Action of cholera toxin on dispersed acini from rat pancreas. Post-receptor modulation involving cyclic AMP and calcium.

In dispersed acini from rat pancreas, cholera toxin caused a significant increase in cellular cyclic AMP but little or no change in amylase secretion. The presence of a secretagogue that causes mobilization of cellular calcium (e.g., cholecystokinin, carbamylcholine, bombesin or ionophore A23187) caused a substantial increase in the effect of cholera toxin on enzyme secretion. Cholera toxin did not alter calcium transport or the changes in calcium transport caused by other secretagogues, and secretagogues that mobilize cellular calcium did not alter cellular cyclic AMP or the increase in cyclic AMP caused by cholera toxin. These results indicate that in dispersed acini from rat pancreas there is post-receptor modulation of the action of cholera toxin by secretagogues that mobilize cellular calcium and that this modulation is a major determinant of the effect of the toxin on enzyme secretion.

Comparison of the effectiveness of ranitidine and cimetidine in inhibiting acid secretion in patients with gastric hypersecretory states.

The H2-histamine receptor antagonists ranitidine and cimetidine were compared for their abilities to control gastric acid hypersecretion on a short- and long-term basis in 22 patients with gastric acid hypersecretory states. Nineteen patients had Zollinger-Ellison syndrome, one patient had systemic mastocytosis, and two patients had idiopathic hypersecretion. The rates of onset of the action of cimetidine and ranitidine were the same. The actions of both drugs were increased by anticholinergic agents, and there was a close correlation between the daily maintenance dose of each drug needed to control acid secretion. However, ranitidine was threefold more potent than cimetidine both in acute inhibition studies and in the median maintenance dose needed (1.2 g per day for ranitidine and 3.6 g per day for cimetidine). Sixty percent of the males developed breast changes or impotence while taking cimetidine and in all cases these changes disappeared when cimetidine was replaced by ranitidine. Treatment with high doses of cimetidine (one to 60 months; median, 11 months) or ranitidine (two to 31 months; median, 14 months) was not associated with hepatic or hematologic toxicity or alterations of serum gastrin concentrations, but ranitidine therapy was associated with a significantly lower serum creatinine level than seen with cimetidine therapy. The results show that both drugs can adequately inhibit acid secretion in patients with gastric hypersecretory states. Both are safe at high doses, but ranitidine is threefold more potent and does not cause the antiandrogen side effects frequently seen with high doses of cimetidine.

Left anterior oblique projection and peak-to-scatter ratio for attenuation compensation of gastric emptying studies.

Compensation for soft-tissue attenuation is necessary for accurate quantitation of nuclear gastric emptying studies. We sought an attenuation compensation method that would require the acquisition of images from a single projection, thus allowing for continuous dynamic acquisition. We investigated the use of the left anterior oblique (LAO) projection and the peak-to-scatter ratio (P/S) method. Phantom studies indicated that the P/S was not only a function of the amount of overlying attenuating material but also a function of the activity in the small intestine. Two models for the P/S method were developed, one that considered the activity in the small intestine and one that did not. A series of 27 patients (21 for solid gastric emptying and six for liquid gastric emptying) were studied comparing the results using the geometric mean (GM) method with the two P/S methods, the LAO and the uncorrected anterior (ANT) projection. The uncorrected ANT view for solid gastric emptying underestimated the percent emptying at 60 min by approximately 7%. The P/S method did not adequately compensate for attenuation. The use of the LAO projection yielded results that were highly correlated and unbiased when compared to the GM method. Accurate estimates of liquid gastric emptying can be obtained without attenuation compensation.

The effect of the Garren-Edwards Gastric Bubble on solid and liquid gastric emptying.

To determine the effect of the Garren-Edwards Gastric Bubble (GEGB) on gastric emptying, radionuclide solid and liquid gastric emptying in 12 obese patients prior to insertion of the GEGB was studied. Four were restudied at one and seven days and ten patients were restudied at twelve weeks with the GEGB in place. There were no significant differences in liquid gastric emptying at one and seven days nor in solid and liquid gastric emptying at twelve weeks. Solid gastric emptying was significantly decreased from a mean of 63% to 31% after one day (P less than 0.05) and returned to preplacement baseline by seven days. These results indicate that gastric emptying is not significantly changed after twelve weeks with the GEGB in place. Therefore, the mechanism of action for weight reduction with the GEGB is not likely to be mediated by an effect on gastric emptying. However, the solid food-induced dyspeptic symptoms commonly noted 1-3 days after placement of the GEGB, which resolve within seven days, are probably explained by transiently delayed solid gastric emptying.

