The effect of vagotomy and antrectomy on serum pepsinogens I and II

Ninety-seven consecutive patients with gastric surgery for peptic ulcer were studied; 86 had duodenal ulcer (DU), and 11 gastric ulcer (GU). DU patients were surgically treated by proximal vagotomy, proximal vagotomy and pyloroplasty, truncal vagotomy and pyloroplasty, or truncal vagotomy and antrectomy. All GU patients were operated on by the Billroth I method. Serum pepsinogen I(S-PG I), serum pepsinogen II (S-PG II), basal acid output (BAO), and maximal acid output (MAO) were determined before and 3 months and 1 year after the operation. The mean preoperative S-PG I concentration in DU patients (154 +/- 7 micrograms/l; mean +/- SE) was significantly higher than that (97 +/- 9 micrograms/l) in GU patients (p less than 0.001). A significant decrease in the mean S-PG I concentration in DU patients was seen 3 months (92 +/- 6 micrograms/l) and 1 year (66 +/- 4 micrograms/l) after the operation (p less than 0.001). This change did not depend on the type of vagotomy. However, this decrease was not seen in all individual patients as it was in BAO values. Moreover, the mean BAO decrease was much greater at 3 months (7% of the preoperative value) and 1 year (23%) after the operation than the respective decrease in S-PG I concentration. There was also no correlation between S-PG I and acid output (BAO and MAO) before and after the operation. In GU patients the decrease in mean S-PG I value after the Billroth I operation was smaller than in DU patients after vagotomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of naloxone on basal and maximum gastric secretion in patients with chronic duodenal ulcer

In 22 men with chronic duodenal ulcer and 15 healthy men effect of a single intravenous injection of 2 mg of naloxone on basis and pentagastrin-stimulated acid output was determined. Naloxone was found to induce a significant decrease in BAO in chronic duodenal ulcer patients; a decrease in BAO in healthy men was insignificant. MAO was not affected by naloxone in both groups. Gastric secretions of potassium, sodium, chloride and mucoprotein were proportional to changes in the volume of the gastric juice. It seems that opioid agonists may play some role in the pathogenesis of duodenal ulcers.     

Helicobacter pylori and Zollinger-Ellison syndrome

Helicobacter pylori (previously Campylobacter pylori) is almost invariably associated with chronic duodenal ulcer disease. The relationship between H. pylori infection and duodenal ulcer in Zollinger-Ellison syndrome is unknown. We investigated the frequency of H. pylori infection in Zollinger-Ellison syndrome and also what effect H. pylori infection had on gastric function in patients with Zollinger-Ellison syndrome. H. pylori infection was diagnosed based on a specific serologic (ELISA) assay based on high-molecular-weight cell-associated proteins of H. pylori. We studied 20 patients with Zollinger-Ellison syndrome; 15 men and 5 women ranging in age from 24 to 71 years, median age 51. Six Zollinger-Ellison syndrome patients had H. pylori infection compared to 100 consecutive patients with chronic recurrent duodenal ulcer disease (P less than 0.05). Pretreatment basal acid output in Zollinger-Ellison syndrome patients ranged from 7.9 to 95.0 mmol/hr, median 35.2. Pentagastrin-stimulated maximal acid output ranged from 8.5 to 132 mmol/hr; median 52.7. Acid secretion was lower in the H. pylori-infected patients than the uninfected patients (BAO 24.5 +/- 6.5 vs 45.4 +/- 6.6, and MAO 44.3 +/- 11.8 vs 67.9 +/- 10.7, for H. pylori infected vs uninfected patients, respectively). The difference in BAO was statistically significant (P less than 0.05). The present results indicate that H. pylori is not a major contributing factor in duodenal ulcer associated with Zollinger-Ellison syndrome. The association of a reduced BAO with H. pylori suggests that these findings may be related.     

Duodenal ulcer in children. Apropos of 28 cases

We present 28 children, 4 to 14 year-old, with duodenal ulcer; there were 21 males and 7 females. In 16 cases, after stimulation with pentagastrin, basal pepsinogen I (PG1), basal gastrinemia and basal acid output (BAO) and maximal acid output (MAO) were measured. Compared to controls, the mean levels of PG1 and gastrin were significantly higher in the patients; 12 children (80%) had high levels of PG1 and the remaining 3 (20%) had normal levels. The blood group O was the most prevalent: 64% of the cases.     

