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The majority of the world population carry the gastric pathogen Helicobacter pylori . Fortunately, most individuals experience only low-grade or no symptoms, but in many cases the chronic inflammatory infection develops into severe gastric disease, including duodenal ulcer disease and gastric cancer. Here we report on a protective mechanism where H. pylori attachment and accompanying chronic mucosal inflammation can be reduced by antibodies that are present in a vast majority of H. pylori carriers. These antibodies block binding of the H. pylori attachment protein BabA by mimicking BabA's binding to the ABO blood group glycans in the gastric mucosa. However, many individuals demonstrate low titers of BabA blocking antibodies, which is associated with an increased risk for duodenal ulceration, suggesting a role for these antibodies in preventing gastric disease., Competing Interests: DECLARATION OF INTERESTS The authors declare the following competing interests: T. Borén and L. Hammarström are founders of Helicure AB and, own the IP-rights to the anti-BabA ABbA-IgG1 (US patent US8025880B2) and own the IP-rights to the gastric cancer vaccine and diagnostics described in the two manuscripts by Bugaytsova et al., 2023 (Patent Application SE 2350423-6).

Few foals escape gastrointestinal disease during the first weeks of life. Diarrhea is an extremely common problem; fortunately, however, it is usually mild and self-limiting. When it is not, the underlying cause is often an infectious agent, such as rotavirus or Salmonella spp. Our understanding of many of the infectious agents causing neonatal diarrhea is far from complete. Gastric and duodenal ulcers are a less common disease of neonatal foals. There has been an apparent increase in the incidence of ulcer disease in foals during the past few years. The most effective way of decreasing serious gastrointestinal disease in foals is through the use of good management practices. Environmental and dietary stress must be minimized, and good hygienic practices should be followed. Unfortunately, the needs of the neonate are often ignored, while attention is focused on the mare during the breeding season.

The pathogenic bacterium Helicobacter pylori is a causative agent of gastric diseases in Bangladesh as well as throughout the world. This study aimed at analyzing the prevalence of H. pylori infection among dyspeptic patients in Chittagong, the second most populous city of Bangladesh, using 16S rRNA-based H. pylori-specific Polymerase Chain Reaction and Campylobacter-like organism test. We found that 67% of the population under study was positive for H. pylori infection. Gastric ulcer and duodenal ulcer disease showed statistically significant association with H. pylori infection; however, no association of H. pylori infection was observed in terms of age and gender. This study would play a crucial role in managing H. pylori-induced gastric diseases by understanding the current trend of H. pylori infection in the Chittagong region of Bangladesh.

Delay of diagnosis of primary adrenal insufficiency (PAI) leads to adrenal crisis which is potentially lethal complication. The objective of our work was an assessment whether the establishment of diagnosis of adrenocortical insufficiency in Poland is so much delayed as assessed in the past. We have analysed data from 60 patients with diagnosis of PAI established in our department during the past 12 years and who are still under our care. We found that the time to diagnosis of primary adrenal insufficiency in Poland exceeds 3 months in every patient and 6 months in patients admitted with symptoms of adrenal crisis. Forty-four percent of patients were diagnosed only just after the hospitalisation due to crisis, despite the evident signs and symptoms of PAI. Lack of appetite and loss of body weight occurred in all patients and for that reason a diagnosis of chronic gastric and duodenal ulcer disease was the most often incorrect diagnosis. After the proper diagnosis and treatment, in the course of 1–11 years of observation, there was only 6 imminent adrenal crises in 5 patients. Our results indicated that training of primary care physicians in the field of recognising and treatment of adrenal insufficiency is still essential.

Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.

BACKGROUND: Patients with duodenal ulcer (DU) have an increased parietal cell mass and sensitivity to secretagogues, with increased acid output.AIM: To determine the effect ofHelicobacter pylorieradication on parietal cell sensitivity and gastric acid secretion.SUBJECTS AND METHODS: Twenty-fiveH pylori-positive DU patients and 18H pylori-negative healthy volunteers were studied. SerumH pyloriimmunoglobulin G, basal acid output and acid secretory response to graded doses of pentagastrin were determined before and after treatment, at six months and at one year. Subjects were randomly assigned to ranitidine or sucralfate treatment for six weeks, and all DU patients received bismuth subsalicylate, metronidazole and tetracycline for the first two weeks.RESULTS:H pyloriwas eradicated in 66% of patients receiving sucralfate and 92% receiving ranitidine. Compared with healthy volunteers, DU patients demonstrated a 2.7-fold greater basal acid output, a 1.3-fold greater peak acid output, significantly higher acid output for each dose of pentagastrin and a 1.38-fold increase in the area under the pentagastrin dose acid response curve. Cure ofH pylori, irrespective of ulcer healing regimen, resulted in a gradual decrease in acid secretory capacity with basal acid output, peak acid output and area under the pentagastrin dose acid response curve returning to healthy volunteer levels by one year. No demonstrable differences were observed in parietal cell sensitivity in all subjects before or after treatment. These data suggest that disturbances in acid secretion inH pylori-positive DU patients are not due to an increased parietal cell sensitivity to pentagastrin but rather due to an increased parietal cell mass with increased capacity to secrete acid, which gradually resolves following cure.

