Gastrin Values Research Articles

Diagnostic value of serum pepsinogen C in patients with raised serum concentrations of pepsinogen A.

Hypopepsinogenaemia A is often found in patients with gastric atrophy and gastric surgery. In these conditions serum pepsinogen C provides additional diagnostic information, especially when expressed as pepsinogen A:C ratio. Hyperpepsinogenaemia A has been shown in patients with duodenal ulcer disease, Zollinger-Ellison syndrome, hypertrophic gastropathy, chronic renal failure, and during omeprazole treatment. As patients with hyperpepsinogenaemia A often overlap in symptoms, endoscopical findings, and serum gastrin values, this study has evaluated whether measurement of serum pepsinogen C in subjects with hyperpepsinogenaemia A can help in differentiating clinical conditions. Serum concentrations of pepsinogen A and C were measured in serologically Helicobacter pylori negative blood transfusion donors (127) as reference population, and in patients with Zollinger-Ellison syndrome (24), duodenal ulcer (50), hypertrophic gastropathy (5), and chronic renal failure (50), and also in reflux oesophagitis patients on longterm omeprazole treatment (28). A low pepsinogen A:C ratio was found in all patients with hypertrophic gastropathy. A pepsinogen A:C ratio above the critical value of 4.7 was found in 14 (70.0%) of the Zollinger-Ellison patients, two (9.5%) of the duodenal ulcer patients, 11 (25.6%) of the patients with chronic renal failure, and in one (7.1%) of the patients receiving longterm omeprazole treatment. In fact, all but three hyperpepsinogenaemia A patients with a pepsinogen A:C ratio greater than 4.7 and normal renal function had the Zollinger-Ellison syndrome. In patients with hyperpepsinogenaemia A, a low pepsinogen A:C ratio may point to hypertrophic gastropathy, while a pepsinogen A:C ratio greater than 4.7 is suggestive for the Zollinger-Ellison syndrome.

Asymptomatic H. pylori infection impairs pH inhibition of gastrin and acid secretion during second hour of peptone meal stimulation.

H. pylori infection is associated with acid-peptic disease, although its role in the pathogenesis is unclear. The purpose of this study was to determine if chronic infection in asymptomatic subjects impairs the inhibition of meal-stimulated gastrin and acid secretion that is observed normally at low intragastric pH. Presence of infection was determined by both C-14 urea breath test and serology. Acid secretion was measured under basal conditions and in response to peptone meal stimulation and pentagastrin. Plasma gastrin concentrations were determined by radioimmunoassay under basal conditions and during peptone meal stimulation. Intragastric titration with 1% peptone during the first hour, and 8% peptone during the second hour, was performed at both pH 7.0 and 2.5 on different days to compare the inhibition of gastrin and acid secretion. Compared to noninfected subjects, asymptomatic individuals infected with H. pylori had significantly increased: (1) basal gastrin values (P < 0.005); (2) 8% peptone-stimulated gastrin responses at both pH 7.0 and 2.5 (P < 0.05); and (3) 8% peptone-stimulated acid output at pH 2.5 (P = 0.01). During the second hour of peptone-stimulation, subjects infected with H. pylori had significantly decreased inhibition of gastrin (52% vs 95%) (P = 0.002) and acid (30% vs 81%) (P = 0.01) secretion from pH 7.0 to 2.5. Thus, chronic infection with H. pylori results in impaired inhibition of gastrin and acid secretion at low intragastric pH during the second hour of peptone meal stimulation. These defects may be unrelated to the pathogenesis of acid-peptic disease, since they occur in asymptomatic subjects infected with H. pylori.

The effect of ranitidine 300 mg at night, ranitidine 300 mg twice daily and placebo on 24-h intragastric pH and 24-h plasma gastrin in healthy subjects

Objective: The aim of this study was to examine the acute effects of ranitidine 300 mg at night and ranitidine 300 mg twice daily on 24-h intragastric acidity and 24-h plasma gastrin levels in a double blind, randomized, placebo-controlled study. Patients and methods: Twelve healthy male subjects were studied. Intragastric acidity was measured by radiotelemetry and 24-h plasma gastrin was derived from hourly blood samples. Both regimens were very effective in reducing median 24-h intragastric acidity, but the twice daily regimen was significantly better than dosing at night (80.5 compared with 71.8%, P < 0.05) by virtue of the greater reduction in daytime acidity (75.6 compared with 45.4%, P < 0.01). There was no significant difference in the effect on nocturnal acidity (95.6 compared with 93.2%). The median integrated 24-h plasma gastrin value increased from 774 pmolh/l on placebo to 1047 pmolh/l on ranitidine 300 mg at night (P < 0.01) and to 1180 pmolh/l on ranitidine 300 mg twice daily (P < 0.01). There was no significant difference in the effect of the two ranitidine regimens on the integrated plasma gastrin levels. Conclusion: Acute treatment with ranitidine 300 mg twice daily results in superior control of 24-h intragastric acidity compared with ranitidine 300 mg at night without a significant increase in plasma gastrin levels.