Tri-annual rhythm of basal acid secretion and secretion stimulated by pentagastrin in duodenal ulcer

Duodenal ulcer is a recurrent disease with seasonal periodicity for pain and complications such as hemorrhage and perforation. Ulcer craters or symptoms seem to occur preferentially in early spring and autumn. Since acid secretion is one of the pathogenetic factors of the disease, we analyzed retrospectively basal and maximal (pentagastrin) acid secretion data obtained in 341 consecutive patients according to the month in which they were obtained. The patients were classified according to the activity of their ulcer (active, non active) and to the level of the peak acid secretion (hypersecretors, normosecretors). Basal acid concentration and output, and peak acid output were, both overall and month by month, higher in patients with active duodenal ulcer disease than in those who were non active, and in hypersecretors than in normosecretors. For all 341 patients as well as for normosecretors and non active ulcer patients, a triannual rhythm was detected for stimulated acid concentration and peak acid output. The highest values were noted in February, June, and October (period: 4 months). The amplitude of these rhythms was 3 to 4 percent, with differences between highest and lowest values of 30.4 mmol/l for concentration and 17.1 mmol/h for peak acid output. These rhythms for acid secretion during the year may contribute to the periodicity of duodenal ulcer events and should be analyzed in association with other factors which could be implied in ulcerogenesis. Moreover, this seasonal periodicity of acid secretion in duodenal ulcer should be taken into account in all therapeutic trials in which acid secretion is analyzed.     

Duodenal ulcer disease: Helicobacter pylori and hyperchlorhydria

Basal and pentagastrin-stimulated gastric acid secretion and basal serum gastrin level were investigated in 55 active duodenal ulcer patients with antral colonization with Helicobacter pylori (HP) and 17 patients without. Our study shows that basal (BAO) and pentagastrin-stimulated gastric acid secretion (MAO and PAO) were significantly higher in HP positive than in HP negative patients with duodenal ulcer disease. There were also a tendency to increase in basal serum gastrin concentration in HP positive patients. We suggest that antral HP increases antral gastrin release and gastric secretion. Increased acid secretion then causes duodenal ulcers by producing a low intraduodenal pH.     

Giant duodenal ulcer

Patients with giant duodenal ulcer (>2 cm) have more ulcer complications (ie, bleeding) than patients with duodenal ulcer in the standard range (0.5–1.5 cm). To evaluate possible differences between patients with giant duodenal ulcer and those with duodenal ulcer in the standard range, we determined basal acid outputs by nasogastric suction, percentage of patients with daily nonsteroidal antiinflammatory drug (NSAID) use, and percentage of ulcer complications in 184 patients with endoscopically documented active duodenal ulcer. Seventeen patients had giant duodenal ulcer, and 167 patients had duodenal ulcer in the standard range. The mean basal acid outputs for the 17 patients with giant duodenal ulcer was 7.9 meq/hr (range 0.0–27.8 meq/hr) and for the 167 patients with duodenal ulcer in the standard range was 9.0 meq/hr (range 0.0–49.1 meq/hr), which were not significantly different. There was a significant difference in the percentages of ulcer complications between the 17 patients with giant duodenal ulcer and the 167 patients with duodenal ulcer in the standard range: 65% compared to 25% (P=0.001), and in the percentages of patients with regular daily NSAID use, during the one month preceding the upper gastrointestinal endoscopy: 53% compared to 8% (P=0.00001). However, a significant association between NSAID use and duodenal ulcer complication was not apparent. These results suggest that the development of giant duodenal ulcer and the significant increase in complications associated with giant duodenal ulcer are not attributable to increased basal acid output, however, they may be attributable to increased NSAID use.     

