Meal-stimulated Serum Gastrin Concentrations Research Articles

Helicobacter pylori infection and fasting plasma glucose concentration

Background—Helicobacter pylori infection raises basal and meal stimulated serum gastrin concentrations and lowers iron stores, which may in turn reduce fasting plasma glucose concentrations in the population. Aim—To determine whether...

Helicobacter pylori infection is associated with low antral somatostatin content in young adults. Implications for the pathogenesis of hypergastrinemia.

Recent studies on the role of Helicobacter pylori in the pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release. We determined meal-stimulated serum gastrin concentrations and antral somatostatin content in 24 asymptomatic volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioimmunoassay in biopsy specimens obtained from the antrum. Fasting and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteers (fasting, 111 +/- 16.3 pmol/l versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 267 +/- 41.2 pmol/l versus 70.1 +/- 2.1 pmol/l; p < 0.01). Antral somatostatin content was 0.764 +/- 0.173 ng/mg and 2.931 +/- 0.414 ng/mg in H. pylori-positive and -negative volunteers, respectively (p < 0.01). Low antral somatostatin content may cause hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this mechanism.

High Doses of Ranitidine in Patients with Reflux Oesophagitis

As in duodenal and gastric ulcer patients, a highly significant correlation between suppression of 24-h intragastric acidity and healing rates in reflux oesophagitis patients was demonstrated by meta-analysis of data obtained from the literature (r = 0.90; p less than 0.001). Furthermore, we have demonstrated in eight patients with reflux oesophagitis that 2-week treatment courses with 300 mg ranitidine twice daily and 300 mg four times daily progressively decreased 24-h intraoesophageal acidity but only moderately elevated basal and meal-stimulated serum gastrin concentrations, significantly below gastrin values obtained after a 2-week treatment course with 20mg omeprazole once daily. Further studies are awaited to demonstrate long-term effects on both healing rates and serum gastrin responses with high doses of histamine H2-receptor antagonists.

Multiple duodenal ulcer: natural history and pathophysiology.

It has not been established whether multiple duodenal ulcer is associated with a different natural history, pathophysiology, and therapeutic response than a single duodenal ulcer. A consecutive series of 96 patients with two or more duodenal ulcers at endoscopy, representing 9.6% of the total number of new patients with duodenal ulcer seen during the period 1980-1985, were compared with a random series of 200 patients with single duodenal ulcer seen in the middle years of this period. Multiple duodenal ulcer was associated with higher (p less than 0.02) male to female ratio, more (p less than 0.05) late onset patients (those with ulcer symptoms starting after age 30 years, more (p less than 0.05) chronic cigarette smokers, and more frequent (p less than 0.05) moderate to severe deformity of the duodenal bulb. More (p less than 0.05) patients with multiple duodenal ulcer had abnormally low D50 derived from pentagastrin dose response tests, indicating that they were more sensitive to gastrin stimulation. Furthermore, their mean fasting and meal stimulated serum gastrin concentrations were significantly higher than those of patients with single ulcer (p less than 0.005), or of controls (p less than 0.05). Compared with single duodenal ulcer, multiple ulcer had significantly lower placebo healing rate, and required a higher dose of misoprostol (1200 v 800 micrograms/day) to achieve a similar healing efficacy at four weeks. We conclude that multiple duodenal ulcer is associated with different clinical features, pathophysiology, and possibly therapeutic response from single duodenal ulcer, and appears to represent the more aggressive side of the ulcer spectrum.

Influence of RP 40749 on basal and meal-stimulated serum-gastrin, serum-pepsinogen I, and gastrin-content of the antral mucosa in duodenal ulcer patients.