Evaluation of pepsinogen, gastrin and antibody response in diagnosing ostertagiasis

Ostertagia ostertagi is widely distributed and is one of the most important parasites affecting young bovine livestock. There is, therefore, a substantial need for sensitive and specific parameters in support of diagnosis of ostertagiasis, especially for subclinical disease related to production losses. In this review, the value and application of pepsinogen, gastrin and antibody response as diagnostic tools are discussed. These three parameters are useful and comparable for confirming clinical disease in calves during their first grazing season. However, their value for detecting subclinical parasitism is questionable. Differences in the course of gastrin and pepsinogen late in the grazing season can be correlated with larval inhibition and the possibility of ostertagiasis Type II. Relatively few serological methods have been developed for the immunodiagnosis of Ostertagia and until now the indirect antibody-detecting enzyme-linked immunosorbent assay (ELISA) has been the method of choice. Antibody measuring methods have several disadvantages, most notably a lack of sensitivity and specificity, which limits their use in longitudinal epidemiological studies. Considering the necessity of cost effectiveness and ease of use, it is anticipated that additional work will result in the enhancement and quality of current immunodiagnostic methods.

Evaluation of a proposed technique to assess unscheduled DNA synthesis and genotoxicity.

Results from a recent, new assay suggest that omeprazole, a potent inhibitor of gastric acid secretion, is genotoxic. The principle of this assay is that the non-proliferating zone of surface gastric epithelial cells can be selectively removed by controlled digestion so that any incorporation of tritiated thymidine into these cells represents unscheduled DNA synthesis. Parietal cells (which are located below the uppermost proliferating cells) and proliferating cells in semiconservative, regular DNA synthesis could always be shown in the digested fraction, and as regular DNA synthesis takes up a thousand fold more thymidine than unscheduled DNA synthesis, any signal from unscheduled synthesis would therefore be swamped. The digestion process was also uneven, as histological analysis showed denuded patches of mucosa, and gland like structures were seen in the digest. Quantification of the number of silver grains over the nuclei showed no increase in low level labelling after omeprazole administration, indicating that there was no unscheduled DNA synthesis. The labelling index of undigested gastric tissue from omeprazole treated rats was not significantly different from that of the control group, despite an increase in the plasma gastrin value.

Pancreatic tumors in multiple endocrine neoplasia type 1: clinical presentation and surgical treatment.

Among 33 patients with endocrine pancreatic tumors due to multiple endocrine neoplasia type 1 (MEN-1), 19 (58%) patients had hypergastrinemia, 7 (21%) patients had hyperinsulinism, and 7 (21%) patients had clinically non-functioning lesions. At least one gross tumor was found in all patients undergoing pancreatic surgery, including those with negative localization studies prior to operation. The patients also had additional macroscopic tumors as well as numerous microadenomas, and the lesions frequently were positive for immunostaining with multiple hormones, mainly pancreatic polypeptide, insulin, glucagon, and somatostatin. Duodenal endocrine lesions were found in 4 of 5 investigated patients and stained with gastrin and somatostatin antibodies. Distal, mainly subtotal pancreatic resection, was performed in 18 patients, eventually combined with caput tumor enucleation or duodenotomy, while a few patients underwent only tumor enucleation or a Whipple procedure. The long-term outcome of operation was most favorable in patients with hyperinsulinism; only 1 patient had clinical recurrence. Patients with hypergastrinemia experienced only transitory lowering of serum gastrin values after pancreatic surgery and 47% of them had or developed metastases. Such tumor spread was seen in 57% of the patients with non-functioning lesions. Nine patients died from progressive tumor disease during follow-up. Consistent with previous studies, we found that surgery is indicated in MEN-1 patients with hyperinsulinism even if a lesion is not visualized by radiology. In addition, these indications should be extended to also include patients with only biochemical markers of disease, including elevations of gastrin, as these indicate the presence of gross tumors.(ABSTRACT TRUNCATED AT 250 WORDS)

Omeprazole-induced hypergastrinemia does not influence growth of colon carcinoma.