Cimetidine vs placebo: complete gastric ulcer pain relief. Six week controlled double blind study without any antacid therapy.

We studied the efficacy of cimetidine or placebo in relieving ulcer pain on 27 endoscopically-proven gastric ulcer outpatients in a randomized controlled prospective double blind trial. There were 12 patients in the cimetidine (1,200 mg daily) treated group and 15 patients in the placebo treated group. No antacid was allowed, but a placebo antacid with no neutralizing capacity was given as needed for pain. The incidence of complete pain relief at 2 and 4 weeks was 58% and 67% in the cimetidine treated patients, and 60% and 80% in the placebo treated patients. At 6 weeks of treatment there was no increase in the number of patients with complete pain relief in either group. There was no significant difference between the 2 groups in the incidence of ulcer pain relief at any of the 3 observation periods. Gastric ulcer healing rates and gastric ulcer pain relief were compared at 2 and 4 weeks. The cimetidine treated group healed 17% with 58% pain relief, and the placebo treated group had no ulcers healed at 2 weeks with 60% complete pain relief. There was no statistical association between ulcer healing and pain relief in both treatment groups at the 2 week evaluation period, but there was statistical association (P less than .05) at 4 weeks. The results of this study demonstrated that in gastric ulcer outpatients treated for 6 weeks: 1) the complete relief of gastric ulcer pain is not influenced by treatment with cimetidine when compared to placebo, and 2) there is no association between complete pain relief and the presence of an endoscopically proven gastric ulcer during the first 2 weeks of treatment with either cimetidine or placebo.

Azulfidine-induced oligospermia.

A patient with Crohn's ileitis was treated with azulfidine (4 gm./day) for 18 months. During the treatment period he was infertile with quantitative and qualitative abnormalities of his spermatozoa. Upon termination of the azulfidine, his semen analysis became normal and his wife subsequently became pregnant. In some patients there appears to be an effect of azulfidine on spermatogenesis that is completely reversible when the drug is withdrawn.

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion.

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.

Definition for idiopathic gastric acid hypersecretion. A statistical and functional evaluation.

Zollinger-Ellison syndrome and other gastric acid hypersecretory states in which a specific etiology is identified are defined as a basal acid output of greater than 15.0 meq/hr. To determine the level of basal acid output that defines idiopathic gastric hypersecretion, basal acid outputs were investigated in normal subjects and patients with duodenal ulcers, and functional and statistical definitions for idiopathic gastric acid hypersecretion were developed. Sixty-five normal subjects were evaluated to define idiopathic gastric acid hypersecretion on a statistical basis, and 22 patients with refractory duodenal ulcers were evaluated to define idiopathic gastric acid hypersecretion on a functional basis. Mean basal acid output for the 65 normal subjects was 3.0 +/- 2.7 meq/hr. Even though the mean basal acid output for the group of 28 normal male subjects was slightly higher than for the group of 37 normal female subjects, the groups were not significantly different. The 95% confidence interval around the mean basal acid output for all normal subjects was 2.4-3.7 meq/hr, with little difference between the male and female groups. The mean basal acid output plus two standard deviations and the mean basal acid output plus three standard deviations for the 65 normal subjects were 8.4 meq/hr and 11.1 meq/hr, respectively. Of 109 patients with active duodenal ulcers treated for eight weeks with standard doses of antisecretory medication, 22 showed no healing as documented by endoscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Ranitidine therapy in patients with idiopathic gastric acid hypersecretion. A prospective study.

