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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).

Aim.This study was conducted to assess the compliance of patients with duodenal ulcer disease during the dispensary observation.Materials and methods.We carried out an examination and a prospective observation of 1896 patients with uncomplicated duodenal ulcer and 43 people with sub- and decompensated scar-ulcerative stenosis of the duodenum.Results. The analysis confirmed that the compliance of patients with duodenal ulcer depends on the professional employment of patients, their gender, the level of education, presence of comorbidity, absence of undesirable effects of the taken medication, contact establishment with the patient, and presence of non-adaptive types of attitude to the disease.Conclusion.The interaction between different factors affecting the compliance should be taken into account when planning the tactics of dispensary observation of patients with uncomplicated duodenal ulcer and after eliminating the complications as wel.

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 current state of public health in Ukraine is characterized as a cri sis. The article analyzes the prevalence of digestive diseases among children aged 0–14 and 15–17 inclusive, and studies the medical and social importance of these diseases impact on the most important peri ods of a growth and development of children and the incidence of the duodenal ulcer disease (DUD) among children. The objective: to examine the prevalence of the peptic duodenal ulcer disease among school children in Ukraine in the practice of family doctors. Materials and methods. The method of semantic evaluation of scien tific instruments and the method of systemic and processing analysis. Results. According to the research program, we studied and analyzed the prevalence of DUD in children in all regions of Ukraine. Particular attention was paid to areas in which the study was conducted (Kyiv City and Kyiv region) [1, 2]. There has been a marked increase in ero sive and ulcerative lesions of the duodenum forms that make up 15–16% of gastroduodenal diseases. The frequency of DUD is 1,6±0,1 per 1000 child population. The severe DUD form and a decrease of the effectiveness of a therapy were recognized. Conclusion. The difference prevalence of digestive diseases among children aged 0–14 years and 15–17 years in the regions of Ukraine are statistically significant and indicates a tendency to increase.

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.

SUMMARY OBJECTIVE: To evaluate the incidence, mortality and cost of non-traumatic abdominal emergencies treated in Brazilian emergency departments. METHODS: This paper used DataSus information from 2008 to 2016 (http://www.tabnet.datasus.gov.br). The number of hospitalizations, costs - AIH length of stay and mortality rates were described in acute appendicitis, acute cholecystitis, acute pancreatitis, acute diverticulitis, gastric and duodenal ulcer, and inflammatory intestinal disease. RESULTS: The disease that had the highest growth in hospitalization was diverticular bowel disease with an increase of 68.2%. For the period of nine years, there were no significant changes in the average length of hospital stay, with the highest increase in gastric and duodenal ulcer with a growth of 15.9%. The mortality rate of gastric and duodenal ulcer disease increased by 95.63%, which is significantly high when compared to the other diseases. All had their costs increased but the one that proportionally had the highest increase in the last nine years was the duodenal and gastric ulcer, with an increase of 85.4%. CONCLUSION: Non-traumatic abdominal emergencies are extremely prevalent. Hence, the importance of having updated and comparative data on the mortality rate, number of hospitalization and cost generated by these diseases to provide better healthcare services in public hospitals. RESUMO OBJETIVO: Avaliar a evolução da Incidência, mortalidade e custo das urgências abdominais não traumáticas atendidas nos serviços de emergência do Brasil durante o período de nove anos. MÉTODOS: Este trabalho utilizou informações do DataSus de 2008 a 2016, (http://www.tabnet.datasus.gov.br). Foram analisados número de internações, valor médio das internações (AIH), valor total das internações, dias de permanência hospitalar e taxa de mortalidade das seguintes doenças: apendicite aguda, colecistite aguda, pancreatite aguda, diverticulite aguda, úlcera gástrica e duodenal, e doença inflamatória intestinal. RESULTADOS: A doença que teve o maior crescimento do número de internações foi a doença diverticular do intestino, com o valor de 68,2%. Ao longo dos nove anos não houve grandes variações da média de permanência hospitalar, sendo que o maior aumento foi o da úlcera gástrica e duodenal, com crescimento de 15,9%. A taxa de mortalidade da doença por úlcera gástrica e duodenal teve um aumento de 95,63%, consideravelmente significante quando comparada com as outras doenças. Todas tiveram seus valores de AIH aumentados, porém, a que proporcionalmente teve o maior aumento nos últimos nove anos foi a úlcera gástrica e duodenal, com um acréscimo de 85,4%. CONCLUSÃO: As urgências abdominais de origem não traumática são de extrema prevalência, por isso a importância em ter dados atualizados e comparativos sobre a taxa de mortalidade, o número de internações e os custos gerados por essas doenças, para melhor planejamento dos serviços públicos de saúde.

