Mean Serum Gastrin Levels Research Articles

Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels.

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.

Effects of Prolonged Metiamide Medication on the Fundic Mucosa: A secretory and histomorphometric study in the rat

Two groups of 10 rats each were treated with metiamide (200 mg per kg, subcutaneously) or with saline (0.15 m , 2 ml per kg, subcutaneously) at 8-hr intervals over 18 days. Eight hours after cessation of the treatment, basal secretion was not significantly altered, except for increased H+ concentration in the metiamide group. Pentagastrin stimulation led to a significant rise in gastric juice volume ( + 18%), H+ concentration (+ 50%), and acid output (+ 27%). In saline-treated controls no changes were observed. Histomorphometric analysis of the fundic mucosa revealed a significant increase in total number (+ 15%), total volume (+ 29%), and volume density (+ 11%) of parietal cells. These changes were attributable to increased volume of the individual parietal cell ( + 13%) and to increased fundic mucosal volume (+ 18%). Stimulated acid output correlated closely with both the total number and total volume of parietal cells. In an additional group of 10 rats mean serum gastrin levels rose significantly 2 hr after a single injection of metiamide (200 mg per kg, subcutaneously) in fasted and nonfasted conditions. It is concluded that in the rat prolonged administration of metiamide induces hypertrophy of the parietal cells, probably via hypergastrinemia, and leads to gastric hypersecretion after discontinuation of the medication.

Studies on the release of extra‐antral gastrin evidence of vagal inhibition in the dog

AbstractSerum gastrin concentration was measured in 3 dogs after a meat meal; basal levels rose significantly after 10 minutes. After antrectomy with a Billroth I, and later a Billroth II anastomosis, the tests were repeated. Basal gastrin levels were unchanged but the rise after meat feeding was abolished. Four antrectomized dogs with a BII anastomosis and cannulae in both the duodenum and stomach were used to examine the effect of duodenal perfusion on serum gastrin. Whether the perfusate was 150 mM NaCl, 150 mM HCl or 0.1% acetylcholine, the mean serum gastrin levels did not differ significantly from basal levels. Transthoracic vagotomy in antrectomized dogs produced a significant rise in basal gastrin levels, but did not restore the response to a meat meal or duodenal perfusion.Parallel studies were conducted in 6 antrectomized, vagotomized patients who had undergone Roux‐en‐Y conversion for postgastrectomy bilious vomiting, and in 2 patients after total gastrectomy. Duodenal perfusion via duodenostomy tubes with 150 mM NaCl, 150 mM HCl, fat emulsion, and an amino acid mixture did not raise serum gastrin above basal levels.Since meat feeding and duodenal perfusion in antrectomized dogs and humans failed to stimulate a rise in serum gastrin, we conclude that the intestinal phase of gastric secretion is unlikely to be mediated by gastrin. The results following vagotomy in the dog suggest that extragastric basal gastrin release is vagally inhibited or that vagotomy interferes with the catabolic destruction of gastrin.

Serum Gastrin Levels in Infants and Children

Fasting serum gastrin concentrations were determined by radioimmunoassay for 124 infants and children free of gastrointestinal disease. Values for the entire group ranged from 1.1 to 167.9 pg/ml (mean, 32.3 pg/ml). Mean serum gastrin levels for children who fasted eight or more hours were 22.5+/-23.9 pg/ml while the mean serum gastrin levels for children who fasted four to eight hours ranged from 42.4+/-33.9 pg/ml to 59.2+/-49.6 pg/ml. The mean serum gastrin levels varied inversely with body surface area among children who fasted the same length of time.

Chronobiological study on serum innumoreactive gastrin RIA levels in patients with liver cirrhosis.

After days of standardized conditions of life and standardized diets, serum gastrin levels were measured in 6 patients with liver cirrhosis on 3 consecutive days and in 14 normal controls on 1 day. Blood samples were drawn every 4 h. In patients as well as in controls, a significant serum gastrin circadian rhythm was noted. The daily mean serum gastrin levels of patients were not significantly different from those of controls. These results suggest a secondary role of the liver in gastrin metabolism.