Colonic mucosa and adenocarcinoma are known to possess gastrin receptors. Recent studies have suggested that some patients with large intestinal cancers and polyps have elevated serum gastrin levels and that gastrin may stimulate growth of colonic neoplasms. The aim of the present investigation was to determine whether endogenous hypergastrinemia--induced by the proton pump inhibitor omeprazole--would influence growth in a subcutaneously implanted murine colonic cancer. The results show that despite a fivefold increase in serum gastrin levels (193 pg/ml median value, range 186-252, in the omeprazole-treated group vs 36 pg/ml median value, range 28-37 in controls), there were no differences in tumor size or survival of tumor-bearing animals. Additionally, there were no differences in serum gastrin values between tumor- (29 pg/ml, range 25-38) and non-tumor- (34 pg/ml, range 25-30) bearing, untreated animals. Endogenous elevation of the serum gastrin hormone to five times the normal level does not demonstrate trophic effects on the murine colon tumor MC-26.

Diagnostic value of gastrin for clinical bovine ostertagiosis.

Gastrin values were evaluated in 130 parasite naive calves, in 61 first season grazing calves during six field trials and in 8 experimentally infected adult immune cows. The gastrin values were linked to pepsinogen levels and daily weight gain. Also the influence of an anthelmintic treatment on pepsinogen and gastrin values was assessed during a clinical outbreak of ostertagiosis in a group of first season grazing calves. Mean gastrin levels in parasite naive calves were 106 pg/ml. Results show that a group mean of 400 pg/ml gastrin in first season grazing calves indicates a reduced daily weight gain but with no obvious clinical signs. During clinical outbreaks mean gastrin levels frequently reached 1,000 pg/ml with a severe weight loss and a mean pepsinogen level of 5,000 mU tyr. The serum gastrin concentration was strongly reduced 4 days post treatment. No gastrin response was noted following an Ostertagia challenge in adult immune cows. The value of gastrin as a diagnostic aid for ostertagiosis is discussed in relation to pepsinogen, the adult worm burden, larval inhibition and the technique involved in assessing gastrin.

Helicobacter pylori-related hypergastrinaemia is not due to elevated antral surface pH. Studies with antral alkalinisation.

It has been postulated that Helicobacter pylori-related hypergastrinaemia is due to bacterial ammonia raising antral surface pH and thus preventing acid inhibition of gastrin release. If true, the infection should not alter gastrin release at neutral intragastric pH. To test this, we have studied basal and meal-stimulated gastrin at uncontrolled pH and at pH greater than 6 in duodenal ulcer patients before and after eradication of H. pylori. The median integrated gastrin response to the meal alone was 2525 ng/l.min (range, 550-8725) before and 725 ng/l.min (range, 250-2925) after eradication of H. pylori (p less than 0.01). The corresponding values when intragastric pH was maintained above 6 were 3700 ng/l.min (range, 1900-14,100) and 1400 ng/l.min (range, 400-3400) (p less than 0.01). The median reduction in gastrin after eradication of H. pylori was thus similar when the meal was taken at uncontrolled pH (61%; range, 0-97%) and at pH greater than 6 (69%; range, 36-89%). Likewise, 5 h of gastric alkalinisation did not cause the basal gastrin values when H. pylori was eradicated to increase to those observed when H. pylori was present. These findings indicate that the hypergastrinaemia is not due to elevated antral surface pH.

Postprandial hypergastrinaemia in patients with colorectal cancer.

Gastrin is trophic to colon cancers that possess gastrin receptors. Whether fasting serum gastrin concentrations are high in patients with colon cancer is controversial. We therefore studied the effect of food on serum gastrin concentrations in patients with colon cancer and control subjects. Fasting serum gastrin was greater, though not significantly so, in patients with colon cancer before surgery (mean (SD) 17.4 (3.6) pmol/l, n = 16) compared with control subjects (12.6 (1.9) pmol/l, n = 14). Postprandial increases in serum gastrin were significantly and persistently higher than normal in the cancer patients. These increases were due to a subset of six patients with serum gastrin concentrations greater than the control mean + 2 SD at 20 and 40 minutes (62 pmol/l-146 pmol/l). Four of the six patients had intra-abdominal metastases. The extent of the increase may well correlate with that of the disease. Surgical resection of the tumour resulted in a fall in serum gastrin values and probably reflects the cause of the hypergastrinaemia. Hypergastrinaemia may, therefore, be an important aetiological factor in colon carcinogenesis.

