Acid Secretion In Patients Research Articles

Effects of Helicobacter pylori Eradication on Gastric Function Indices in Functional Dyspepsia: A Prospective Controlled Study

Background: To date, it is unclear whether Helicobacter pylori infection is associated with disturbances of gastric emptying or acid secretion in patients with functional dyspepsia (FD). Our aim was to investigate whether, in the long run, cure of H. pylori infection significantly influences gastric emptying of solids, acid secretion, and gastrin and pepsinogen I (PGI) release in patients with FD. Methods: Thirty-eight consecutive H. pylori-positive patients with FD, whose complaints were scored for severity and frequency on the basis of a validated symptom questionnaire, were initially enrolled in the study. They were randomized to receive an eradicating regimen consisting of omeprazole plus clarithromycin and tinidazole for 1 week or full-dose ranitidine for 3 weeks. In 33 patients (18 H. pylori-cured and 15 with persistent infection) basal and pentagastrin-stimulated acid secretion, fasting and meal-induced gastrin concentrations, fasting serum PGI levels, and gastric emptying of solids were determined before and 6 months after therapy. Results: In the 18 H. pylori

The acid response to gastrin distinguishes duodenal ulcer patients from Helicobacter pylori–infected healthy subjects

Background & Aims: Helicobacter pylori–induced hypergastrinemia is accompanied by increased acid secretion in patients with duodenal ulcer (DU) but not in infected healthy volunteers. The aim of this study was to investigate the mechanism underlying this difference. Methods: Thirty-four H. pylori–negative and 20 H. pylori–positive healthy volunteers and 15 H. pylori–positive patients with DU were studied. Maximal acid output and sensitivity to gastrin (gastrin concentration required to achieve 50% maximal acid output) were assessed by examining the dose response to gastrin 17. Inhibitory control was tested by comparing the maximal acid response to cholecystokinin octapeptide with that for gastrin 17. Results: Sensitivity to gastrin was similar in patients with DU (median, 69.5 ng · L −1; range, 26.2-142) and H. pylori– negative healthy volunteers (median, 82.2 ng · L minus;1; range, 17.7-410); H. pylori–positive healthy volunteers were less sensitive than either (164.5 ng · L minus;1; range, 44.8 to >3360 ng · L −1). Patients with DU had higher maximal acid output (51.2 mmol · h minus;1; range, 30.8-73.7 mmol · h −1) than either infected healthy volunteers (37.8 mmol · h −1; range, 0.0-65.0 mmol · h −1; P< 0.04) or uninfected healthy volunteers (35.3 mmol · h −1; range, 21.3-67.3 mmol · h −1; P < 0.002). The maximal acid output in both groups of healthy subjects was similar. The proportion of maximal acid output to gastrin 17 achieved by cholecystokinin was similar in patients with DU (36.6%; range, 21.5%-58.2%) and H. pylori–negative healthy volunteers (28.7%; range, 5.9%-85.8%). Conclusions: A combination of decreased sensitivity to gastrin in infected healthy volunteers and increased maximal acid secretory capacity in patients with DU underlies their different acid response to H. pylori–induced hypergastrinemia. GASTROENTEROLOGY 1998;114:50-57

How Does Helicobacter pylori Cause Mucosal Damage? Its Effect on Acid and Gastrin Physiology

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor a and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor α in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1β, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.

