Mean Serum Gastrin Concentration Research Articles

Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

Elevated gastrin concentration leading to gastritis is explained as the effect of change in the density of D and G cells. The aim of the study was to determine and compare fasting serum gastrin concentrations, G and D cell densities in gastric antrum mucosa in children with chronic gastritis and in children with no gastritis or Helicobacter pylori infection. A total of 184 patients aged 6-18 years, with chronic abdominal pain underwent endoscopic examination. We created three groups: I--patients with chronic gastritis and H. pylori infection; II--patients with chronic gastritis but no H. pylori infection; III--patients with neither gastric mucosal abnormalities nor H. pylori infection. G and D cell densities were determined in the biopsy specimens (using Rbalpha H Gastrin & Somatostatin antibodies). Fasting serum gastrin concentrations were measured using a Beckmann gamma-counter and a GASK-PR kit. The mean serum gastrin concentration in group I was higher when compared with group II (p = 0.04) and group III (p = 0.019). No statistically significant differences were found between groups II and III (p = 0.91). There were no statistically significant differences in G and D cell densities between groups. The mean G/D cell ratios in groups I and III were almost identical. The mean fasting serum gastrin concentration was higher in children with both chronic gastritis and H. pylori infection compared with patients without infection or without antral inflammation. No difference in the G cell density or D cell density in children was found, regardless of the presence or absence of gastritis or H. pylori infection.

Effect of propranolol on secretin-induced gastrin release and secretin-induced tachycardia in patients with the Zollinger-Ellison syndrome

The mechanism for secretin-induced gastrin release in the Zollinger-Ellison syndrome is uncertain. We evaluated whether the stimulatory effect of intravenous secretin on gastrin release was partly mediated through a beta-adrenergic stimulatory mechanism. Serum gastrin concentrations and heart rate were monitored in six patients with the Zollinger-Ellison syndrome. Secretin (2 clinical units/kg) increased mean serum gastrin concentrations from 1558 pg/ml basally to a peak of 3683 pg/ml (136% above baseline). This increase was not altered by pretreatment with 2 mg of propranolol intravenously, a dose which in previous studies blocked terbutaline-induced gastrin release. Secretin increased heart rate by 14 beats/min (20% above base-line) and this also was not altered by propranolol pretreatment. Thus, the stimulatory effects of secretin on gastrinoma cells and the heart do not appear to be mediated by beta-adrenergic receptors.

Effects of Preoperative Anxiety on Gastric Fluid Acidity and Volume

The aim of this study was to evaluate the effect of preoperative anxiety on the gastric pH and volume. We studied 96 female patients aged 16-60 yr who underwent elective gynecological surgery. We classified the subjects into 2 groups, those presenting preoperative anxiety scores using visual analogue scale (VAS, 0-10) less than 5 (L-group, n=59), and those with 5 and more (H-group, n=37). Immediately after tracheal intubation, gastric contents were aspirated using a 14-F multiorifice nasogastric tube. The gastric acidity and volume of the two groups were not statistically different. Mean pH were 3.0±1.8 and 3.0±2.0 in each group (L-group and H-group) and mean gastric volume (mL) were 15.3±11.7 and 11.8±11.8, respectively. Nine (15.3%) patients in the L-group were considered to be 'at risk i.e. gastric pH <2.5 and volume >25 mL' and one patient (2.7%) in the H-group (p<0.05). The mean serum gastrin concentrations in both groups were similar (21.6±9.8 vs. 20.2±11.0 pg/mL). The pH and volume of preoperative gastric contents were not correlated with the preoperative anxiety. The results suggest that a low level of preoperative anxiety can be considered a risk factor for aspiration pneumonitis.