Pathophysiologic effects of Ostertagia ostertagi in calves and their prevention by strategic anthelmintic treatments

SUMMARY Pathophysiologic effects of Ostertagia ostertagi infection and their prevention by strategic anthelmintic treatments were studied in 3 groups each of 6 steer calves. Group-1 calves were noninfected controls. Group-2 calves were inoculated with 100,000 third-stage larvae on the 1st and 28th days of the experiment and grazed on pasture initially free of contamination. Group-3 calves were on a similar regimen as those in group 2, but were also treated with ivermectin 9 days after each larval inoculation. Group-2 calves had increased plasma pepsinogen and gastrin values and decreased weight gains, and total serum protein and albumin concentrations from the 2nd week of infection onward. They were anemic at 10 to 12 weeks and had lower carcass and meat quality at slaughter. Strategic anthelmintic treatments were effective in preventing these effects and calves in groups 1 and 3 had similar performances. On the basis of our findings, high pepsinogen values were related to worm burdens, whereas high gastrin concentrations were related to gastric lesions.

Elevated Serum Gastrin Levels in Patients with Colorectal Neoplasia

Gastrin stimulates the growth of some human colon adenocarcinomas grown in vitro or as xenografts in nude mice. To evaluate the possibility of elevated plasma gastrin levels in patients with adenomatous polyps or colorectal cancer, we carried out a radioimmunoassay in subjects fasting overnight and undergoing colonoscopy. The study included 190 patients who were divided into three groups: controls (n = 65), those with benign adenomas (n = 63), and those with adenocarcinomas (n = 62). The mean values of plasma gastrin in the cancer group (112.71 +/- 16.65 pg/ml) were significantly higher than those of the control group (40.41 +/- 1.88 pg/ml) as well as those of the polyp group. Mean plasma gastrin values in the polyp group (54.27 +/- 5.29 pg/ml) were also significantly higher than those of the control group. In the cancer group, 32 of 62 patients (51.6%) had gastrin levels greater than the control mean +2 SD, as opposed to only 10 of 63 (15.9%) in the polyp group. The number, size, histologic type, and presence of dysplasia in the polyp group and the location or Dukes' stage in the cancer group had no significant influence on gastrin levels in this study. Preliminary results in cancer patients with elevated preoperative gastrin levels show a postoperative reduction in six of seven patients. The exact cause and role of hypergastrinemia in tumor growth in such patients remains to be determined. Measurements taken both before and after colectomy coupled with a systematic search for specific gastrin receptors would be useful.

Multiple Endocrine Neoplasia Type 1: A 10-Year Prospective Screening Study in Four Kindreds*

A total of 80 individuals in 4 kindreds with multiple endocrine neoplasia type 1 (MEN 1) have been subjected to repeated biochemical screening during a 10-yr period with the principal aim being to analyze characteristics of the developing pancreatic lesion. Age at presentation of the MEN 1 trait averaged 18 yr in 7 previously unaffected individuals, and this effect of the screening procedure represented a lowering by almost 2 decades. Pancreatic endocrine involvement was recognized at a mean age of 25 yr and constituted the presenting lesion in a majority of the patients. A standardized meal test and basal values of serum pancreatic polypeptide, insulin, proinsulin, and gastrin were the most efficient markers for the pancreatic lesion and preceded signs of pancreatic tumors upon radiological examinations by a mean of 3.5 yr. A 75% penetrance of the islet cell disease and 90% for primary hyperparathyroidism within the affected individuals equalled the prevalences reported in autopsy studies. Two of the kindreds showed signs of intrafamilial homogeneity with respect to the profile of peptide excess (P less than 0.05) and considerable discrepancy in the malignant potential of the pancreatic lesions. The results of early detection and surgical intervention of the pancreatic tumors in MEN 1 suggested an impact on morbidity, while any effect on the mortality of these individuals remains to be clarified.