Aim. To evaluate prevalence of electrical instability of the heart in persons with stressogenic professions by a complex evaluation of the parameters of clinical and functional methods of investigation.Material and methods. Totally 154 men included with AH of I-II stages; first group consisted of 78 motormen and their assistants having stressogenic profession, second grup consisted of 76 persons with minimal psychoemotional tension. A clinical and functional investigation was performed.Results. In 1st group "possible existence" of delayed atrial and ventricular potentials was twice and three times (resp.) more prevalent comparing to the 2nd (with p=0,0001 and p=0,0002, resp.). A rigid circadian index in the 1st group was 1,7 times more prevalent (Х2=10,5; p

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.

DOI: http://dx.doi.org/10.3329/medtoday.v23i2.13098 Medicine TODAY Vol.23(2) 2011 pp.67-71

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.

SUMMARY Intraluminal pH was measured simultaneously in the stomach and duodenal bulb with six small, glass electrodes tied together at 1.5-cm intervals. Ten patients with duodenal ulcer disease were studied under fasting conditions and for 3 h after a standard liquid meal on three occasions: day 1, before treatment; day 8, when the proton pump blocker omeprazole had been taken in a daily dose of 30 mg for 7 days consecutively, including the day of the pH study; day 9, 24 h after the last dose of omeprazole. Mean hydrogen ion activity and the percentage of time with pH below 3 was calculated from the digital pH data sampled at a frequency of 1 per second from each electrode. On day 8, five of the patients were permanently anacidic (pH > 4) in the stomach and duodenum, while the food-stimulation broke off anacidity for shorter periods in the other five patients. The pH pattern in the duodenal bulb was markedly altered in all patients with disappearance of the typical pH fluctuations, and a decrease in the time that the pH was below 3 from a median value of 30% before treatment to 0% in seven patients and close to 0% in three patients. On day 9, a large patient-to-patient variation was observed in gastric pH: three patients were still anacidic, four were markedly suppressed, but three patients reached near pre-treatment acidity. Duodenal bulb acidity was still decreased significantly on day 9 in all patients, with post-prandial pH below 3 for less than 5% of the time, compared with 30% before treatment.