Impact of Helicobacter pylori infection on serum gastrin in haemodialysis patients

Helicobacter pylori infection is associated with increased gastrin release in patients with normal renal function. Hypergastrinaemia is a common finding in haemodialysis patients and, in many cases, may be linked to H. pylori infection. The aim of this study was to examine the effect of H. pylori infection, and its eradication, on elevated gastrin levels in haemodialysis patients. Eighty-nine dyspeptic patients were included in the study. While 44 patients had normal renal function, the remaining 45 were end-stage renal failure patients. Patients were assigned to one of four groups according to their H. pylori and renal function status. Infected patients were re-evaluated after 2 months following eradication treatment. Serum gastrin levels were measured in these groups both before and after eradication treatment. Haemodialysis patients with H. pylori infection had higher serum gastrin levels than did H. pylori negative haemodialysis patients (321+/-131 pg/ml vs 154+/-25 pg/ml) (P<0.05). Mean serum gastrin concentration was 152+/-21 pg/ml in the non-uraemic H. pylori-positive group. This value was 58+/-17 pg/ml in the non-uraemic H. pylori-negative group (P<0.05). There were significant decreases in serum gastrin levels from pre- to post-eradication of H. pylori in the infected haemodialysis and non-uraemic patient groups (312+/-131 pg/ml to 179+/-85 pg/ml and 152+/-21 pg/ml to 72+/-2.4 pg/ml respectively, P<0.05). Four patients in group Ib and 5 patients in group IIb who had persistent infection did not have a decrease in serum gastrin level. All patients with successful eradication had a decrease in serum gastrin concentration. Our findings suggest that H. pylori infection contributes to hypergastrinaemia in haemodialysis patients. More research is needed regarding the clinical consequences of hypergastrinaemia in these individuals.

Effect of the somatostatin analog octreotide on gastric mucosal function and histology during 3 months of preoperative treatment in patients with acromegaly.

To study the effects of the somatostatin analog octreotide on gastric mucosal function and histology during short-term (3 months) preoperative treatment in patients with acromegaly. Open design clinical study. 10 patients were studied before treatment with octreotide (pre-tx), on day 1 of 300 microg octreotide/day (d300), after 1 week on 300 (w300), 600 (w600) or 1500 (wl500) microg octreotide/day, and after an additional 2.5 months on 1500 microg octreotide/day (M3). An 8h gastrin profile was obtained and ambulatory intragastric 23h pH-metry carried out at the indicated time points. Gastroscopy was performed at pre-tx and M3 and multiple mucosal biopsy specimens taken. The mean serum gastrin concentration at first declined during octreotide therapy to a nadir at w1500, then recovered despite ongoing therapy (probably in response to reduced gastric acidity) and was similar to pre-tx values at M3 (mean+/-S.E.: 87+/-26, 50+/-11 and 98+/-46ng/l for pre-tx, w1500 and M3 respectively; P<0.05, pre-tx vs w1500). Gastric acidity had also declined at d300(P<0.05, d300 vs pre-tx), then recovered (despite the increase in the octreotide dose), but declined again at M3 (mean pH (95% confidence interval): 2.4 (1.7-3.2), 3.3 (2.4-4.3), 2.6 (1.8-:3.5, n=8) and 2.9 (1.6-4.2, n=7) at pre-tx, d300, w1500 and M3 respectively). The gastrin concentration at M3, although similar to pre-tx values, remained inadequately low for the reduced gastric acidity. The reduction in gastric acidity was marked during the daytime (0900-2200 h; P<0.01, d300 vs pre-tx and P=0.028, M3 vs pre-tx). However, while the stimulated postprandial gastric acid secretion was reduced at d300 (P<0.01, d300 vs pre-tx) and at M3 (n=7; P=0.027, M3 vs pre-tx), fasting and preprandial acidity was not affected. During the night, gastric acidity was reduced from 2200 to 0300 h, but the reduction was less marked than during the daytime. Paradoxically, the physiological intermittent late nocturnal reduction in acidity ('pH peaks' (0300-0800 h)) was abolished rather than enhanced. No patient acquired new Helicobacter pylori infection. The mean gastritis scores for antrum and body (n=8, Sidney classification) increased marginally from 1.7 to 1.9 (chronicity) and from 0.7 to 0.9 (atrophy), while the activity score was slightly reduced from 1.2 to 1.0. Three months of preoperative octreotide treatment profoundly and persistently altered gastric mucosal function (gastrin suppression, reduced acidity), but caused only minor variations in the pre-existing gastritis scores.

Gastric gland degeneration induced in monkeys by the CCK-B/gastrin receptor antagonist CI-988.