Inhibition of Gastrin Release Induced by Fundic Distension, Evidence of a Defective Inhibition in Duodenal Ulcer Patients

The serum gastrin response to an infusion of gastrin-releasing peptide (GRP), with or without simultaneous fundic distension, was studied in healthy volunteers and in patients with duodenal ulcer disease before and after a complete proximal gastric vagotomy (PGV). We also studied the effect of fundic distension alone on gastrin release and intraluminal gastric pressure in healthy volunteers and in patients after PGV. We observed an increased intraluminal pressure in patients after PGV compared with healthy subjects. During fundic distension with 600 ml of air no significant increase in gastrin values was observed in healthy subjects or in duodenal ulcer patients. In healthy subjects fundic distension significantly inhibited the gastrin response to the higher dose of GRP. This inhibitory effect exerted by fundic distension was counteracted by cholinergic blockade. In contrast, fundic distension did not alter the gastrin response to GRP in duodenal ulcer patients, suggesting a defective inhibitory mechanism in duodenal ulcer patients. After PGV, GRP infusion resulted in an enhanced gastrin response, and fundic distension seemed to facilitate the gastrin-stimulatory effect of GRP. This supports the concept of a vagally dependent inhibitory oxyntopyloric mechanism and that fundic distension can elicit both inhibitory and stimulatory secretory mechanisms.

Pyloric Antrum Gastrin Cell Hyperplasia after Jejunum or Colon Transposition: Effects of Jejunal or Colonic Mucosa on G Cells

Jejunal or colonic segments are currently used as esophageal substitutes after resection of intractable peptic stenoses. The present study was carried out in order to investigate the effects of the jejunal or colonic mucosa on antral gastrin (G) cells. Colonic or jejunal patches with intact vascular supply were sutured to the pyloric antrum or the higher portion of the gastric body in 40 rats. Ten further animals were used as controls. Three to 4 months after surgery, the serum gastrin levels were weekly determined in fasted (24 h) and freely fed rats using radioimmunoassay. The pyloric antrum was then removed, and the G cell density was assessed with an immunoperoxidase method. Transposal of the colonic mucosa to the antrum increased G cell density and basal serum gastrin levels, while grafting of the jejunal mucosa did not. G cell proliferation proved to be dependent on the topographic location of the colonic patch with respect to the pyloric antrum. Serum gastrin values in freely fed rats tended to be greater in the colon-to-antrum transposition group than in the other experimental groups, but the difference was not significant. In conclusion, variations between the properties of the jejunal and colonic mucosa would include their uneven effects on antral G cells.

Gastric Parietal, Chief, and G-Cell Densities in Chronic Renal Failure

We calculated morphometrically the amount of antral gastrin-producing (G) cells and body parietal and chief cells in gastric biopsy specimens from 30 undialysed patients with chronic renal failure (CRF) and from sex- and age-matched controls. The CRF patients had raised fasting serum gastrin levels, whereas these were normal in the controls (mean, 290 +/- 283 (+/- SD) ng/l (n = 27) versus 33 +/- 36 (n = 30)). Serum gastrin values of the patients and controls correlated positively with G-cell density (r = 0.501, n = 36, p = 0.002), as did the maximal acid output of the CRF patients with parietal cell density (r = 0.617, n = 14, p = 0.019). In CRF patients the densities of G, parietal, and chief cells were higher than those in the controls (G cells, 351 +/- 151 (+/- SD) cells/mm2, n = 21 versus 211 +/- 90, n = 16, p = 0.002; parietal cells, 299 +/- 94, n = 15 versus 224 +/- 72, n = 14, p = 0.025; chief cells, 886 +/- 346, n = 15 versus 743 +/- 182, n = 14, p = 0.181). The results agree with previous findings indicating that hyposecretion of gastric acid in CRF does not derive from decreased capacity for acid secretion but rather from the inhibition of acid output. Increased parietal cell density in CRF patients gives cause to suspect that the maximum acid output might even in raised, possibly depending on the permanent hypergastrinaemic state with its trophic influence on the gastric body mucosa.

