Maximal Acid Output Research Articles

Gastro-oesophageal reflux disease in Asia.

Gastro-oesophageal reflux disease (GORD) occurs more frequently in Europe and North America than in Asia but its prevalence is now increasing in many Asian countries. Many reasons have been given for the lower prevalence of GORD in Asia. Low dietary fat and genetically determined factors, such as body mass index and maximal acid output, may be important. Other dietary factors appear to be less relevant. Increased intake of carbonated drinks or aggravating medicines may influence the increasing rates of GORD in some Asian countries but no strong evidence links other factors, such as the age of the population, smoking or alcohol consumption, to GORD. The management of GORD in Asia is similar to that in Europe and North America but the lower incidence of severe oesophagitis in Asia may alter the approach slightly. Also, because Asians tend to develop stomach cancer at an earlier age, endoscopy is used routinely at an earlier stage of investigation. Gastro-oesophageal reflux disease is essentially a motility disorder, so short-term management of the disease can usually be achieved using prokinetic agents (or histamine (H2)-receptor antagonists). More severe and recurrent GORD may require proton pump inhibitors (PPI) or a combination of prokinetic agents and PPI. The choice of long-term treatment may be influenced by the relative costs of prokinetic agents and PPI.

Oral and intravenous dosage forms of pantoprazole are equivalent in their ability to suppress gastric acid secretion in patients with gastroesophageal reflux disease

OBJECTIVE: The aim of this study was to assess the ability of pantoprazole to maintain gastric acid suppression in patients with gastroesophageal reflux disease who are switched from an oral ( p.o.) to an intravenous ( i.v.) dosage form. METHODS: A total of 65 patients with gastroesophageal reflux disease were administered either 40 or 20 mg of p.o. pantoprazole daily for 10 days, then were switched to either a matching dose of i.v. pantoprazole or to placebo for 7 days. Acid output (basal and maximal) was measured at the end of the p.o. treatment period and on the first and last days of i.v. therapy. In the primary efficacy analysis, the acid output values at the end of the p.o. pantoprazole treatment were compared with those at the end of the i.v. treatment. Safety was monitored by periodic vital sign measurements, clinical laboratory evaluations, ophthalmic examinations, electrocardiograms, and reports of adverse events. The data were tested by an analysis of covariance and by Wilcoxon signed rank and t tests. RESULTS: Maximal acid output (mean ± SD) in the 40 mg and 20 mg pantoprazole group after p.o. treatment was 6.5 ± 5.6 mEq/h and 14.5 ± 15.5 mEq/h, respectively; whereas, at the end of the i.v. treatment period, the values were 6.6 ± 6.3 mEq/h and 11.1 ± 10.2 mEq/h, respectively. In patients given i.v. placebo, acid output was significantly ( p < 0.05) increased to 29.2 ± 13.0 mEq/h by day 7. Both p.o. and i.v. pantoprazole dosage forms had similar favorable safety and tolerability profiles. CONCLUSIONS: The p.o. and i.v. formulations of pantoprazole (40 and 20 mg) are equivalent in their ability to suppress gastric acid output. The i.v. form of pantoprazole offers an alternative for gastroesophageal reflux disease patients who are unable to take the p.o. formulation.

The effect of severe undernutrition, and subsequent refeeding on digestive function in human patients.

Severe undernutrition may adversely affect gut function. To investigate the effects of severe undernutrition and subsequent refeeding on human digestive function. Severely undernourished patients (body mass index (BMI) < 17 kg/m2) were studied before, and after a period of intensive nutritional support. Standard intestinal absorption tests (faecal fat and urinary xylose excretion), pentagastrin-stimulated acid secretion, and cholecystokinin octapeptide (CCK-8)-stimulated pancreatic enzyme secretion tests were performed. In addition, duodenal biopies were taken to assess gut mucosal morphology. Findings were evaluated in comparison to a group of normal healthy volunteers. Mean BMI of the patients prior to nutritional support was 13.41 kg/m2, with improvement to 16.12 kg/m2 after. Duodenal histology showed evidence of villous atrophy in six of 14 (43%) undernourished patients. Mean xylose excretion following a 5 g oral dose was 0.62 g/5 h in the group of undernourished patients prior to nutritional support (normal > 1 g/5 h), with improvement to 1.40 g/5 h (P < 0.01) after feeding. Maximal gastric acid output was significantly impaired in the undernourished group, as compared to the controls (6.94 mEq/l vs 25.53 mEq/l, P < 0.02), with a significant improvement to 12.30 mEq/l (P < 0.05) following nutritional support. Pancreatic enzyme output was significantly reduced (amylase 830.9 U/h vs 2304 U/h, P < 0.01; lipase 38.0 U/h vs 118.6 U/h, P < 0.01; trypsin 119.7 U/h vs 341.4 U/h, P < 0.01). Following a period of nutritional support there was a significant improvement in amylase and lipase outputs to 1819 U/h and 85.5 U/h, respectively (P < 0.01). These levels were not significantly different from the normal controls. Trypsin output, however, remained significantly impaired at 174.3 U/h (P < 0.01). Severe undernutrition is associated with significant impairment of digestive function, with improvement occurring following nutritional support. These changes may affect initial tolerance to enteral feeding, particularly in those patients with co-existent gut disease.