Gastric effects of subchronic treatment with the cholecystokinin-B (CCK-B)/gastrin receptor antagonist CI-988 were investigated in cynomolgus monkeys. In preliminary range-finding studies, CI-988 was given orally to 1 monkey per sex for 14 days at doses of 50, 100, 200, and 500 mg/kg/day. Subchronic studies of CI-988 were subsequently conducted using 5 monkeys per sex at doses of 0, 5, 25, and 75 mg/kg for 4 or 13 wk. High-dose monkeys were dosed initially at 100 mg/kg, but the dose was not well tolerated and was decreased to 75 mg/kg after 8 days of treatment. One male monkey at 75 mg/kg was euthanatized in extremis on day 23. In the range-finding study, minimal to moderate, multifocal to diffuse degeneration of gastric glands, primarily in the fundic region, was observed at 100 mg/kg and above, with frank gastric mucosal atrophy occurring at 200 and 500 mg/kg. Minimal to mild gastric gland degeneration was also observed in the subchronic study after 4 wk at 25 and 75 mg/kg, but histopathologic gastric changes were remarkably absent after 13 wk. Mucosal height in the stomach fundus was decreased 19.8% in 75-mg/kg males at week 4, and although gastric mucosa appeared histologically normal after 13 wk, mucosal height remained 28.6% less than that of controls. In females at 75 mg/kg, fundic mucosal height was decreased 7% and 5% at weeks 4 and 13, respectively, but decreases were not statistically significant. Mean serum gastrin concentrations were increased 10-fold in males only after 4 wk at 75 mg/kg, but were comparable to controls during week 13. CI-988-induced gastric gland degeneration is consistent with antagonism of gastrin's trophic activity toward gastric mucosa. Notwithstanding decrements in gastric mucosal height, disappearance of mild histopathologic findings despite continued treatment with the ligand suggests some degree of adaptation to subchronic CCK-B/gastrin inhibition, although the mechanism of accommodation has yet to be delineated.

Serum gastrin and blood glucose levels during halothanenitrous oxide anaesthesia and strabismus surgery in children

The purpose of this study was to determine whether serum gastrin levels are increased by reflexogenic stimuli applied to the extrinsic muscles of the eye. Serum gastrin and blood glucose concentrations were measured in ten normal children aged between 5 and 12 yr during general anaesthesia with halothane and nitrous oxide and during strabismus surgery. Fasting basal concentrations of gastrin (33.6 +/- 14.8 pg.ml-1) and of glucose (4.43 +/- 0.72 mmol.L-1) were in the normal range of values for children. Intravenous atropine (0.01 mg.kg-1), general anaesthesia with halothane in nitrous oxide and oxygen by mask for three minutes, tracheal intubation, extraocular muscle stimulation and surgical stress did not cause any variation in the mean serum gastrin concentration. On the contrary, tracheal intubation and surgical stress increased blood glucose concentrations (P less than 0.05). There was no difference in the serum gastrin levels after extraocular muscle stimulation between children with positive or negative oculocardiac reflexes (44.5 +/- 16.7 pg.ml-1 vs 38 +/- 14.7 pg.ml-1, respectively). The incidence of vomiting predischarge was 60 per cent. Serum gastrin levels did not differ between children who vomited and children who did not (44.3 +/- 18.5 pg.ml-1 vs 47.1 +/- 16.9 pg.ml-1, respectively). Vomiting after strabismus surgery cannot be attributed to high gastrin serum levels. Consequently, it is unlikely that vomiting after strabismus surgery is linked to an "oculogastric reflex" with the vagus nerve as the efferent pathway.

Variable Contribution of Gastrin to Gastric Acid Secretion After a Meal in Humans