One hundred twenty-four patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) were prospectively evaluated and treated with ranitidine twice a day. Fifty-four patients (44%) required standard doses of ranitidine 300 mg/day for adequate treatment, and the other 70 patients (56%) required increased doses of ranitidine (mean 994 mg/day, range 600-3000 mg/day). Mean basal acid outputs for these two groups were 14.0 and 16.6 meq/hr, respectively, which were not significantly different. Nevertheless, there was a significant correlation between basal acid output and daily ranitidine dose required for therapy (r = 0.18, P = 0.05). The duration of ranitidine therapy consisted of: < 1 year (N = 46), 1 year (N = 16), 2 years (N = 19), 3 years (N = 22), 4 years (N = 15), 5 years (N = 6). Only five patients required progressive increases in ranitidine during the time of treatment, which consisted of an average of 0.5 dose adjustments per year. No side effects occurred with any of these high doses of ranitidine. These results indicate that, as in Zollinger-Ellison syndrome, ranitidine is effective therapy for patients with idiopathic gastric acid hypersecretion; however, markedly increased doses as large as 3000 mg/day may be required.

Idiopathic gastric acid hypersecretion. Comparison with Zollinger-Ellison syndrome.

Many patients with acid-peptic disease have idiopathic gastric acid hypersecretion defined as a basal acid output > 10.0 meq/hr; however, a significant proportion have basal acid outputs > 15.0 meq/hr, which is within the range found in Zollinger-Ellison syndrome. Although idiopathic gastric acid hypersecretion is more common than Zollinger-Ellison syndrome, it is important that these two disorders be differentiated because of differences in treatment and natural history. In the present study, we compared 124 patients with idiopathic gastric acid hypersecretion and 137 patients with Zollinger-Ellison syndrome. There were no significant differences with regard to age at diagnosis, history of upper gastrointestinal hemorrhage, nausea, vomiting, and family history of duodenal ulcer and other acid-peptic disease. However, significant differences were observed between patients with idiopathic gastric acid hypersecretion and patients with Zollinger-Ellison syndrome with regard to percentage of males: 77% compared to 64% (P = 0.008), mean serum gastrin: 60 pg/ml compared to 3679 pg/ml (normal < 100 pg/ml) (P < 0.001), mean basal acid output: 15.4 meq/hr compared to 47.0 meq/hr (P < 0.001), mean age at onset of symptoms: 33 years compared to 41 years (P < 0.001), mean duration of symptoms before diagnosis: 11 years compared to five years (P < 0.001), percentage with abdominal pain: 67% compared to 82% (P = 0.00004), percentage with diarrhea: 12% compared to 75% (P < 0.000001), percentage with pyrosis: 58% compared to 40% (P = 0.003), percentage with duodenal ulcer: 53% compared to 74% (P < 0.000001), and percentage with esophagitis: 31% compared to 42% (P = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Basal gastric acid secretion in nonulcer dyspepsia with or without duodenitis.

Nonulcer dyspepsia with or without duodenitis and duodenal ulcer disease are often considered to be a spectrum of the same acid-peptic process. Some reports evaluating basal gastric acid secretion in nonulcer dyspepsia and duodenal ulcer disease have supported that impression; however, results from different studies have been mixed. In order to compare basal gastric secretory profiles in nonulcer dyspepsia and duodenal ulcer disease, we determined basal acid outputs in 66 consecutive patients with the diagnosis of nonulcer dyspepsia. All patients with nonulcer dyspepsia had at least a three-month history of epigastric abdominal pain, and all had negative upper gastrointestinal endoscopies except for 14 with duodenitis. The 66 patients with nonulcer dyspepsia were compared to 40 asymptomatic normal subjects and 114 patients with endoscopically documented duodenal ulcer disease. There was no significant difference in mean basal acid output among all 66 patients with nonulcer dyspepsia (2.9 +/- 2.7 meq/hr), the group of normal subjects (3.2 +/- 2.7 meq/hr), the 14 patients with nonulcer dyspepsia with duodenitis (3.0 +/- 2.1 meq/hr), and the 52 patients with nonulcer dyspepsia without duodenitis (2.9 +/- 2.9 meq/hr). However, mean basal acid output of the patients with duodenal ulcer disease (9.1 +/- 7.6 meq/hr) was significantly higher than all the other groups (P less than 0.001). The gastric acid secretory profiles determined in this study do not appear to support the view that nonulcer dyspepsia with or without duodenitis and duodenal ulcer disease are a spectrum of the same acid-peptide process.