Carbonic Anhydrase Inhibitors. Part 91. Metal Complexes of Heterocyclic Sulfonamides as Potential Pharmacological Agents in the Treatment of Gastric Acid Secretion Imbalances

Zinc, magnesium, aluminum and copper complexes of several potent, clinically used carbonic anhydrase (CA) sulfonamide inhibitors, such as acetazolamide, methazolamide, ethoxzolamide and benzolamide were tested for their possible applications as antacids, in experimental animals. Gastric acid secretion parameters 3 days after treatment with these CA inhibitors (2 × 500 mg, twice a day), in dogs with chronic gastric fistulas, led to the observation that the gastric acid parameters BAO (the basal acid output), and MAO (the maximal acid output after stimulation with histamine) were drastically reduced, as compared to the same parameters in animals that did not receive these enzyme inhibitors. These are promising results for the possible use of metal complexes of heterocyclic sulfonamides as treatment alternatives (alone or in combination with other drugs) for gastric acid secretion imbalances.

Gastric Function in Dogs with Naturally Acquired GastricHelicobacterspp. Infection

The association ofHelicobacter pyloriwith gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship ofHelicobacterspp. infection to gastric disease in dogs is unclear. The objective of this study was to determine ifHelicobacterinfection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquiredHelicobacterspp. infection were studied before and after (4 and 29 days) the attempted eradication ofHelicobacterspp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific‐pathogen‐free,Helico‐bacter‐freeBeagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection withHelicobacter felis‐ andH bizzozeronii‐liks organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin‐stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P= .09) toward higher meal‐stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin‐stimulated maximal acid output (mmol HC1/ kg0 75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P&lt; .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA withHelicobacter‐specificprimers indicated persistence ofHelicobacterDNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression ofHelicobacterspp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquiredHelicobacterspp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastricHelicobacterspp. in dogs.

Morphological and functional restoration of parietal cells inHelicobacter pylori associated enlarged fold gastritis after eradication

BACKGROUND/AIMHelicobacter pylori infections are associated with hypochlorhydria in patients with pangastritis. It has previously been shown that eradication of H pylori leads to an increase in acid secretion in H...

Inhibition of pentagastrin-induced gastric acid secretion by intravenous pantoprazole: a dose-response study

OBJECTIVE: The purpose of this study was to compare the gastric acid inhibitory ability of increasing doses of intravenous ( i.v.) pantoprazole with that of i.v. famotidine and placebo. Pentagastrin was infused continuously in healthy subjects as a model for patients with Zollinger-Ellison syndrome. METHODS: Pentagastrin (1 μg/kg/h) was infused to stimulate maximum acid output in 39 subjects over a 25-h period. After 60 min of pentagastrin infusion, subjects received a single dose of i.v. pantoprazole (20, 40, 80, or 120 mg), i.v. famotidine (20 mg), or saline placebo. The variables measured were onset of response (time until acid output fell to <10 mEq/h), duration of response (time acid output remained <10 mEq/h), and cumulative acid output over 24 h. RESULTS: All doses of i.v. pantoprazole produced a dose-dependent suppression of acid output to <10 mEq/h. Single i.v. doses of pantoprazole, 80 and 120 mg, suppressed acid output by >90% in all subjects for ≤21 h and had an onset of action of <1 h. CONCLUSIONS: Intravenous pantoprazole has a rapid onset and a clear dose-related effect, with a significantly longer duration of action than that of i.v. famotidine.

