose acid response curve returning to healthy volunteer levels by one year. No demonstrable differences were observed in parietal cell sensitivity in all subjects before or after treatment. These data suggest that disturbances in acid secretion inH pylori-positive DU patients are not due to an increased parietal cell sensitivity to pentagastrin but rather due to an increased parietal cell mass with increased capacity to secrete acid, which gradually resolves following cure.

Gastric acid secretion response in the Cebus apella: a monkey model of chronic Chagas disease

The objective was to study the secretory pattern, both basal and stimulated either by histamine (0.1 mg/kg) or pentagastrin (64 ug/kg) in eighteen Cebus apella monkeys chronically infected with different T. cruzi strains (CA1, n=10; Colombian, n=4 and Tulahuen, n=4) and to describe the morphological findings in the gastrointestinal tract in twelve infected (6 sacrificed and 6 spontaneously dead) and four healthy monkeys. All infected monkeys and 35 healthy ones were evaluated by contrast X-ray examination. No differences were observed in basal acid output between control and infected groups. Animals infected with the Tulahuen and Colombian strains showed significant lower values of peak acid output in response to histamine or pentagastrin (p<0.01 and p<0.05 respectively; "t" test) in comparison to the controls. Barium contrast studies showed enlargement and dilatation of the colon in three infected animals. Histopathological lesions were seen in 75% of the autopsied animals either in colon alone (33%) or both, in colon and esophagus (42%). The normal secretion observed in the CA1 infected group could be due to a lower virulence of the strain, a lower esophagic tropism or the necessity of a longer post-infection time to cause lesions.

Measurement of Blood Cortisol and Acid Output in Patients with Duodenal Ulceration and Normal Subjects During Insulin Hypoglycaemia

1. The blood cortisol and gastric acid responses to insulin hypoglycaemia were investigated in 18 healthy control subjects and 14 patients with endoscopically proven duodenal ulceration. 2. In both controls and patients, insulin hypoglycaemia caused blood cortisol and acid output to rise and peak simultaneously, the rises being significantly greater in patients with duodenal ulcer than in control subjects. 3. The peak acid output and the base to peak cortisol increments were also found to be significantly greater in patients with duodenal ulcer than in control subjects (P < 0.001 and P < 0.005 respectively). 4. We conclude that insulin hypoglycaemia causes stimulation of the sympathetic and parasympathetic nervous systems and of the hypothalamo-pituitary-adrenal axis, resulting in the simultaneous elevation of gastric juice acidity and blood cortisol levels. We have shown that synchronous rises in gastric acid and blood cortisol occur during insulin hypoglycaemia and that these rises are greater in patients with duodenal ulcer.

Effect of luminal somatostatin on pentagastrin-stimulated gastric acid secretion in the rat

The perfused rat stomach was used to investigate the effect of intragastrically administered somatostatin (S-14) on basal and pentagastrin-stimulated gastric acid secretion. Intravenous injection of pentagastrin (10 micrograms/kg body wt) induced a peak acid output (PAO) of 6.3 +/- 0.45 mu eq H+. With luminal perfusion of the stomach by S-14 (100 micrograms X kg-1 X min-1), no significant inhibition of gastric acid secretion was observed (PAO: 5.9 +/- 0.6 mu eq H+). The same dose of S-14 administered intravenously significantly inhibited acid secretion (PAO: 1.7 +/- 0.4 mu eq H+) as did intravenous injection of neutralized S-14-containing gastric perfusate obtained by perfusion from a different rat stomach (PAO: 1.9 +/- 0.5 mu eq H+). Intravenous injection of a saline gastric perfusate containing no S-14 did not alter gastric acid secretion (PAO: 6.3 +/- 0.7 mu eq H+). It is concluded that S-14 does inhibit gastric acid secretion when administered systemically but not by intraluminal application.