Four hundred and sixty-four patients with duodenal ulcer disease received continuous maintenance treatment with ranitidine for up to 9 years. Treatment failure was defined as either the first symptomatic recurrence of ulcer or the first ulcer recurrence accompanied by haemorrhage. Life tables were constructed using the Kaplan-Meier product-limit method; comparisons of survival curves were performed using the log-rank test; and multivariate analysis was carried out using the Cox proportional hazards model. Results. The proportion of patients remaining free from symptomatic recurrence of ulcer during maintenance treatment with either 150 mg/day or 300 mg/day ranitidine was: 95% at 1 year; 88% at 3 years; 86% at 5 years; and 81% at 7 and 9 years (95% C.I. 76-86%). Young age and the absence of exposure to non-steroidal anti-inflammatory drugs (NSAIDs) at the time of diagnosis of ulcer were shown to increase the likelihood of developing ulcer recurrence. The rate of ulcer recurrence after 9 years of maintenance treatment (17%) was significantly less than that after 5 years without active anti-ulcer therapy (80%), P = 0.0001. The proportion of patients who remained free from ulcer haemorrhage during maintenance treatment was: 99.1% at 1 year and 98.1% at 5 and 9 years (95% C.I. 96.7-99.6%). The risk of haemorrhage was significantly greater in patients who were not receiving active treatment (12.4% at 5 years) than in patients receiving maintenance treatment (less than 2% at 9 years), P = 0.0001 (log-rank test). Patients who had originally presented with haemorrhage had an increased risk of further ulcer bleeding compared with patients who presented with pain (P = 0.0013). A significantly greater proportion of patients with NSAID-associated duodenal ulcers remained free from ulcer recurrence during maintenance treatment compared with patients suffering from 'idiopathic' ulcers (P = 0.0238), although there was no difference between the two groups in respect of haemorrhage during maintenance treatment. Conclusions. (a) Continuous maintenance treatment with ranitidine for up to nine years successfully prevents ulcer recurrence in more than 80% of patients with duodenal ulcer disease. (b) Young age increases the risk of ulcer recurrence during maintenance treatment with ranitidine. Ulcers associated with NSAID-intake at the time of diagnosis have a lesser risk of recurrence during maintenance treatment. (c) The risk of haemorrhage in patients with ulcer disease receiving maintenance treatment with ranitidine for nine years was less than 2% compared with greater than 12% in untreated patients observed for 5 years.(ABSTRACT TRUNCATED AT 400 WORDS)

Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection 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 of H. pylori infection 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. This study was under taken at the Department of surgery, Narayana medical college, Nellore from January 2007 to July 2008. A total of 150 patients with duodenal ulcers, gastric ulcers, antral gastritis, gastric carcinoma and dyspepsia of any kind were studied. Maximum number of cases were in the age group of 31 years to 50 years among both sexes and number of cases gradually decreased after 50 years of age in males and females. Males were more in number and male to female ratio is (2.75:1) approximately 3:1.

Helicobacter pylori strains harboring the vacAs1, cagA and babA2 have been associated with ulcer disease (UD). We compared the prevalence of these different genotypes and adhesive properties in H. pylori infected patients with UD in four European countries. Genomic DNA was isolated from 314 H. pylori strains: Germany (GER; n=92), Sweden (SWE, n=74), Portugal (POR, n=91) and Finland (FIN, n=57). The frequencies of babA2 genotype varied from 35% to 60%. Triple-positive strains (vacAs1+, cagA+ and babA2+) were significantly associated with UD in GER and POR and were closely correlated with UD in FIN, but not in SWE. Classification as triple-positive strains had a higher specificity for detection of UD in GER, POR and FIN than type1 or cagA+ strains. In vitro adhesion assays revealed that Swedish strains showed high adhesion properties and were thus correlated with the diagnosis of UD, although PCR detected the babA2 gene at lower frequencies and failed to show a correlation with UD. This finding appears to reflect allelic variations of the babA2 gene in SWE, although adhesive properties of the strains are retained.

Helicobacter pylori infection has been identified as a pathogenic factor in a number of gastroduodenal diseases, most importantly in gastric and duodenal ulcer disease. This association and the development of H. pylori eradication therapies has had a tremendous influence on the surgical therapy for these disorders. Decades ago, surgery was the therapy of choice for gastric and duodenal ulcers. Now, however, the first line of therapy includes treatment of H. pylori infection, suppression of gastric acid secretion, and protection of gastric mucosal barriers combined with a range of endoscopic procedures. These developments have had a major impact on the indications for surgery in benign gastroduodenal diseases. In addition, advances in our understanding of the pathogenetic mechanisms of H. pylori infection have also changed our views of gastric mucosa-associated lymphoid tissue lymphoma, gastric cancer, and gastroesophageal reflux disease.