Helicobacter pylori infection potentiates the inhibition of gastric acid secretion by omeprazole

BACKGROUNDOmeprazole has a greater intragastric pH elevating effect in Helicobacter pylori positive than negative subjects. Ammonia production byH pylori has been suggested as a probable mechanism.AIMSTo assess the effect ofH...

Maleic acid and succinic acid in fermented alcoholic beverages are the stimulants of gastric acid secretion.

Alcoholic beverages produced by fermentation (e.g., beer and wine) are powerful stimulants of gastric acid output and gastrin release in humans. The aim of this study was to separate and specify the gastric acid stimulatory ingredients in alcoholic beverages produced by fermentation. Yeast-fermented glucose was used as a simple model of fermented alcoholic beverages; it was stepwise separated by different methods of liquid chromatography, and each separated solution was tested in human volunteers for its stimulatory action on gastric acid output and gastrin release. Five substances were detected by high-performance liquid chromatography and were analyzed by mass spectrometry and 1H-13C nuclear magnetic resonance spectroscopy. At the end of the separation process of the five identified substances, only the two dicarboxylic acids, maleic acid and succinic acid, had a significant (P < 0.05) stimulatory action on gastric acid output (76% and 70% of fermented glucose, respectively), but not on gastrin release. When given together, they increased gastric acid output by 100% of fermented glucose and by 95% of maximal acid output. We therefore conclude that maleic acid and succinic acid are the powerful stimulants of gastric acid output in fermented glucose and alcoholic beverages produced by fermentation, and that gastrin is not their mediator of action.

Rebound hypersecretion after omeprazole and its relation to on-treatment acid suppression and Helicobacter pylori status

Background & Aims: There have been conflicting reports regarding acid secretion after treatment with omeprazole. This study examined acid secretion after treatment with omeprazole and its relation to Helicobacter pylori status and on-treatment gastric function. Methods: Twelve H. pylori–negative and 9 H. pylori–positive subjects were examined before, on, and at day 15 after an 8-week course of 40 mg/day omeprazole. On each occasion, plasma gastrin, intragastric pH, and acid output were measured basally and in response to increasing doses of gastrin 17. Results: In the H. pylori–negative subjects at day 15 after omeprazole treatment, basal acid output was 82% higher ( P < 0.007) and maximal acid output 28% higher ( P < 0.003) than before omeprazole. The degree of increase in maximal acid output was related to both on-treatment pH and on-treatment fasting gastrin levels, being 48.0% in subjects with an on-treatment pH of >4 vs. 21.0% in those with a pH of <4 ( P < 0.02) and 49.2% in subjects with an on-treatment gastrin of >25 ng · L −1 vs. 19.8% in those with a fasting gastrin of <25 ng · L −1 ( P < 0.006). At day 15 after omeprazole treatment, the H. pylori–positive subjects showed a heterogeneous response with some having increased acid output and others persisting suppression. Conclusions: Rebound acid hypersecretion occurs in H. pylori–negative subjects after omeprazole treatment. Its severity is related to the degree of elevation of pH on treatment. Persisting suppression of acid secretion masks the phenomenon in H. pylori–positive subjects. GASTROENTEROLOGY 1999;116:239-247

Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection.

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.

Effects of Helicobacter pylori on gastritis, pentagastrin-stimulated gastric acid secretion, and meal-stimulated plasma gastrin release in the absence of peptic ulcer disease

Objective: There is strong evidence accumulating that chronic infection with Helicobacter pylori ( H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis. Methods: H. pylori status was assessed by CLO test and histology (two biopsies each from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender. Gastritis score was assessed by a pathologist, who was unaware of the acid secretory data. Following determination of BAO, the relation of pentagastrin and gastric acid secretion was established with a cumulative pentagastrin dose response curve for the dose range 0.03–6.0 μg/kg −1 h −1 and MAO (V max) and pentagastrin sensitivity (ED 50) were determined. Basal and postprandial gastrin release was measured by radioimmunoassay. Results: There was a significant higher gastritis score in the H. pylori-positive compared with the H. pylori-negative subjects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. pylori-negative groups. No correlation was seen between the gastritis score, basal acid output (BAO) peak acid output (PAO), maximum acid output (MAO), ED 50 values and the plasma gastrin values. There was, however, a considerable larger variation of the PAO and MAO data of the H. pylori-infected subjects and >50% of the respective data was above or below the relatively low range of the respective values of the noninfected subjects. Conclusions: H. pylori-induced gastritis does not regularly enhance maximum acid output in nonulcer patients, nor does it modify the sensitivity of the parietal cell to gastrin. H. pylori infection is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum acid secretory capacity in certain subgroups of patients.