Do non-steroidal anti-inflammatory drugs cause duodenal ulcer? Evaluation of basal acid output and ulcer complications

Non-steroidal anti-inflammatory drug (NSAID) use and basal acid outputs determined by nasogastric suction were evaluated prospectively in 184 patients with endoscopically documented duodenal ulcer. The mean basal acid output and percentage of gastric acid hypersecretion for duodenal ulcer patients who used NSAID were compared with duodenal ulcer patients who did not use NSAID to determine whether patients using NSAID who develop duodenal ulcer have basal acid outputs in the normal range or in the duodenal ulcer range. Results were compared with 65 normal subjects and 105 patients with nonulcer dyspepsia. There were no significant differences with regard to the percentage of male gender, mean age, mean basal acid output, percentage of gastric acid hypersecretion and percentage of cigarette smoking history between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not. However, significant differences were observed between duodenal ulcer patients who used NSAID and duodenal ulcer patients who did not use NSAID with regard to the percentage of bleeding duodenal ulcer (59 compared with 23%; p= 0.0008) and the percentage of patients with giant duodenal ulcer (41 compared with 5%; P= 0.00001). These results suggest that NSAID use does not cause duodenal ulcer but does make pre-existing duodenal ulcer worse by causing duodenal ulcer complications.     

The effects of smoking and nicotine on the parietal cell mass of human beings and rats

Abstract On 94 patients with duodenal ulcer and 44 controls, parietal cell mass (PCM), as derived from pentagastrin-stimulated peak acid output (PAO), was significantly greater in chronic cigarette smokers than in non-smokers. Smokers and non-smokers did not differ in their fasting and postprandial serum gastrin concentrations, and in the frequency of familial ulcer, although basal acid output (BAO) and BAO/PAO were significantly higher in smokers, suggesting the presence of hypervagotonia. Chronic hypodermic administration of depot nicotine in rats resulted in significant dose-dependent increase in PAO and PCM as determined histologically, supporting the results of the human studies. Acute administration of nicotine, however, did not cause any increase in acid output, indicating that it had no effect on parietal cell function. Chronic nicotine administration also led to significant increase in antral G cell mass as determined by immunohistochemical labeling, and in peptone-stimulated serum gastrin. The effects on PCM and G cells were abolished by the simultaneous administration of atropine. Nicotine induced gastric electrical and motor activities in rats similar to those induced by carbachol, and the effects of both agents could be blocked by atropine. Nicotine had no effect on gastric mucosal blood flow in rats as estimated by neutral red clearance. We conclude that cigarette smoking in man and chronic nicotine administration in rats cause parietal cell hyperplasia, plus, in rats, G cell hyperplasia, possibly through a cholinergic mechanism.     

Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers

BACKGROUND AND AIM: Antral somatostatin interacts with gastric acid secretion. We aimed to investigate the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with Helicobacter pylori (H. pylori) infection. METHODS: Twenty-eight patients (21 male, 7 female) with H. pylori-positive gastric ulcer were treated with dual therapy. Before and 4-8 weeks after the therapy, the histology of biopsy specimens, basal acid output (BAO) and maximal acid output (MAO) after stimulation with tetragastrin were assessed. Somatostatin concentration in the gastric juice was measured by radioimmunoassay, and somatostatin output during either the basal or gastrin-stimulated period was also examined. RESULTS: Eradication was successful in 22 patients. Before treatment, the acid and somatostatin output were inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin-stimulated somatostatin output were observed. Eradication had no effect on atrophy and MAO. There was a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition, irrespective of H. pylori infection. CONCLUSIONS: The present results suggest that recovery of gastric BAO may be caused by an improvement in corpus neutrophil infiltration, but not by an increase in parietal cell volume or a change in atrophy. Also, there was an increase in basal and gastrin-stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers.     

Helicobacter pylori and gastric acid output in peptic ulcer disease

Helicobacter pylori is associated with peptic ulcer, and a causal relationship has been postulated. We investigated the association betweenHelicobacter pylori and gastric acid output. Two hundred forty-one patients were studied: 173 with duodenal ulcer, 51 with gastric ulcer (41 corpus, 10 prepyloric), and 17 with combined gastric and duodenal ulcer. In 194 patients (80%),Helicobacter pylori could be demonstrated histologically from gastric antral biopsies. The presence or absence ofHelicobacter pylori was not influenced by age, sex, or use of tobacco or analgesics. Patients with duodenal ulcer or combined gastric and duodenal ulcer had similar gastric acid outputs irrespective of the presence or absence ofHelicobacter pylori. However, gastric ulcer patients withHelicobacter had higher basal and maximal acid outputs when compared to patients withoutHelicobacter (mean basal output: 4.1 mmol/hr vs 2.4,P<0.05; mean maximal output 19.5 mmol/hr vs 14.4,P<0.05). AlthoughHelicobacter pylori is associated with both gastric ulcer and duodenal ulcer, its significance may be different in the two diseases.     