Peptic ulcers generally appear in the stomach and the first segment of the duodenum as a result of mucosal erosion caused by pepsin and gastric acid secretion, with up to 70% of these occurring amongst patients aged 25-64. Currently, endoscopic procedures combined with proton pump inhibitors are considered the gold standard for managing complicated peptic ulcers, leaving surgical management as an option for endoscopic management failure or in scenarios such as incoercible bleeding, perforation, penetration and intestinal occlusion. Penetration of a gastric ulcer to adjacent organs is a rare complication; penetration to the liver and endoscopic diagnosis is even rarer. We have presented the case of a 54 year old diabetic male, who presented to the emergency room with upper gastrointestinal bleeding due to a chronic duodenal ulcer, with haemodynamic instability, requiring surgical management, revealing penetration to the liver with rupture of the right hepatic artery. The patient successfully recovered after surgery and was discharged 7 days after surgical intervention. We did not find any similar case reports in the current literature

The study was conducted in the gastroenterological department of Donetsk City Children Clinical Hospital No. 1. The study involved 120 children aged 12-17 years old with erosive and ulcerative changes in the duodenal mucosa on the background of Helicobacter pylori persistence. All patients were divided into four groups of comparison. Patients of group I received omeprazole + amoxicillin + nifuratel, group II – amoxicillin + clarithromycin + colloidal bismuth subcitrate, group III – omeprazole + clarithromycin + nifuratel, group IV – omeprazole + clarithromycin + amoxicillin. The efficiency of different methods of Helicobacter pylori eradication in children with duodenal ulcer and erosive bulbitis has been studied. None of the schemes of anti-HP therapy used allows to achieve Helicobacter pylori elimination in 100% of the cases in children with destructive changes of duodenal mucosa. It has been found that the combination of clarithromycin and amoxicillin with omeprazole or colloidal bismuth subcitrate allows to achieve eradication of Helicobacter pylori in 80% of cases in children with erosive and ulcerative changes in the duodenal mucosa. It is necessary to develop new, combined, more effective schemes for the treatment of erosive-ulcerative changes in the duodenal mucosa, which would be available and safe for application in pediatric practice., В условиях гастроэнтерологического отделения Городской детской клинической больницы №1 г. Донецка обследовано 120 детей с эрозивно-язвенными изменениями слизистой оболочки двенадцатиперстной кишки на фоне персистенции Helicobacter pylori в возрасте от 12 до 17 лет. Все пациенты были разделены на четыре группы сравнения. Пациенты I группы в качестве антихеликобактерной терапии получали омепразол + амоксицил- лин + нифурател, II группы – амоксициллин + кларитромицин + коллоидный субцитрат висмута, III группы – омепразол + кларитромицин + нифурател, IV группы – омепразол + кларитромицин + амоксициллин. Изучена эффективность различных схем антихеликобактерной терапии в лечении детей с язвенной болезнью двенадцатиперстной кишки и эрозивным бульбитом. Ни одна из использованных схем антихеликобактерной терапии не позволяет добиться эрадикации Helicobacter pylori у детей с деструктивными изменениями слизистой оболочки двенадцатиперстной кишки в 100% случаев. Установлено, что комбинация антибактериальных препаратов кларитромицина и амоксициллина в сочетании с омепразолом либо колоидным субцитратом висмута позволяет добиться эрадикации Helicobacter pylori в 80% случаев у детей с эрозивно-язвенными изменениями слизистой оболочки двенадцатиперстной кишки. Необходимым является разработка новых комбинированных, более эффективных схем лечения эрозивно-язвенных изменений слизистой оболочки двенадцатиперстной кишки, которые были бы доступны и безопасны для применения в педиатрической практике., В умовах гастроентерологічного відділення Міської дитячої клінічної лікарні №1 обстежено 120 дітей з ерозивно-виразковими змінами слизової оболонки дванадцятипалої кишки на тлі персистенції Helicobacter pylori віком від 12 до 17 років. Усі пацієнти були розділені на чотири групи порівняння. Пацієнти I групи в якості антихелікобактерної терапії отримували омепразол + амоксицилін + ніфурател, ІІ групи – амоксицилін + кларитро- міцин + колоїдний субцитрат вісмуту, III групи – омепразол + кларитроміцин + ніфурател, IV групи – омепразол + кларитроміцин + амоксицилін. Вивчена ефективність використання різних трикомпонентних схем антихелікобактерної терапії у лікуванні дітей з виразковою хворобою дванадцятипалої кишки та ерозивним бульбітом. Жодна з використаних схем антихелікобактерної терапії не дозволяє домогтися ерадикації Helicobacter pylori у дітей з деструктивними змінами слизової оболонки дванадцятипалої кишки у 100% випадків. Встановлено, що використання комбінації антибактеріальних препаратів кларитроміцину та амоксициліну у поєднанні з омепразолом або колоїдним субцитратом вісмуту дає змогу досягнути ерадикації Helicobacter pylori у 80% випадків у дітей з ерозивно-виразковими змінами слизової оболонки дванадцятипалої кишки. Необхідною є розробка нових комбінованих, більш ефективних схем лікування ерозивно-виразкових змін слизової оболонки дванадцятипалої кишки, які були б доступні і безпечні для застосування в педіатричній практиці.