Interpretation of Postvagotomy Endoscopic Congo Red Test Results in Relation to Ulcer Recurrence 5 to 12 Years after Operation

Background: The aim of the present study was to estimate, after vagotomy, the location and extension of residual vagal innervation of the gastric corpus mucosa by using the endoscopic Congo red test (ECRT) and its relation to recurrent ulcer (RU), as well as the results of quantitative gastric acid tests: basal acid output (BAO), maximal acid output (MAO), and nocturnal acid output (NAO). Methods: A total of 271 consecutive vagotomized duodenal ulcer (DU) patients were studied 5 to 12 years (mean 8 years) after the operation. In all cases gastroscopy and ECRT were performed simultaneously. ECRT was considered positive if a red to black-blue (pH <3.0) color change of the gastric corpus mucosa occurred within the first 3 minutes, and the cases were classified as having small extension (SE), ie, one or more areas with a diameter of 1 to 30 mm, or large extension (LE), ie, 20% or more of the gastric corpus showing residual vagal innervation. No red to black-blue changes (pH >3.0) were attributed to negative ECRT. BAO, MAO, and NAO were determined preoperatively and postoperatively in 108 cases out of 271 and correspond with ECRT results. Results: Recurrent ulcer occurred in 18 out of 135 ECRT-positive and in 1 out of 136 ECRT-negative cases. RU occurred 5 times more frequently in LE than SE cases ( P <0.05). The postoperative mean values of BAO, MAO, and NAO were significantly higher in ECRT-positive than in ECRT-negative cases ( P <0.001), and higher in LE than in SE cases ( P <0.01; for NAO, P >0.05). Conclusion: ECRT is a practical and reliable method in the evaluation of postvagotomy DU patients: Negative ECRT practically includes recurrent ulcer risk; positive ECRT of large extension is related to fivefold higher recurrent ulcer risk compared with ECRT of small extension; and ECRT reflects BAO, MAO, and NAO results and can be used instead of them as a less time-consuming procedure, which is more convenient for the patient.

Cholinergic stimulation augments maximal (penta) gastrin-stimulated acid secretion in man

In the vascularly perfirsed isolated rat stomach, maximal histamine stimulated acid secretion is higher than maximal gastrin stimulated, and the former may be augmented by concomitant cholinergic stimulation. The purpose of the present study was to examine whether maximal pentagastrin stimulated acid secretion may be augmented by concomitant vagal stimulation in man. Eight students (one female, seven males) gave an informed written consent to participate in the study. Each subject was studied thrice after an overnight fast, and with an interval at least of one week. On the first day maximal pentagastrin stimulated acid secretion was assessed by giving pentagastrin at a dose of 0.1 ~tg/kg/min which previously has been shown to give maximal gastrin stimulated acid secretion. On day two, acid secretion was stimulated by insulin induced hypoglycemia applying glucose clamp technique establishing a blood glucose level of around 2.1 mmol/1 for a 30 min period. On day three, gastric acid secretion was simultaneously stimulated with pentagastrin and hypoglycemia. Insulin induced hypoglycemia was more short-lived than that stimulated by pentagastrin. Therefore maximal acid output (MAO) was higher when stimulated by pentagastrin than by insulin hypoglycemia. Peak acid output (PAO) was, however, closely similar. The combined stimulation induced an increase in PAO in all subjects when compared with that stimulated by pentagastrin or hypoglycemia alone. The augmentation of pentagastrin stimulated PAO when applying hypoglycemia simultaneously was from 5 to 50% with a median value around 20%. The present study shows that insulin induced hypoglycemia to stimulate the vagal nerves and thus gastric acid secretion, is a safe procedure when utilizing the glucose clamp technique. Moreover, pentagastrin stimulated acid secretion does not represent maximal gastric secretory capacity in man.