Parietal cell vagotomy performed with fundoplication for esophageal reflux

Reduction of acid secretion is an important aspect of medical treatment of reflux esophagitis. Truncal vagotomy and drainage procedures used in conjunction with antireflux procedures to reduce acid secretion in patients with gastroesophageal reflux were unsatisfactory. This study reviews the results of parietal cell vagotomy used in conjunction with a 360-degree fundoplication to determine if reduction of acid by this form of vagotomy was beneficial to patients with gastroesophageal reflux. Between March 1973 and May 1993, 94 private and 64 Veterans Administration patients underwent parietal cell vagotomy and Nissen type fundoplication for esophageal reflux. Esophagogastroduodenoscopy (EGD), gastric analysis, cine-esophagogram, and 24-hour esophageal pH and motility studies were performed preoperatively on VA patients. Private patients underwent EGD, cine-esophagogram, and sometimes pH and motility studies. Similar studies were performed postoperatively if the patient permitted. The major technical alteration made during the study was the addition of posterior gastropexy to the operations performed between March 1978 and January 1987. Patients were considered failures if dysphagia and reflux symptoms were moderate but operation not contemplated (Visick III) or symptoms were severe and reoperation had been performed or was contemplated (Visick IV). There were no operative deaths. There were 25 operative failures; dysphagia contributed to failure in 4, reflux in 11, and dysphagia and reflux in 10 patients. Reoperation was required in 6 patients. There was no statistical difference in acid secretion inhibition for patients with or without postoperative reflux symptoms. The cumulative probability for operative failure was 9.3 +/- SE 4.2% for patients who underwent posterior gastropexy and 22.9 +/- SE 4.6% (P <0.02) for those who did not. Parietal cell vagotomy with Nissen fundoplication is a safe operation. The exposure created by PCV protected the vagi from injury. The study design made it impossible to determine whether PCV improved the results of fundoplication but the failure rate was significantly (P <0.02) reduced by the addition of posterior gastropexy. This may have lessened the risk of disintegration of the wrap that might be more likely to occur after PCV.

Cure of Helicobacter pylori Infection Improves Gastric Acid Secretion in Patients with Corpus Gastritis

Background: For more than 30 years it has been known that gastric acid secretion is inversely related to the extent and severity of corpal gastritis. We therefore evaluated the effect of cure of Helicobacter pylori infection on basal and pentagastrin-stimulated acid secretion. Methods: Basal acid output (BAO) and maximal acid output (MAO) were assessed in 11 H. pylori-infected dyspeptic patients (8 women and 3 men; mean age, 28 years) before and after successful anti-H. pylori therapy. Results: The gastritis index was significantly lower after therapy and was associated with an increase in both BAO and MAO after cure of the H. pylori infection (BAO from 0.3 mmol/h to 3.1 mmol/h and MAO from 4.8 mmol/h to 19 mmol/ h). Basal and stimulated acid concentrations also increased (29.1 ± 36.6 to 54 ± 31 mmol/1 and 72.5 ± 46 to 120.1 ± 30 mmol/1, respectively, for basal and stimulated acid concentrations; P < 0.05 for peak and MAO, P = 0.07 for BAO). Conclusion: Gastric acid secretion increased into the normal range after successful treatment of, pylori infection, suggesting that gastric function can recover to normal or almost normal after cure of H. pylori infection.

Evaluation of 24-hour gastric acidity in patients with hepatic cirrhosis

Background/Aims: Data from previous studies on gastric acid secretion in patients with hepatic cirrhosis are controversial, due, at least in part, to the possible interference of liver failure and altered gastric mucosal microcirculation on the pharmacological action of the substances used to stimulate the parietal cell. For this reason, we wished to investigate the circadian pattern of gastric acidity by means of continuous 24-hour pH monitoring, which permits measurement of pH fluctuations in a nearly physiological manner and does not require any pharmacological stimulus. Methods. Forty-nine patients with liver cirrhosis of different aetiology were recruited for this study. They underwent 24-hour gastric pH-metry with an eletcrode positioned in the gastric corpus, and their pattern of gastric acidity was compared with that of 49 healthy subjects, matched for age and sex. In a subgroup of 31 patients with cirrhosis, antral pH was recorded in addition to body pH in order to assess whether there are regional differences in gastric acidity. Results. The circadian, daytime and nocturnal gastric acidity of patients with cirrhosis was significantly lower ( p<0.05-0.001) than that of contr ls. In the 31 patients studied with two electrodes, antral pH was higher ( p<0.05) than body pH only during the night. The prevalence of Helicobacter pylori infection was rather low (42%) in our patients. Conclusions. There is a marked hypoacidity over the circadian cycle in patients with cirrhosis compared to controls, and the greatest difference between them is visible during the nocturnal hours. Also, in patients with liver cirrhosis the pH in the antrum is higher than that in the body of the stomach during the night for reasons that need to be elucidated.

Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease

Background & Aims : The mechanism by which Helicobacter pylori predisposes to duodenal ulcers (DUs) remains unclear. The aim of this study was to investigate the effect of the infection on acid secretion. Methods : Acid output was examined basally and in response to gastrin-releasing peptide (GRP) and gastrin in healthy volunteers with and without H. pylori infection and in patients with DUs before and after eradication of the infection. Results : Compared with H. pylori-negative healthy volunteers, patients with DUs with H. pylori had the following abnormalities of acid secretion: (1) threefold increase in basal acid output, (2) sixfold increase in acid response to GRP, (3) increased maximal acid response to exogenous gastrin, (4) increased ratio of basal acid output to maximal gastrin-stimulated output, and (5) increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output. All of these abnormalities resolved fully after H. pylori eradication except for increased maximal acid output to gastrin, which was unchanged. Infected healthy volunteers showed a threefold increase in acid response to GRP that resolved after eradication of H. pylori infection. Conclusions : These disturbances in acid secretion caused by H. pylori infection are consistent with impaired inhibitory control and are likely to be relevant to the mechanism by which the infection predisposes to DU.

Suppression of acid secretion in peptic ulcer disease.

Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic drugs had only modest inhibitory effects on acid secretion, many side effects, and uncertain efficacy. Controlled trials using antacids demonstrated the value of reducing gastric acidity for healing duodenal ulcer. The discovery of histamine-2 (H2) receptor antagonists in the 1970s and the introduction of H+,K(+)-ATPase inhibitors in the 1980s made reduction of acid secretion the first-choice modality for healing and preventing recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from the stomach. However, antibiotic eradication of Hp can be difficult, often requiring simultaneous administration of a drug that suppresses acid secretion. Therefore, H2 and proton pump inhibitors continue to play a role in the management of duodenal and gastric ulcers associated with Hp and also play a primary role in the therapy of other acid-related disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gastrinoma (Zollinger-Ellison syndrome) and other acid hypersecretory states.

Parenteral control of gastric acid hypersecretion in patients with Zollinger-Ellison syndrome

Parenteral control of gastric acid hypersecretion in patients with Zollinger-Ellison syndrome is increasingly required; however, existing methods of determining the required dose are cumbersome and not applicable in all centers. A previous study suggested that the required parenteral dose of histamine H2-receptor antagonists correlated with the previous oral dose. In the present study, in 31 patients with Zollinger-Ellison syndrome we evaluated the hypothesis that an effective parenteral histamine H2-receptor antagonist dose could be predicted from the previous oral dose. Twenty-three patients were taking oral ranitidine (mean 1.3 g/day), six patients famotidine (152 mg/day), and two patients cimetidine (1.8 g/day). Each patient was treated with a continuous intravenous infusion of the equivalent dose of ranitidine (mean dose 1 mg/kg/hr with 35% requiring 0.5 mg/kg/hr, 49% 1 mg/kg/hr, 3% 1.5 mg/kg/hr, 10% 2 mg/kg/hr, and 3% 2.5 mg/kg/hr. This dose of ranitidine acutely controlled acid secretion (< 10 meq/hr) in all patients. To evaluate long-term efficacy and safety, 20 patients were maintained on this dose through the peri- and postoperative periods. Mean duration was 7.1 days with 25% treated 3-5 days, 40% 6-8 days, 30% 8-10 days, and 5% > 10 days. The predicted dose continued to control acid secretion in 95% of patients with one patient requiring one dose adjustment. No biochemical, clinical, or hematological toxicity was seen, although ranitidine was stopped in one patient because of skin rash. These results demonstrate that the parenteral dose of ranitidine required to control acid secretion in patients with Zollinger-Ellison syndrome can be predicted from the oral dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Flow cytometry and Zollinger-Ellison syndrome: Relationship to clinical course

Background: With successful means of controlling gastric acid secretion in patients with Zollinger-Ellison syndrome, the gastrinoma itself is becoming the major determinant of long-term survival. No methods have yet been described to predict which tumors will have more malignant courses thereby indicating which patients should undergo aggressive surgery or antitumor therapy. Because DNA analysis, using flow cytometry, has proved helpful in this regard in other tumors, the current study was designed to evaluate its utility in gastrinoma patients. Methods: Flow cytometry was performed on 81 paraffin-embedded gastrinoma specimens from 59 patients. Results were compared with preoperative patient characteristics, findings at surgery, and postoperative follow up. Results: Tumors were diploid in 54% of patients, near diploid in 15%, pure tetraploid in 0%, nontetraploid aneuploid in 25%, and multiple stem line aneuploid in 5%. All patients with multiple stem line aneuploid tumors had widespread metastases whereas all patients with nontetraploid aneuploid tumors had localized or regional disease. Median S phase percentage was 3.6. S phase percentages were higher in patients with widespread metastatic disease than in patients with localized or regional disease. Disease extent also correlated closely with fasting serum gastrin level. After removing this variable with logistic regression analysis, the significant correlation between disease extent and DNA analysis persisted. Conclusions: DNA analysis of gastrinoma tissue specimens correlates independently with the extent of disease and may be useful in planning therapeutic strategies for patients with Zollinger-Ellison syndrome.