Helicobacter pylori(H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link betweenH. pyloriinfection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication ofH. pyloriinfection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. Against this concept there are issues that need explanation such as the reason why only a minority of infected persons develop duodenal ulceration when infection withH. pyloriis widespread. There is evidence thatH. pyloriinfection has been prevalent for several centuries, yet duodenal ulceration became common at the beginning of the twentieth century. The prevalence of duodenal ulceration is not higher in countries with a high prevalence ofH. pyloriinfection. This paper debate puts forth the point of view of two groups of workers in this field whetherH. pyloriinfection is the primary cause of duodenal ulcer disease or a secondary factor.

The author examines the clinical impact of findings from a key international workshop on acid peptic disorders, “Appropriate acid suppression for the healing of acid-related diseases,” and from an important meeting which summarized results of a cross-Canada study of the symptomatic treatment of dyspepsia due to esophagitis and duodenal ulcer disease.

BACKGROUND: Information about gastric acid secretion and gastric acidity can be obtained using several techniques but, presently, continuous intragastric pH recording is probably the one applied most frequently. This paper aims to review the technical aspects and some important applications of intragastric pH monitoring in research and clinical practice. METHODS: Literature review. RESULTS: Most studies on intragastric pH are performed with either glass or antimony electrodes. Optimal measurement of 24-h intragastric pH requires accurate calibration of the pH measuring system, exact positioning of the pH electrodes, and a sufficient sample rate. Depending on the aim of the study the results of intragastric pH monitoring are expressed either as median H+ activity or as median pH values. Gastric acidity shows a circadian rhythm, modified by buffering meals and nocturnal duodenogastric reflux. In health, age, gender and smoking habits are known to influence gastric acidity. In duodenal ulcer disease an increased gastric acidity is found and in patients with gastric ulcer gastric acidity is decreased. In GERD, no relation between reflux oesophagitis and gastric acidity is found. Helicobacter pylori affects intragastric pH most pronounced during acid inhibitory therapy, both in DU patients and in healthy subjects. In the absence of H. pylori the effect of proton-pump inhibitors on intragastric pH is much less than in the presence of the microorganism, whereas the effect of ranitidine on intragastric pH is barely affected by the H. pylori status. CONCLUSIONS: Despite some limitations, intragastric pH monitoring provides important information about gastric acidity

Exogenously administered zinc compounds have been shown to possess anti-ulcer activity against a wide variety of ulcerogenic agents, both in laboratory animal models and in human peptic ulcer disease. However, a strong possibility exists that endogenous zinc may also play an important role during noxious events by various mechanisms. Therefore, the aim of this study was to focus on the changes of endogenous zinc serum and tissue concentrations in cysteamine-induced duodenal lesions. We used atomic absorption spectropho- tometry to determine the tissue and serum concentrations of zinc in normal (control) rats and those with cysteamine-induced duodenal ulcers. The results obtained in this study indicated that the onset, development and spontaneous healing of ulcer lesions were associated with certain shifts in zinc serum and tissue concentrations. Prior to ulcer formation, a significant increase was noted in serum zinc values. With the onset of duodenal lesions, zinc serum concentrations significantly decreased, while there was a significant increase in duodenal tissue concentrations when compared to healthy control animals. Zinc tissue concentrations decreased and returned to starting values by the end of the first week of spontaneous healing. This decrease in zinc tissue concentration corresponded to the healing rate of the duodenal ulcers. Serum zinc concentrations also returned to starting values within the first week period. These observations indicate and confirm that zinc could play an important role in duodenal ulcer disease and represent a natural defense system in the body.

Intraluminal duodenal pH was recorded using a combined miniature electrode and logged digitally every 10 or 20 seconds for five hours (basal/meal/drink) in eight control subjects and 11 patients with duodenal ulcer (five on and off treatment with cimetidine). Over the whole test there were no significant differences in duodenal mean pH or log mean hydrogen ion activity (LMHa) between control subjects and patients with duodenal ulcer, but there were significantly longer periods of duodenal acidification (pH less than 4) and paradoxically more periods of duodenal alkalinisation (pH greater than 6) in the duodenal ulcer group compared with controls. After a meal duodenal mean pH and LMHa fell significantly in both controls and patients with duodenal ulcer, with more periods of duodenal acidification and alkalinisation in the duodenal ulcer group. An exogenous acid load (Coca-Cola) significantly increased the periods of duodenal acidification, and reduced alkalinisation, in both groups. Cimetidine significantly increased mean pH and LMHa and abolished the brief spikes of acidification in four of five patients with duodenal ulcer. Peak acid output (but not basal acid output) was significantly correlated with duodenal mean pH and LMHa but not with the periods of duodenal acidification. Smoking did not affect duodenal pH in either group.

1 The effects of mianserin (60 mg) have been studied on nocturnal and pentagastrin-stimulated gastric secretion. 2 Mianserin reduced pentagastrin-stimulated gastric acid secretion by 38%, pepsin by 40% and secretory volume by 45% during a 1 h test. 3 Twelve-hour overnight secretion of acid was reduced by 37%, while secretion of pepsin was reduced by 43% and secretory volume by 51%. 4 No adverse effects were noted. 5 These findings, which achieve statistical significance, suggest the need for further study to evaluate the possible role of mianserin in the therapy of duodenal ulcer disease.