Comparison of omeprazole and ranitidine in treatment of refractory gastroesophageal reflux disease in patients with gastric acid hypersecretion.

Secretion of gastric acid and volume, serum gastrin concentration, and ambulatory 24-hr esophageal pH monitoring were evaluated prospectively in 12 patients with idiopathic gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr) undergoing treatment for refractory chronic long-standing pyrosis. Treatment lasted six months and consisted of three months of ranitidine (mean 2150 mg/day, range 1200-3000 mg/day), followed by three months of omeprazole (mean 33 mg/day, range 20-60 mg/day). Both ranitidine and omeprazole significantly reduced gastric acid output (P less than 0.001) and gastric volume output (P less than 0.001) compared to a basal evaluation and resulted in complete disappearance of pyrosis. Total reflux time (percent 24 hr intraesophageal pH less than 4) was significantly reduced by ranitidine (P less than 0.02) and omeprazole (P less than 0.001) compared to basal evaluation; however, the effects of omeprazole were significantly greater than ranitidine (P less than 0.05). Omeprazole caused a significant increase in serum gastrin concentration compared to both basal and ranitidine (P less than 0.05). Endoscopically documented erosive esophagitis was present in nine of the 12 patients, and seven of the 12 patients had Barrett's epithelium. All 12 patients had complete resolution of pyrosis and healed esophagitis by six months, but no significant endoscopic regression was observed in the extent of Barrett's epithelium. No side effects occurred with these high doses of ranitidine or omeprazole. These results indicate that high-dose ranitidine and omeprazole are effective therapy for refractory gastroesophageal reflux disease. However, with omeprazole, total reflux times are reduced more than with ranitidine, often into the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation between basal acid output and daily ranitidine dose required for therapy in Barrett's esophagus.

We prospectively evaluated basal gastric acid secretion in 42 consecutive patients with Barrett's esophagus to determine the optimal dose requirement for an H2-receptor antagonist in relation to the gastric acid secretory status of each patient. All patients with Barrett's esophagus had pyrosis and 31 of the 42 patients had erosive esophagitis. Mean extension of Barrett's epithelium was 6.9 cm (range 2-17 cm). Mean basal acid output for the patients with Barrett's esophagus was 8.0 +/- 5.2 meq/hr, which was significantly different compared to a group of 65 normal subjects with mean basal acid output of 3.0 +/- 2.7 meq/hr (P less than 0.001). There was no correlation between basal acid output and extension of Barrett's epithelium. All patients with Barrett's esophagus were treated with ranitidine, with 24 requiring standard-dose (300 mg/day) and 18 requiring increased doses (mean 1170 mg/day, range 600-2400 mg/day) for complete healing of esophagitis and disappearance of pyrosis. There was a significant correlation between basal acid output and daily ranitidine dose required for therapy (r = 0.52, P less than 0.001). Fifteen of the 42 patients with Barrett's esophagus (36%) had gastric acid hypersecretion. There was a significant association between gastric acid hypersecretion defined as a basal acid output of greater than 10.0 meq/hr and a requirement for increased daily ranitidine doses (greater than 300 mg/day) (P less than 0.0002). No side effects occurred with any of these high doses of ranitidine. We conclude that as a group, patients with Barrett's esophagus have significantly higher basal acid outputs than normal subjects and many require increased therapeutic doses of ranitidine.(ABSTRACT TRUNCATED AT 250 WORDS)

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastroesophageal reflux disease in the elderly: more severe disease that requires aggressive therapy.