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.

BACKGROUND: Although the eradication ofHelicobacter pyloriis of primary importance when initiating treatment, it is also important to have a strategy for patients who areH pylori-negative, fail to demonstrate eradication or have a tendency to become re-infected or relapse.PATIENTS AND METHODS: In a double-blind, parallel-group clinical trial of 928 patients (from 70 centres in 16 countries) with duodenal ulcers who after a short term study had relief of symptoms and healed ulcers proved endoscopically, 308 were randomly assigned to receive omeprazole 10 mg in the morning, 308 to receive omeprazole 20 mg in the morning and 312 to receive ranitidine 150 mg at bedtime for up to 12 months. Symptoms were assessed every three months and endoscopy repeated at three, six and 12 months, or more often if indicated by recurrence of symptoms. The safety screening included basal serum gastrin concentrations and gastric mucosal histopathology.RESULTS: The remission rates up to 12 months were 87% for the omeprazole 20 mg group, 71% for the omeprazole 10 mg group and 63% for the ranitidine group. Omeprazole 20 mg differed significantly from both omeprazole 10 mg (P=0.0001, 95% CI 9 to 23) and ranitidine (P=0.0001, 95% CI 17 to 31). There was no statistically significant difference between omeprazole 10 mg and ranitidine over the 12-month period, but the 95% confidence interval allowed differences between 0% and 16% in favour of omeprazole at 12 months. A Cox regression analysis revealed that longer treatment courses to heal, smoking, a long ulcer history and young age negatively contributed to the odds of staying in remission. The treatments were well tolerated. There was a slight increase in basal serum gastrin concentrations, reflecting the different degrees of acid inhibition induced by the three treatments. No dysplastic or neoplastic lesions were found in any biopsies.CONCLUSIONS: More duodenal ulcer patients are maintained in remission with omeprazole 20 mg daily than with omeprazole 10 mg daily or with ranitidine 150 mg at bedtime.

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.

Background and aims: Although the role of H. pylori in peptic ulcer disease is no longer in dispute, certain aspects of eradication therapy in this condition have yet to be settled. Uncertainties still surround the relationship between Helicobacter pylori status and ulcer healing, the efficacy of eradication therapy in alleviating acute symptoms and healing ulcers, and the prognosis after eradication with respect to recurrence of symptoms, ulcers and complications. The present literature review, encompassing studies published up to October 1995, specifically addresses these issues. Results: Pooled data show that eradication therapy heals 90% of duodenal ulcers and 85% of gastric ulcers, while individual studies repeatedly confirm that it is more effective at healing ulcers than conventional treatment with anti-secretory drugs. Recent reports indicate that triple therapy regimens for 1 week, provided they include an anti-secretory drug, are sufficient to achieve high rates of healing and rapid symptom relief. A detailed analysis of the data, particularly those from studies reporting healing rates in relation to H. pylori status after eradication therapy, provides strong evidence that eradication of H. pylori produces ulcer healing. Follow-up studies show that ulcer recurrence and complications are rare after eradication treatment in patients with either gastric or duodenal ulcer disease. However, while ulcer symptoms are infrequent during follow-up, a proportion of patients appear to develop gastrooesophageal reflux after eradication. Conclusions: H. pylori eradication is highly effective in promoting ulcer healing and preventing subsequent ulcer recurrence. These beneficial effects of eradication therapy are observed in patients with either gastric or duodenal ulcers which are associated with H. pylori infection.