The enterochromaffin-like (ECL) cell. Physiological and pathophysiological role.

Histamine has a central role in the regulation of gastric acid secretion. This histamine is produced by and released from the enterochromaffin-like (ECL) cell which accordingly has a key-regulatory role in the oxyntic mucosa. Gastrin and the vagal nerves stimulate the formation and release of histamine from the ECL cell. Moreover, gastrin and the vagal nerves also stimulate the proliferation of the ECL cell. An increased ECL cell density may partly explain the increased acid secretion in patients with duodenal ulcer, particularly in patients with Zollinger-Ellison syndrome. The reduced potency of histamine-2 blockers in patients with Zollinger-Ellison syndrome is probably due to increased histamine release by an elevated ECL cell mass. Prolonged and profound hypergastrinemia may lead to ECLomas. Moreover, a proportion of diffuse gastric carcinomas may originate from ECL cells.

Omeprazole

Omeprazole is the first of a new class of drugs, the acid pump inhibitors, which control gastric acid secretion at the final stage of the acid secretory pathway and thus reduce basal and stimulated acid secretion irrespective of the stimulus. In patients with duodenal or gastric ulcers, omeprazole as a single 20 mg daily dose provides more rapid and complete healing compared with ranitidine 150 mg twice daily or 300 mg at nighttime, or cimetidine 800 or 1000 mg/day. Patients poorly responsive to treatment with histamine H2-receptor antagonists respond well to omeprazole--most ulcers healed within 4 to 8 weeks of omeprazole 40 mg/day therapy. Omeprazole 20 or 40 mg/day has been administered as maintenance therapy for peptic ulcer disease for up to 5.5 years with very few ulcer recurrences. In patients with erosive or ulcerative oesophagitis, omeprazole 20 or 40 mg/day produces healing in about 80% of patients after 4 weeks, and is superior to ranitidine with respect to both healing and symptom relief. Healing rates of greater than 80% are achieved after 8 weeks in patients with severe reflux oesophagitis unresponsive to H2-receptor antagonists. Maintenance therapy with a daily 20 mg dose prevents relapse in about 80% of patients over a 12-month period. Omeprazole is considered to be the best pharmacological option for controlling gastric acid secretion in patients with Zollinger-Ellison syndrome. Daily dosages of 20 to 360 (median 60 to 70 mg successfully reduce basal acid output to target levels (less than 10 mmol/h or less than 5 mmol/h in patients with severe oesophagitis or partial gastrectomy) during treatment for up to 4 years. Omeprazole is well tolerated in short term studies (up to 12 weeks); the reported incidence of serious side effects (about 1%) being similar to that seen in patients treated with an histamine H2-receptor antagonist. The longer term tolerability of omeprazole has been investigated in patients treated for up to 5.5 years. Slight hyperplasia, but no evidence of enterochromaffin-like (ECL) cell dysplasia or neoplasia or ECL cell carcinoids has been reported. ECL cell carcinoids have been observed in rats after life-long treatment with high doses of omeprazole or ranitidine, or in rats with partial corpectomy; the weight of experimental evidence indicates that this is a result of prolonged hypergastrinaemia.(ABSTRACT TRUNCATED AT 400 WORDS)

Use of omeprazole in patients with Zollinger-Ellison syndrome

Omeprazole, a substituted benzimidazole, has been shown to be a potent inhibitor of gastric acid secretion in patients with Zollinger-Ellison syndrome (ZES). We review our experience, as well as the published data on 210 patients with ZES who have required omeprazole for control of gastric acid hypersecretion over the past seven years. The dose of omeprazole required in individual patients ranged from 10 to 180 mg/24 hr with 20-60% requiring a split dosage regimen. Omeprazole was effective in approximately 99% of the patients over a period ranging from 0.5 to 54 months. Twenty-four percent of patients required an increase in omeprazole dose, while 26% required a decrease in dose. Adverse effects attributable to omeprazole were reported in 2% of patients, and in all cases, they were mild (ie, rash, constipation, headache). There was no effect of omeprazole on serum gastrin concentration or on gastric endocrine cells in three studies. Although one patient with multiple endocrine neoplasia, type-I syndrome (MEN-I) in this series developed a gastric carcinoid while taking omeprazole, evidence is presented that suggests the presence of MEN-I per se may be important in determining the development of gastric carcinoid in patients with ZES. It is concluded that omeprazole is safe and effective in patients with ZES, and in these patients, it is the drug of choice for the management of gastric acid hypersecretion. However, yearly assessment is indicated to clearly evaluate the long-term risk of gastric carcinoid as well as therapy directed at the gastrinoma itself.