Serum gastrin level in early childhood.

Serum gastrin concentration was measured in newborns and infants with no gastrointestinal disorders, in the fasting state and after food stimulation. Mean fasting concentration in 14 newborns aged 1 to 12 days (130 . 4 pg/ml +/- 11 . 4 SE) was significantly higher than the mean value in 23 infants aged 1.5 to 22 months (101.4 +/- 6.6 pg/ml). Ingestion of the usual milk meal resulted in a definite rise of the serum gastrin level in the 5 subjects tested (3 newborns and 2 infants). The mean fasting serum gastrin level in 6 babies with hiatus hernia and gastro-oesophageal reflux was found to be no different from the corresponding value in 8 age-matched controls. However, a conspicuously raised fasting gastrin concentration was observed in one infant with lower oesophageal dyskinesia. The results indicate that the release of gastrin and the reactivity of the hormone-producing sites to food stimulation in early life are similar to those in adult humans. No defect of gastrin release was shown in patients with gastro-oesophageal reflux.

Serum gastrin levels before and after vagotomy and pyloroplasty or vagotomy and antrectomy.

Abstract Fasting serum gastrin concentrations and rates of basal and maximum gastric acid secretion were measured in patients with duodenal ulcer before and at least six months after either antrectomy with vagotomy or pyloroplasty with vagotomy. The mean serum gastrin level after antrectomy and vagotomy was substantially and significantly (p less than 0.001) reduced; this decrease was accompanied by more than 90 per cent reduction in both basal and stimulated acid secretion. In sharp contrast, although gastric acid secretion was reduced, no fall in fasting serum gastrin concentrations was observed after pyloroplasty with vagotomy. These results indicate that reductions in gastric acid secretion after vagal transaction, with pyloroplasty, cannot be interpreted as consequences of reductions in vagally stimulated gastrin release; more probable mechanisms include modification of the sensitivity of the parietal-cell mass to gastrin or interruption of more direct vagal effects on acid-secreting cells.

Serum Gastrin Levels in Patients with Peptic Ulcer Disease

Fasting serum gastrin concentrations were measured by radioimmunoassay in serum from 67 patients with peptic ulcer disease and 102 hospitalized patients without recognized gastrointestinal disease of similar age and sex distribution. Unlike patients with the Zollinger- Ellison syndrome, patients with ordinary peptic ulcer disease were not found to have serum mean fasting gastrin levels elevated when compared with this control population. The mean fasting serum gastrin level for the control population was 165 pg per ml (± 28 se). The mean serum gastrin level for the patients with peptic ulcer disease was 98 pg per ml (± 12 se). The serum gastrin concentrations for patients with gastric ulcers, pyloral-antral ulcers, and duodenal ulcers were 126 (± 41 se), 118 (± 6.8 se), and 82 (± 11.5 se) pg per ml, respectively. Mean fasting serum gastrin levels in the control population were found to increase with increasing age. It was speculated that these increasing fasting serum gastrin levels with increasing age may reflect the effects of achlorhydria (and less complete forms of reduced acid secretion) in removing the usual inhibition of gastrin release due to antral acidification.

Immunochemical measurement of elevated levels of gastrin in the serum of patients with pancreatic tumors of the Zollinger-Ellison variety.

Abstract A radioiodine-immunoassay technic was used to measure fasting serum gastrin levels in four patients with the Zollinger-Ellison syndrome and 24 patients without gastrointestinal diseases. Serum gastrin levels in all the patients with the Zollinger-Ellison syndrome exceeded by approximately tenfold or greater the mean serum gastrin level of 425 μμg per milliliter in the control population. Gastrin was identified immunochemically in an extract derived from a pancreatic islet-cell tumor from one of the patients with the Zollinger-Ellison syndrome.