The purpose of these experiments was to determine the contribution of gastrin to the acid secretory response to eating in healthy human subjects. To simulate the gastric and intestinal phases of eating, a meal was homogenized and then infused into the stomach through a nasogastric tube. At the same time, the cephalic phase of acid secretion was activated by sham feeding. With this simulated meal, mean serum gastrin concentration increased from a basal value of 43 +/- 9 pg/ml to an average postprandial gastrin concentration over 2 h of 121 +/- 25 pg/ml. Gastrin release after this simulated meal was similar to gastrin release after a normally eaten meal in the same 12 subjects. Gastric acid secretion in response to the simulated meal, which was measured by in vivo intragastric titration, averaged 24.2 +/- 2.4 mmol/h. To determine how much of this postprandial acid secretion could be attributed to gastrin, gastrin 17 I was infused intravenously in the same subjects on a separate day and acid secretion and serum gastrin concentrations were measured. By relating serum gastrin concentration during gastrin 17 infusion to concomitant acid secretion, we determined that an average postprandial serum gastrin concentration of 121 pg/ml could result in an acid secretion rate of 21.5 mmol/h, 89% of the actual acid secreted after the simulated meal in these subjects. However, in individual subjects, the amount of gastrin released after a meal could produce as little as 51% or as much as 162% of actual postprandial acid secretion. Thus, in individual human subjects the contribution of gastrin to acid secretion after a meal is variable.

Effect of Gastric Alkalinization on Serum Gastrin Concentrations in Humans

Previous studies have shown that alkalinizing the stomach with sodium bicarbonate for periods up to 3 h does not cause an increase in serum gastrin concentration. We evaluated the effect of a 5-h period of continuous intragastric alkalinization on serum gastrin concentration in 12 healthy humans and 12 asymptomatic duodenal ulcer patients. On the first day, intragastric pH was maintained between 6.0 and 7.0 for 5 h by infusing 0.3 N sodium bicarbonate into the stomach. On the second day, an identical amount of sodium bicarbonate was infused intravenously while intragastric pH was permitted to remain at its natural level for 5 h. Serum gastrin concentration was also measured in each subject and patient after infusion of a homogenized steak meal. In both healthy subjects and duodenal ulcer patients, mean serum gastrin concentrations were significantly (p less than 0.05) higher after 5 h of intragastric bicarbonate infusion than after 5 h of intravenous bicarbonate infusion during which intragastric pH remained at its natural level. Increases in serum gastrin concentration with alkalinization averaged 23% and 30% of the increases in serum gastrin after a homogenized steak meal in the same subjects and patients, respectively. We conclude that continuous gastric alkalinization for 5 h increases serum gastrin concentrations in humans.

The effect of vasoactive intestinal polypeptide on meal-stimulated gastric acid secretion in man.

The effect of vasoactive intestinal polypeptide (VIP) on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Acid secretion was stimulated by instillation of a 10% solution of peptone, which was adjusted to pH 5.5, circulated through the stomach via a double-lumen gastric tube by a peristaltic pump. The acid secretion was estimated by continuous titration by a pH-stat. The subjects were studied twice on separate days, receiving an intravenous infusion of either VIP (1 microgram/kg/h) or saline. No effect on acid secretion was found. Mean serum gastrin concentration rose from 42 pmol/l to 150 pmol/l during meal stimulation and was unaffected by infusion of VIP. Plasma VIP concentration during infusion of saline was 6.8 pmol/l and during VIP infusion, 82.8 pmol/l. Plasma VIP concentration was unaffected by the peptone meal.

Serum gastrin I concentrations of mother and newborn immediately after birth.

Serum gastrin I (GLU-GLY-PRO-TRYP-LEU(GLU)6-ALA-[formula, see text]-GLY-TRY-MET-ASP-PHE-CO-NH2) concentrations were investigated by radioimmunoassay in 50 mothers and their newborn infants immediately after birth. The mean serum gastrin concentration in maternal blood was 52.80 +/- 13.37 (SD) pg/ml, and in cord blood 84.12 +/- 42.90 (SD) pg/ml. Both values were significantly higher than serum gastrin levels found in normal, healthy, nonpregnant women (Mean +/- SD = 32.34 +/- 18.35 pg/ml). There were no statistically significant differences in the cord serum gastrin concentrations with respect to sex, weight and length of the infant and age and parity of the mother.

Neonatal gastric motility in dogs: maturation and response to pentagastrin.