Comparison of maximal acid output and gastrin response to meals in Chinese and Scottish normal and duodenal ulcer subjects.

Maximal acid output (MAO) after pentagastrin stimulation and gastrin response to a standard meal was studied in 100 control and 200 duodenal ulcer subjects from each of two ethnic groups, Scots and Chinese. The acid output was significantly higher in the Scots than in the Chinese for both controls and duodenal ulcer patients. Despite correction for differences in body stature by expressing MAO as a function of the body weight, these differences persisted. In 45 pairs of closely matched patients with duodenal ulcer, the differences between the two ethnic groups remained significant, irrespective of whether MAO was expressed in absolute or weight corrected values. This indicates that differences in age, sex, family history, or duration of illness did not account for differences in acid output. In 20 pairs of normal control and 45 pairs of duodenal ulcer patients the fasting and post-prandial serum gastrin levels did not differ, significantly between the two ethnic groups. The proportion of acid normosecretors was significantly higher in the Chinese duodenal ulcer patients than in the Scottish. The reason for these differences in the gastric acid output between the two ethnic groups is not known and needs to be studied further.     

Gastric acid response to modified sham feeding in patients with duodenal ulcer: Is increased vagal tone the cause of basal acid hypersecretion?

In order to test the hypothesis that increased basal vagal tone causes basal acid hypersecretion in duodenal ulcer (DU), the effect of sham feeding on gastric acid secretion was studied in 26 patients with DU and 20 healthy controls. Basal acid output (BAO), sham feeding-stimulated acid output (SAO) and peak histamine-stimulated acid output (PAO) were significantly higher in DU patients compared with healthy controls (P less than 0.01). The BAO/PAO ratio in DU patients (0.28 +/- 0.03) was not significantly different from that of healthy subjects (0.19 +/- 0.03), indicating that the higher BAO in DU patients group, as a whole, was due to a higher parietal cell mass. The basal subtracted response to sham feeding expressed as a fraction of secretory capacity [(SAO-BAO)/PAO], which correlates inversely with the basal vagal tone, was not significantly different in the patients and control subjects (0.27 +/- 0.03 versus 0.3 +/- 0.03; P greater than 0.05). Based on the data from the healthy controls, a ratio of BAO/PAO greater than 0.44 was defined as abnormal (using 95% confidence limits) and it indicated marked basal acid hypersecretion. Four of 26 DU patients had basal acid hypersecretion (that is, BAO/PAO greater than 0.44), but only two of them did not show an increase over their basal rate of secretion in response to sham feeding. All other DU patients, including two with marked basal acid hypersecretion, and all healthy controls showed an appreciable increase in their acid secretion in response to sham feeding.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gastrin sensitivity in duodenal ulcer.

The sensitivity to pentagastrin measured as D50C, the dose required for half maximal acid output (MAO) corrected for basal acid output, in 200 patients with active duodenal ulcer was significantly (p less than 0.001) higher than that in 36 age- and sex-matched controls, and was above the normal limit in 27% of the patients. The distribution of D50C was significantly different between early onset and late onset patients, defined as patients whose ulcer symptoms started at respectively age less than or equal to 30 years and age greater than 30 years. Among patients whose MAO/kg body weight was within 2 SD of the normal mean as established previously in 100 normal subjects, gastrin sensitivity was significantly greater in late onset than in early onset patients, and in those who were positive than in those who were negative for familial ulcer dyspepsia. Among patients with abnormally large MAO, the reverse was true, gastrin sensitivity being greater in early rather than in late onset patients, and in patients negative rather than in those positive for familial ulcer dyspepsia. These findings suggest that gastrin hypersensitivity is a distinct physiological abnormality in duodenal ulcer, the increased gastrin sensitivity in some patients with normal MAO has a genetic basis but the lateness in onset of their disease also suggests an environmental origin, and the increased gastrin sensitivity in some patients with abnormally large MAO is related to environmental factors encountered early in life.     

Gastric acid and pancreatic polypeptide responses to modified sham feeding: indication of an increased basal vagal tone in a subgroup of duodenal ulcer patients.