Eighteen patients with active duodenal ulcer were treated with a novel antisecretory drug, RP 40749, either 100 mg or 150 mg as a daily nocturnal dose for 28 days. In these patients we evaluated the clinical course, endoscopic healing rates after 28 days, routine laboratory parameters, basal serum gastrin and pepsinogen I levels, meal-stimulated serum gastrin concentration, and the gastrin content of the antral mucosa. All nine patients receiving 150 mg RP 40749 and eight of nine patients receiving 100 mg RP 40749 healed their ulcers completely within 28 days, becoming rapidly symptom-free after an average of three days. The basal (53.8 +/- 5.2 vs 99.8 +/- 11.4 pg/ml) and meal-stimulated serum gastrin levels (109.2 +/- 12.1 vs 189.2 +/- 16.7 pg/ml) rose significantly after treatment with RP 40749, as did the gastrin content of the antral mucosa (11.3 +/- 2.1 vs 26.0 +/- 5.1 micrograms/g), suggesting increased synthesis and secretion of gastrin. Between the 100 mg and 150 mg groups, no significant differences in response were observed. Serum pepsinogen I levels (64.9 +/- 7.3 vs 147.9 +/- 17.9 ng/ml) increased after treatment; the increase after 150 mg RP 40749 was significantly greater than that after 100 mg RP 40749. The increase of serum pepsinogen levels are probably due to a spillover effect resulting from a blockade in exocrine secretion into the lumen. There were no relevant changes in routine laboratory parameters.

Effect of oral nalmefene, an opiate-receptor antagonist, on meal-stimulated gastric acid secretion and serum gastrin concentration in man

We evaluated whether nalmefene, an orally administered opiate-receptor antagonist, would inhibit gastric acid secretion in response to a meal in healthy humans. On separate days either 50 mg nalmefene or a placebo tablet was administered by mouth 90 min before a blenderized steak meal was infused into the stomach through a nasogastric tube. Compared to placebo, nalmefene inhibited meal-stimulated acid secretion in each of 6 subjects studied ( P < 0.05). During the second and third hours after the meal, nalmefene inhibited mean acid secretion by 16%. Nalmefene also resulted in significantly higher meal-stimulated serum gastrin concentrations than placebo ( P < 0.05) even though intragastric pH was kept constant at 5.0 in both experiments. These studies indicate that an orally administered opiate-receptor antagonist can inhibit gastric acid secretion in response to a meal in humans, yet increase meal-stimulated serum gastrin concentrations.

The Type of Anastomosis after Selective Gastric Vagotomy and Precise Antrectomy Is of No Importance for Basal and Postprandial Serum Gastrin Concentration

Twenty-six patients were treated for duodenal or recurrent ulcer with selective gastric vagotomy plus precise antrectomy--that is, complete removal of the entire antrum. Sixteen had a gastroduodenal anastomosis and 10 a gastrojejunal anastomosis. Fasting and protein meal-stimulated serum gastrin concentration was measured in 10 patients before antrectomy and in all after the operation. Fasting serum gastrin concentration was reduced and food-stimulated gastrin response abolished irrespective of the type of the anastomosis. It is concluded that a postprandial gastrin rise means retained antral tissue in the gastric remnant and that neither protein nor mechanical stimulation of the passage of food through the duodenum stimulates the duodenal G-cells to gastrin release.

Gastric Acid Hypersecretion in Cystic Fibrosis

SummaryIncreased basal and/or pentagastrin‐stimulated gastric acid secretion was observed in 31 of 40 cystic fibrosis (CF) patients as compared to 13 age‐matched control volunteers. Fasting serum gastrin level for 20 CF patients of 67.7 ± 11.1 pg/ml (ranging from 10 to 145 pg/ml) was normal. Mealstimulated serum gastrin concentrations were not significantly higher for seven CF patients as compared to nine normal subjects. In a rat bioassay, serum extracts from six CF patients produced gastric acid secretion comparable to 250 ng/ml of pentagastrin; significantly (p &lt; 0.01) greater than the responses produced by serum extracts from six normal subjects. There was no significant correlation of severity of pulmonary disease or steatorrhea with acid secretory results. Fourteen of 16 CF patients biopsied had evidence of proximal small intestinal injury which correlated with basal acid output elevation. Gastric acid hypersecretion in CF patients is due to nongastrin secretagogues and is a cause of proximal small intestinal injury.

Effect of one-month treatment with cimetidine on gastric secretion and serum gastrin and pepsinogen levels

The inhibitory effects of cimetidine on gastric acid and pepsin secretion were studied before and after 1 month of treatment with 300 mg of cimetidine four times a day in 15 male duodenal ulcer patients. Cimetidine inhibited both pentagastrin- and peptone meal-stimulated acid secretion significantly better before, than after, 1 month of treatment. Similarly cimetidine inhibited pentagastrin-stimulated pepsin secretion significantly better before treatment. Meal-stimulated serum gastrin concentrations were significantly higher after treatment. The mechanism(s) of these effects was not apparent.