Postnatal changes in the pH of gastric secretions, gastric motility, serum gastrin concentration, and response of the stomach to pentagastrin administration were studied in 15 beagle puppies from birth to 5 wk of age. Motility was monitored manometrically via twin-lumen catheters 3--6 h postprandially. Mean gastric pH was stable at 5.85 until the 7th postnatal day when pH decreased to 3.45; pH then increased to a mean value of 4.95 through the 18th day. Antral contractions increased from 0.2 contractions per min on the day of birth to a maximum 2.3 contractions per min on the 11th day and then gradually declined. Pentagastrin (8.0 microgram/kg sc) had no effect on gastric pH or motility until the 2nd postnatal wk. Pentagastrin inhibited the rate and peak pressure of antral contractions from the 2nd through the 5th wk. Mean serum gastrin concentrations in six puppies were greater than values for adult dogs, attaining a preweaning maximum on the 9th day.

Increased plasma noradrenaline and serum gastrin in patients with duodenal ulcer

Serum gastrin, serum insulin, plasma noradrenaline, plasma adrenaline, pulse rate and blood pressure were measured repeatedly during 24h in six patients with duodenal ulcer and in six control subjects. Mean serum gastrin concentration was 3-4 times higher in duodenal ulcer patients than in controls during both the day and at night. Serum insulin was the same in both groups of subjects. Overnight fasting and mean supine plasma noradrenaline as well as mean supine pulse rate were significantly higher in duodenal ulcer patients than in controls. Plasma adrenaline and arterial blood pressure were the same in patients and controls. These results suggest that sympathetic nervous activity is increased in patients with duodenal ulcer. The increased sympathetic nervous activity may mean that duodenal ulcer patients are subject to more stress than normal subjects or may be compensatory to increased vagal nervous activity presumed by some authors to be present in such patients.

The effect of metramide on the prolonged serum gastrin response to feeding observed in patients with duodenal ulcer.

The response of serum gastrin to a meal has been studied in 11 normal subjects and 16 patients with duodenal ulceration. The mean serum gastrin concentration rises after a meal to similar peak values in both normal subjects and duodenal ulcer patients, and fall to basal values with 3 hours in normal subjects. In duodenal ulcer patients the peak concentration is sustained throughout the 3 hour test period, and this response is not affected by the administration of Metiamide. It is concluded that the control of gastrin release is defective in duodenal ulceration, and this may be due to a failure of the antral pH feedback mechanism. Gastrin may be a primary pathogenetic factor in duodenal ulceration.

Differences in rates of gastrin release in normal persons and patients with duodenal-ulcer disease.

To compare gastrin release in response to a physiologic stimulus in normal persons and in patients with duodenal-ulcer disease, serum gastrin levels were measured in 22 patients with duodenal ulcer and 10 control subjects before ingestion of a protein-rich meal (180 g of beef) and five 15-minute intervals thereafter. The mean fasting serum gastrin concentration for the 22 patients with duodenal ulcer (76 ± 7.0 S.E.M. pg per milliliter) did not differ from that of the control subjects (71 ± 9.4 pg per milliliter). However, mean serum gastrin concentrations in the patients with duodenal ulcer were significantly greater than those of the control subjects 45, 60, and 75 minutes after feeding. The integrated gastrin response to feeding in these patients (99 ± 25 per cent) substantially and significantly (p less than 0.01) exceeded that of the control population (44 ± 10 per cent). Thus, increased gastrin release occurs in response to feeding in such patients as compared with normal persons, and, in spite of the absence of fasting hypergastrinemia, indicates the potential importance of gastrin in the hypersecretory state that frequently characterizes duodenal-ulcer disease.

Relations between serum gastrin levels and rates of gastric hydrochloric acid secretion.

Fasting venous serum gastrin concentrations and both unstimulated and maximum-stimulated gastric hydrochloric acid secretory rates were determined in 168 subjects. The patients included 55 with duodenal peptic-ulcer disease, nine with gastric ulcers and 69 with assorted gastrointestinal abnormalities, and 35 control subjects without recognized gastrointestinal diseases. Fasting serum gastrin concentrations were measured by radioimmunoassay and compared for groups of patients with differing rates of basal and stimulated gastric acid secretion. There was, in general, an inverse relation between fasting serum gastrin concentrations and rates of gastric hydrochloric acid secretion. Fasting serum gastrin concentrations in patients with duodenal-ulcer disease were not found to be significantly greater than those of the control subjects. However, mean serum gastrin concentrations in the patients with gastric-ulcer disease were found to be significantly greater than those of both the control subjects and the patients with duodenal-ulcer disease.