The effect of sham feeding upon gastric acid secretion and pancreatic polypeptide release was investigated in 28 patients with duodenal ulcer in order to evaluate whether high basal vagal activity is the cause of basal acid hypersecretion in patients with duodenal ulcer and basal secretion higher than 30% of their peak acid output. The patients were divided into two groups based on the ratio of basal/pentagastrin stimulated peak acid output (BAO/PAO) was higher or lower than 0.30: group A n = 19 (BAO/PAO less than or equal to 0.30) and group B n = 9 (BAO/PAO greater than 0.30). Gastric acid response to sham feeding (SAO) was significantly higher than basal level in group A (SAO: 11.4 mEq/h (2.5-20.1) vs BAO: 5.2 mEq/h (0.8-22.9), p less than 0.01, median (range)) while in group B the acid secretion did not increase with sham feeding (SAO: 9.6 mEq/h (4.5-13.6) vs BAO: 8.8 mEq/h (6.3-13.8) ns, median (range)). A negative correlation (r= -0.6118226, p less than 0.01) was found between acid increase expressed as basal subtracted sham feeding response (SAO-BAO) and BAO/PAO ratio of the entire group of duodenal ulcer patients (n = 28) suggesting that the greater is basal acid secretory capacity the smaller is acid increase in response to residual vagal activation. Pancreatic polypeptide response to sham feeding was higher in group A than in group B but no correlation (r = 0.20, n = 28) nor individual covariation was found between acid and pancreatic polypeptide secretions during vagal stimulation. sham feeding did not change serum gastrin. It is concluded that an increased vagal stimulation seems to be the cause of basal hypersecretion in a subgroup of patients with duodenal ulcer. The lact of correlation between the pancreatic polypeptide and acid responses to vagal stimulation interferes with the reliability of pancreatic polypeptide as indicator of vagal tone on gastric parietal cells.     

Gastric ulcers differ from duodenal ulcers evaluation of basal acid output

Patients with pyloric channel and prepyloric gastric ulcers are often considered to have an ulcer diathesis similar to patients with duodenal ulcers, while patients with more proximal gastric ulcers (ie, fundus, body, antrum) are excluded. To evaluate possible differences in basal acid outputs with regard to gastric ulcer location, basal acid outputs were determined by nasogastric suction in 80 patients with endoscopically documented benign active gastric ulcers. The results were compared to 65 normal subjects and 155 patients with endoscopically documented duodenal ulcers. There were no significant differences in basal acid outputs among the 80 patients with gastric ulcers with regard to location (ie, fundus-body, antrum, prepyloric, channel), and no significant differences compared to the 65 normal subjects. However, basal acid output for the 155 patients with duodenal ulcers was significantly different from the 80 patients with gastric ulcers (P<0.05) and the 65 normal subjects (P<0.05). Basal acid outputs tended to be higher and there was more gastric acid hypersecretion when gastric ulcers were located near the pylorus. However, irrespective of gastric ulcer location, basal acid outputs were higher in patients with duodenal ulcers. Seventy-one of the 80 patients with gastric ulcers were treated for eight weeks with standard doses of antisecretory medications, and endoscopic healing or nonhealing was documented. In 60 patients their gastric ulcers completely healed, while 11 patients had nonhealed gastric ulcers. There were no significant differences between the two groups with regard to gender, mean age, or basal acid output. The gastric acid secretory profiles determined in this study do not appear to support the view that prepyloric and pyloric channel gastric ulcers are similar to duodenal ulcers.     

Maximum acid output to graded doses of pentagastrin and its relation to parietal cell mass in Chinese patients with duodenal ulcer.

In groups of Chinese patients with duodenal ulcer and controls, increasing the dose of pentagastrin from the standard dose of 6 ug/kg or 12 ug/kg did not result in any change in the maximum acid output (MAO). Comparison of the MAO thus obtained with that reported in series of Occidental subjects suggested that the Chinese subjects had smaller MAO. Using the method of Card and Marks (1960), the parietal cells of resected stomachs were counted in a group of Chinese patients with duodenal ulcer. It was found that the parietal cell mass (PCM) correlated with the MAO, both PCM and MAO were significantly small in the Chinese series as compared with the Scottish series, but the acid output per unit parietal cell mass (MAO per 10(9) parietal cells) was not different in the two groups. These observations suggested that the Chinese patients with duodenal ulcer had smaller parietal cell mass compared with the Westerners.     