Role of acid suppressants in patients with Zollinger–Ellison Syndrome

Virtually all symptoms in patients with Zollinger-Ellison syndrome are due to acid hypersecretion, thus the control of acid secretion is the first and most important step in the management of patients with this syndrome. Antisecretory medication is prescribed as soon as the diagnosis of Zollinger-Ellison syndrome is made, as patients may bleed or perforate with little warning. Acid output is reduced to less than 10 mmol/h to heal mucosal lesions, but in patients with a Billroth I or II gastrectomy and those with severe oesophagitis and stricture formation, acid output is reduced to less than 5 or less than 1 mmol/h. Acid output and not symptomatic response is a reliable guide of the adequacy of therapy. In sufficient doses, all H2-receptor antagonists are useful; however, side effects associated with cimetidine therapy limit its use. The ratio of potencies of cimetidine:ranitidine:famotidine is 1:4:32. Ranitidine given as a 50-mg intravenous bolus, followed by a continuous infusion of 0.5 mg.kg/h, controls acid hypersecretion acutely in patients with Zollinger-Ellison syndrome. Acid output is checked after 4 h, and the dose increased until acid output is less than 10 mmol/h. In 70% of patients with Zollinger-Ellison syndrome, 1 mg.kg/h reduces acid output to less than 10 mmol/h; however, doses up to 4 mg.kg/h have been used. When patients are switched to oral ranitidine, a useful dosage conversion is to administer 1.5 times the total daily intravenous dose in four equal doses every 6 h. Four doses of oral drug are given before the infusion is stopped. Six hours after the first/last oral dose, acid output is checked. In our patients, the mean dose of ranitidine was 2100 mg/day (range, 450-9200 mg/day). No serious toxicity was observed. Omeprazole, which has a long duration of action and is a potent inhibitor of gastric acid secretion, has simplified management. Once-daily dosing is sufficient in most patients, and a reasonable starting dose is 60 mg daily. The dose may be increased to 120 mg once daily; if this dosage fails to control acid secretion, 60 mg is administered every 12 h. In our studies, the median dose was 90 mg/day (range, 20-120 mg/day). Omeprazole was more effective than H2-receptor antagonists in providing symptom relief and mucosal healing and did not cause significant toxicity. In particular, no gastric carcinoid tumours developed during four years of use. Omeprazole is, therefore, the treatment of choice for control of acid secretion in patients with Zollinger-Ellison syndrome.(ABSTRACT TRUNCATED AT 400 WORDS)

Stress ulceration in the intensive care unit: use of H2‐receptor antagonists

H2-receptor antagonist drug therapy is the mainstay of peptic ulcer treatment in the USA. About 75% of patients in intensive care units receive parenteral H2-antagonists. The rationale for their use is that parenteral H2-antagonists offer about a four-fold protective effect compared with placebo against significant upper gastrointestinal haemorrhage. Parenteral administration of H2-receptor antagonists appears to be preferred to oral antacid or sucralfate regimens because of ease of administration and, perhaps, lower treatment costs. Recommended dosage schedules for intravenously administered H2-receptor antagonists are at fixed intervals, 6- to 8-h intervals for cimetidine and ranitidine and 12-h intervals for famotidine. These dosage schedules assume a fixed dose-response relationship (i.e. a given dose of H2-antagonist results in equivalent acid suppression throughout the circadian, or 24-h, period). However, human basal gastric acid secretion exhibits circadian variation, with peak rates occurring during the evening hours. Recent evidence from 24-h continuous intragastric pH studies in fasting patients with healed duodenal ulcer suggests that larger doses of intravenous H2-antagonists are required in the evening than in the morning to achieve equivalent acid suppression. These findings are consistent with a changing H2-antagonist dose/acid-inhibiting response over the circadian period. Continuous infusion has the advantage of providing consistent and sustained suppression of gastric acid secretion in patients at risk for stress ulceration. Results of a double-blind, randomized, crossover study indicated that equally effective suppression of acidity and time-to-onset of pharmacological effect can be achieved with and without priming bolus doses of ranitidine, and presumably other H2-receptor antagonists as well.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty‐four‐hour intragastric acidity and nocturnal gastric secretion in gastric ulcer patients—the effects of cimetidine