OBJECTIVE: To evaluate gastroesophageal reflux disease in the elderly (people > or = 60 yr). METHODS: Basal gastric acid secretion was prospectively determined in 228 consecutive patients with symptomatic gastroesophageal reflux disease who had upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (n = 98), erosive esophagitis (n = 87), or Barrett's esophagus (n = 43). RESULTS: Patients > or = 60 yr (n = 66) had significantly more esophageal mucosal disease (erosive esophagitis, Barrett's esophagus) than patients < 60 yr (n = 162)--81% versus 47% (p = 0.000002, Fisher's exact test). Furthermore, 87% of patients > or = 70 yr had esophageal mucosal disease. For each decade from < 30 yr to > or = 70 yr, there was a significant increase in esophageal mucosal disease (p = 0.002; chi 2 test, 23.96); however, there were no significant differences in severity of pyrosis symptoms or in mean basal acid output for each decade. When 146 of the 228 patients with gastroesophageal reflux disease were given enough ranitidine (mean, 630 mg/d; range, 300-3000 mg/d) for the relief of all pyrosis symptoms and healing of all esophageal mucosal disease, there were no significant differences in ranitidine therapy between each decade. CONCLUSIONS: Elderly patients with pyrosis symptoms severe enough to require upper gastrointestinal endoscopy have gastroesophageal reflux disease with more esophageal mucosal disease (erosive esophagitis, Barrett's esophagus) than patients < 60 yr, and like younger patients, may require markedly increased doses of ranitidine as large as 2400 mg/d for effective therapy.

Giant duodenal ulcer. Evaluation of basal acid output, nonsteroidal antiinflammatory drug use, and ulcer complications.

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.

Basal acid output and gastric acid hypersecretion in gastroesophageal reflux disease. Correlation with ranitidine therapy.

The purpose of this study was to evaluate possible differences in basal gastric acid secretion with regard to severity of gastroesophageal reflux disease. Basal acid output was determined by nasogastric suction in 228 patients with gastroesophageal reflux disease who received upper gastrointestinal endoscopy and were diagnosed with either pyrosis alone (N = 98), erosive esophagitis with or without pyrosis (N = 87), or Barrett's esophagus (N = 43). Mean basal acid output for the 228 patients with gastroesophageal reflux disease was 6.5 +/- 5.6 meq/hr, which was significantly different from 65 normal subjects with a mean basal acid output of 3.0 +/- 2.7 meq/hr (P < 0.0001). Compared to normal subjects, mean basal acid outputs significantly differed for patients with pyrosis (P < 0.05), esophagitis (P < 0.01), and Barrett's esophagus (P < 0.01). There was also a significant difference in mean basal acid output between the patients with pyrosis and Barrett's esophagus (P < 0.01). Nineteen of the 98 patients with pyrosis (19%), 24 of the 87 patients with esophagitis (28%), and 15 of the 43 patients with Barrett's esophagus (35%) had gastric acid hypersecretion (basal acid output greater than 10.0 meq/hr). One hundred forty-six patients with gastroesophageal reflux disease were treated with ranitidine in doses that resulted in complete healing of esophagitis and disappearance of pyrosis. Ninety-three patients responded to ranitidine 300 mg/day; however, 53 patients required increased dose of ranitidine (mean 1205 mg/day, range 600-3000 mg/day).(ABSTRACT TRUNCATED AT 250 WORDS)

Age does not affect basal gastric acid secretion in normal subjects or in patients with acid-peptic disease.

OBJECTIVES: To determine whether basal acid output was affected by patient age. METHODS: Basal acid output determined by nasogastric suction was prospectively evaluated in normal subjects (n = 65) and patients with gastroesophageal reflux disease (n = 228), gastric ulcer (n = 81), duodenal ulcer (n = 184), and nonulcer dyspepsia (n = 105). RESULTS: There was no correlation between basal acid output and age for the normal subjects and the patients with gastroesophageal reflux disease, gastric ulcer, duodenal ulcer, and nonulcer dyspepsia. However, there was a significant inverse correlation between age and basal acid output for the 33 male patients with gastric ulcer (r = -0.41, p < 0.05) and the 130 male patients with duodenal ulcer (r = -0.18, p = 0.05). Furthermore, mean basal acid outputs were significantly higher for male patients than for female patients with gastroesophageal reflux disease (p < 0.001), gastric ulcer (p < 0.05), and duodenal ulcer (p < 0.001). Mean basal acid output for the 184 patients with duodenal ulcer was significantly higher than the mean basal acid output for the 228 patients with gastroesophageal reflux disease (p < 0.001), and both were significantly higher than mean basal acid outputs for the normal subjects and the patients with gastric ulcer and nonulcer dyspepsia (p < 0.0005). CONCLUSIONS: Basal acid output can vary with gender and acid-peptic disease process; however, basal acid output does not vary with regard to age of subject.