Repeated pentagastrin-stimulated gastric acid secretory tests carried out in the evaluation of the pharmacodynamics of a new histamine H2-receptor antagonist, SK&F 93479

Single doses of 10 mg or 20 mg intravenously or 25 mg or 40 mg orally of a new histamine H2-receptor antagonist, SK&F 93479, have been administered to 31 patients with peptic ulcer disease. BAO and MAO were measured before and repeated during a 26-h period after drug administration. In a separate group of 17 patients the mean coefficients of variation of BAO and MAO measured in this manner were 53% and 20%, respectively. If this variation in the placebo group is taken into account, BAO was significantly inhibited at all dose levels during the 3rd h after dosing, and a significant effect was still seen during the 25th h after 40 mg orally with a mean reduction of 77%. Mean inhibitions of MAO during the 4th h after dosing of SK&F 93479 were significant at all dose levels, and a significant effect could still be seen during the 26th h for the two oral doses. The mean inhibitions of MAO measured during the 4th and 10th h after dosing were after 10 mg intravenously 44% and 11%, after 20 mg intravenously 59% and 11%, after 25 mg orally 57% and 21%, and after 40 mg orally 75% and 46%. The percentage inhibition of MAO during the 10th h correlated with plasma concentrations (r = 0.64, p less than 0.01). SK&F 93479 is a potent inhibitor of acid secretion with a long duration of action.     

Do Anticholinergics Interact with Histamine H2 Receptor Antagonists on Night Intragastric Acidity in Active Duodenal Ulcer Patients?

The effect of administering low doses of famotidine or ranitidine alone or in combination with an M1-receptor-selective antagonist, pirenzepine, on night intragastric acidity was evaluated in 16 active duodenal ulcer patients to verify 1) whether anticholinergics and H2-antagonists have a synergic effect on inhibition of night gastric acidity, and 2) whether patients with vagal hypertone are more sensitive to anticholinergics than the remainder of the duodenal ulcer population. The endogastric pH was continuously recorded for 12 h (8 PM-8 AM) after random, single-blind administration of one of the following drug regimens: 20 mg famotidine, 150 mg ranitidine, 50 mg pirenzepine, 20 mg famotidine plus 50 mg pirenzepine, and 150 mg ranitidine plus 50 mg pirenzepine. Six patients with a basal acid output:peak acid output BAO:PAO greater than 0.3 were considered "vagal hypertone" subjects. Night gastric acidity inhibition was -39.6% with pirenzepine (p less than 0.001) and -73.7% and -71.5% with famotidine or ranitidine (p less than 0.001 vs. pirenzepine). The simultaneous administration of pirenzepine with famotidine or ranitidine provoked only a slight, insignificant increase in percent suppression, 5.1% and 6.3%, respectively, and did not modify either the time lag to onset of anti-H2 action or the duration of action. Patients with a BAO:PAO greater than 0.3 were not more sensitive to anticholinergic treatment than other duodenal ulcer patients. Our study furnishes evidence that combined administration of anti-H2 and anticholinergics is not significantly better than anti-H2 alone, in active duodenal ulcer patients.     

Sham Feeding—Pentagastrin Test in Healthy Subjects and Peptic Ulcer Patients

The acid response to a combined sham feeding-pentagastrin test was studied in 27 patients with gastric ulcer (GU), 47 patients with pyloric or prepyloric ulcer (PU), 65 patients with duodenal ulcer (DU), and 29 healthy subjects (HS). In each group basal acid secretion (BAO) and peak acid output to sham feeding (PAO_Sh) and to pentagastrin (PAO_Pg) were significantly correlated. After correction for body weight these variables were equivalent in men and women. DU patients showed basal hypersecretion, not only due to a greater secretory capacity, since the BAO/PAO_Pg ratio was significantly higher than in non-DU groups. The response to vagal activation was also increased in DU patients. Thus the ratio PAO_Sh/PAO_Pg amounted to 0.52 in DU, compared with 0.34-0.36 in non-DU subjects (p < 0.001). The relative acid responses were similar in healthy subjects and GU and PU patients. Thus DU patients seem to have a vagal hyperfunction that might be due to defective inhibitory mechanisms, for which there is supporting evidence, or might be caused by a possible vagal hyperactivity, which is a speculation.