In a double-blind randomized study, the profile of 24-h intragastric acidity and nocturnal gastric secretion was measured in a group of patients with healed gastric ulcer on placebo and 400 mg cimetidine b.d. and 800 mg nocte. Neither cimetidine regimen significantly decreased daytime intragastric acidity, but the 800 mg nocte dose caused a significant decrease in both nocturnal acidity (18.1 to 5.5 mmol/L; P less than 0.05) and acid output (11.0 to 1.7 mmol 7 h; P less than 0.05). The decrease in nocturnal gastric secretion by 400 mg cimetidine b.d. was not significant. As in duodenal ulcer, 800 mg cimetidine nocte will effectively suppress night-time acid secretion in patients with gastric ulcer while leaving acid secretion during the day unaffected.

Elevated gastric acid secretion in patients with Barrett's metaplastic epithelium.

Gastric acid secretion in response to a protein meal and to exogenously administered synthetic human gastrin 17-I was measured in patients with Barrett's esophagus, patients with uncomplicated gastroesophageal reflux, and normal age- and sex-matched controls. Acid secretion, both basally and in response to gastrin 17-I, was significantly greater in patients with Barrett's esophagus compared to normal individuals without reflux. Basal gastrin levels and meal-stimulated levels of the hormone were similar among all three groups. Sensitivity to gastrin, expressed as the concentration causing half-maximal acid secretion, was also similar among the study groups. It is speculated that elevated basal acid production in Barrett's esophagus may contribute to the pathogenesis of the disorder.

Effect of smoking on gastric acid secretion in patients with duodenal ulcer

The effect of smoking on gastric secretion was studied in 15 consecutive patients with duodenal ulcer--six normosecretors (basal acid output less than or equal to 3 mEq/h), and nine hypersecretors (basal acid output greater than 3 mEq/h). The volume, acid output, acid concentration, and pH of the gastric juice measured before, during and after 1 h of smoking did not show any significant difference in these patients taken as a single group, or when the normosecretors and hypersecretors were analysed as separate groups (P greater than 0.05 for each parameter in each group). The higher acid output before and during smoking in hypersecretors than in normosecretors was due to the higher acid concentration in the gastric juice (P less than 0.01). Study of the pH curves of the gastric juice after acute smoking showed that hypersecretors had a lower pH for a longer duration compared with normosecretors. This could make the hypersecretors with a history of chronic smoking more prone to developing duodenal ulcer.

Gastrointestinal transit and gastric acid secretion in patients with achalasia

Previous studies suggest that patients with achalasia exhibit degenerative changes of extraesophageal nerve fibers. We investigated whether these morphological alterations are associated with functional abnormalities of the gastrointestinal tract. Patients with achalasia had a normal acid secretory response (5.5 +/- 1.5 mmol/hr) to vagal stimulation when compared to controls (6.0 +/- 5.3 mmol/hr). However, the half time of gastric emptying of liquids was significantly shorter in patients with achalasia (10.4 +/- 1.8 min) than in control subjects (19.3 +/- 11.3 min) (P less than 0.01). Although there was a tendency towards a more rapid gastrointestinal transit in patients with achalasia, these changes failed to reach statistical significance. It is concluded that patients with achalasia have a gastric emptying disorder that could either be explained by a selective defect of extraesophageal vagal inhibitory nerve fibers or as an epiphenomenon occurring as a consequence of impaired esophageal emptying.

Loss of Efficacy of Famotidine in the Control of Gastric Acid Secretion in Patients with Zollinger-Ellison Syndrome Reversed by Omeprazole

(1989). Loss of Efficacy of Famotidine in the Control of Gastric Acid Secretion in Patients with Zollinger-Ellison Syndrome Reversed by Omeprazole. Scandinavian Journal of Gastroenterology: Vol. 24, No. sup166, pp. 180-180.