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

Antigastric Autoantibodies and Gastric Secretory Function in Helicobacter pylori-Infected Patients with Duodenal Ulcer and Non-Ulcer Dyspepsia

Background: Autoantibodies against epitopes located at the canaliculi of human parietal cells occur in about 30% of Helicobacter pylori-infected patients. This has led to the hypothesis that gastric secretory function could be inhibited by anticanalicular autoantibodies in H. pylori gastritis. Methods: Forty-four H. pylori-infected patients with and without duodenal ulcers were screened for anticanalicular autoantibodies by means of immunohistochemistry. Plasma gastrin levels and basal and maximal gastric acid output were determined. Results: Fasting gastrin levels were significantly increased in the group with anticanalicular autoantibodies. In the group of patients with non-ulcer dyspepsia the presence of anticanalicular autoantibodies was significantly correlated with an impaired basal acid secretion. Conclusions: Antigastric autoimmunity in H. pylori gastritis seems to be relevant for gastric hyposecretion either directly by inhibiting the proton pump or indirectly through the development of gastric mucosa atrophy.

Helicobacter pylori independent chronological change in gastric acid secretion in the Japanese

Background—Gastric acid secretion in Japanese subjects decreases with aging. One of the possible causative mechanisms of this attenuated acid secretion is speculated to be aHelicobacter pylori induced chronic gastritis. The...

Changes in acid secretion over the years. A 30-year longitudinal study.

We studied the effect of aging on gastric acid secretion in 11 physicians who had augmented histamine tests while at medical school in 1962. One of them had a duodenal ulcer at the time. The augmented histamine test was repeated in 1991 and, in addition, upper gastrointestinal endoscopy was done to exclude peptic ulcer and to obtain biopsies for histologic analysis and assessment of Helicobacter pylori status. The mean basal acid output decreased from 7.3 to 1.9 mEq/hr during the 30-year period of follow-up (p < 0.001), and the mean maximum acid output decreased from 29.9 to 20.3 mEq/hr (p < 0.01). The maximum acid output data showed a profound decrease in 4 of the 11 participants, a lesser decrease in 4, and a minimal increase in the remaining 3. Histologic analysis suggested a greater likelihood of atrophic gastritis, H. pylori infection, or both in participants showing a pronounced decrease in acid secretion with aging.

Effects of TRH on gastric acid secretion: A model for human study

The possible effects of TRH administration on different parameters of gastric function were studied in 10 patients with different gastrointestinal complaints. Basal (BAO) and pentagastrin stimulated (6 μg pentagastrin/kg bw sc) maximal (MAO) acid output were determined and serum levels of TSH, total and free thyroxine (T4 and FT4), triiodothyronine (T3) were measured. After determinations of BAO and MAO and the hormones indicated above, one group of patients received a TRH injection (0.2 mg protirelin) intravenously. The second group of patients was injected with atropine (atropinum sulfuricum, 1 mg, iv). At different times following the injections in both groups of patients BAO, MAO and serum levels of TSH, total and free T4, T3, gastrin were determined. Injection of TRH resulted in an increase in TSH and with some delay in thyroxine and gastric acid levels. Atropine treatment was followed by a decrease in gastric acid secretion and a small decrease in TSH and no changes in the values of the other studied hormones. The results suggest a complex interrelationship between TRH, vagal system and pentagastrin-dependent gastric acid secretion operating in human subjects.

Thoracoscopic vagotomy for recurrent ulcer after previous gastric operation.

Recurrent peptic ulcer after previous gastric operation is a difficult surgical problem and abdominal re-operation is associated with significant morbidity, mortality and recurrence rate. The authors report on five patients with recurrent ulcers who, after previous gastric operation, were treated with thoracoscopic vagotomy. All patients tolerated the procedure well without complications, and the median hospital stay was 5 days. Endoscopy confirmed healing of the ulcers in all patients. Pre-operative and postoperative gastric acid studies showed a significant postoperative reduction in both basal and maximal acid output (P < 0.05). In a follow-up period of 18-33 months, one patient had a recurrent ulcer presenting with bleeding. Gastric biopsy revealed presence of Helicobacter pylori and repeated gastroscopy after a course of H. pylori eradication treatment showed a healed ulcer. The other four patients were asymptomatic. We conclude that thoracoscopic vagotomy is a simple and safe procedure for the treatment of recurrent ulcers after previous gastric operation, but the long-term results need further assessment.