Acute Effects of Continuous Nasogastric Tube Feeding on Gastric Function: Comparison of a Polymeric and a Nonpolymeric Formula

The acute effects of continuous intragastric administration of 1500 ml (4200 kJ/liter) of a polymeric and of a nonpolymeric formula on gastric function were studied in 15 healthy subjects. During 450 min 1500 ml, containing 6300 kJ (1500 kcal), was given through a nasogastric tube. At regular intervals the volume, the pH, the titratable acidity, and the pepsin activity of the gastric contents and the plasma gastrin concentration were determined. Maximal observed intragastric volumes occurred after 120 min (118 +/- 16 ml during polymeric formula, 212 +/- 37 ml during nonpolymeric one) and volumes subsequently halved (at 450 min 68 +/- 13 and 104 +/- 16 ml, respectively). During the administration of both polymeric and the nonpolymeric formula intragastric pH fell progressively to 3.15 and 2.67, respectively, at 450 min. Incremental plasma gastrin values increased between 120 and 450 min from 7 to 12 ng/liter during the polymeric formula. During the nonpolymeric one it stabilized after 120 min at 12 ng/liter. When the whole test periods were considered integrated, mean intragastric volumes tended to be larger during the nonpolymeric formula (153 +/- 23 ml) than during the polymeric formula (107 +/- 12 ml), but this difference was not statistically significant. Median integrated mean pH was lower during the nonpolymeric formula (2.89) compared with the polymeric one (3.26). Despite the limitation that the investigations were performed in healthy subjects only, it is concluded from this study that the risk of aspiration during continuous nasogastric tube feeding is probably greatest during the first few hours of administration because of the larger intragastric volumes.(ABSTRACT TRUNCATED AT 250 WORDS)

H+K+-ATPase Antibodies in Autoimmune Gastritis: Observations on the Development of Pernicious Anemia

The prevalence and development of antibodies to H+,K+-ATPase were investigated with a sensitive enzyme-linked immunosorbent assay in 86 patients with autoimmune atrophic gastritis (type A). Sixty-nine of the patients had pernicious anemia, and 17 had simple atrophic gastritis. Elevated titers were found in 93% of pernicious anemia probands. Women had higher levels than men: 3.24 versus 1.58 U/l (p = 0.002) (upper reference limit, 0.55 U/l). The antibody levels did not change over 1-4 years, but a gradual decrease in titers over decades was observed. All patients with pernicious anemia had low levels of pepsinogen A, a product of the gastric chief and mucous neck cells (median, 8.5 micrograms/l; reference range, 10-90 percentile, 64.4-195.5 micrograms/l), and elevated serum gastrin values (greater than 55 pmol/l) were found in 87%. Serum pepsinogen A, but not serum gastrin, correlated with H+,K(+)-ATPase antibody titers (r = 0.35, p = 0.01). In the 17 cases with simple atrophic gastritis, H+,K(+)-ATPase antibodies correlated inversely with fundic mucosal gland destruction. The data indicate that H+,K(+)-ATPase antibody titers reflect the immune responsiveness of a given patient as well as the antigenic amount, dependent on the degree of mucosal destruction and the duration of the disease.

Influence of suckling on plasma concentrations of somatostatin, insulin and gastrin in lactating women

The effects of suckling on plasma somatostatin, insulin and gastrin values were evaluated in eight nursing women on the 3rd to 4th day postpartum. Plasma prolactin levels were also determined. Prolactin levels increased in response to suckling, as expected. Insulin levels also rose, whereas somatostatin and gastrin concentrations did not change after suckling. It is possible that the suckling-induced hyperinsulinemia blunts the somatostatin response to suckling in humans.

Is antral gastrin important in the resistance of duodenal ulcers to H2 receptor antagonists or in recurrent ulceration after highly selective vagotomy?

Basal serum gastrin, integrated gastrin response to a meal, and integrated gastrin response to insulin induced hypoglycaemia were measured in 60 patients with duodenal ulcer before and after elective highly selective vagotomy to determine whether antral gastrin has a role in resistance to H2 receptor antagonist treatment which the patients had received before surgery or in the development of recurrent ulceration after vagotomy. The basal gastrin, integrated gastrin response to a meal, and the integrated gastrin response to insulin were similar in patients whose ulcers healed after H2 receptor agonist treatment or were refractory to at least three months of this treatment. The same parameters measured before or after highly selective vagotomy were similar in patients who eventually developed recurrent ulceration compared with those who did not. As expected the basal and meal stimulated (but not insulin stimulated) serum gastrin values increased after highly selective vagotomy. Ulcer patients with particularly high gastrin values (whether basal or stimulated) were not more resistant to H2 receptor antagonist treatment or prone to develop ulcer recurrence after highly selective vagotomy. This study suggests that antral gastrin is not important in 'resistance' of duodenal ulceration either to H2 receptor antagonist treatment or to highly selective vagotomy.