Sir, I greatly enjoyed Dr David Grimes’ review ‘An epidemic of coronary heart disease’.1 An epidemic of a completely different disease, duodenal ulcer, occurred during almost exactly the same time, which seems rather unlikely to have been a coincidence. David Grimes describes the fact that coronary heart disease was rare before the first world war, then became increasingly common in the 1920s and then, after peaking in the late 1960s, has declined in incidence steadily ever since. Duodenal ulcer disease shows a very similar time scale. Duodenal ulcers were rare before the early 1900s. Although this was partly due to the lack of radiological diagnosis, dramatic events such as perforation or fatal haemorrhage were obvious to doctors, and such events provide the most reliable data for estimating ulcer incidence around a 100 years ago. The work of surgeons such as Moynihan2 made it possible to recognize the typical symptoms. William Osler, then working in Johns Hopkins Hospital, Baltimore, wrote in the third edition of his textbook of medicine, published …

Although the connection of microRNAs (miRNAs) to some diseases is well established, their involvement in chronic infections such as Helicobacter pylori has received less attention. The aim was to compare miRNA expression profiling in patients with duodenal ulcer (DU) due to H. pylori infection with that in infected patients without DU and in uninfected patients. The miRNA expression profile was determined by microarrays in antral mucosal samples from well-characterized dyspeptic patients (n = 46). The most significant set of miRNAs was subsequently analysed in an independent validation group of patients (n = 42). Transcripts for IL8, IL12p40, IL12p35 and IL23p19, the signalling molecules MYD88, GATA6, SOCS2 and STAT6 and H. pylori virulence factors cagA and VacA were analysed. Microarray experiments showed that 17 miRNAs were deregulated in the mucosa of H. pylori-infected patients. No significant differences were observed between normal and DU patients. PCR confirmed the up-regulation of miR-9, miR- 146a, miR-155 and miR-650 and the down-regulation of miR-96 and miR-204 in the independent validation set of patients. Importantly, miR-9, miR-96, miR-146a and miR-650 expression was specific to chronic-active gastritis. H. pylori-infected patients showed higher levels of IL8 and IL12p40 mRNAs and lower levels of GATA6 and SOCS2 mRNAs. The antral mucosa of patients with non-active or chronic-active gastritis showed significantly lower levels of GATA6, MYD88, SOCS2 and STAT6 mRNAs compared with patients without gastritis. The down-regulation of these factors was not correlated with the expression of any of the validated miRNAs. The exact role of the miRNA changes observed will require further study.

A retrospective study of 31 consecutive bleeding duodenal ulcer (DU) patients and, as controls, 62 active DU subjects without bleeding episodes was conducted in order to ascertain whether bleeding DU patients have particular clinical or functional characteristics. The patients were followed for 15.6 and 17.4 months, respectively, after diagnosis. The following parameters were taken into account: sex, age, family history of ulcer, blood group (ABO system), ulcer pain, nonsteroidal anti-inflammatory drug (NSAID) consumption, cigarette smoking, alcohol and coffee consumption, ulcer site, fasting serum gastrin and pepsinogen group A, basal acid output (BAO), and maximal acid output (MAO). Statistics were gathered using the Student's t test and Fisher's exact test. Bleeding DU patients had less ulcer pain ( P P

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.

Distinct virulence factors of Helicobacter pylori have been associated with clinical outcome of the infection; however, considerable variations have been reported from different geographic regions. Data on genotypes of African H. pylori isolates are sparse. The aim of this study was to determine the prevalence of specific genotypes of H. pylori in Nigerian patients with duodenal ulcer and non-ulcer dyspepsia. H. pylori was cultured from endoscopic biopsies obtained from 41 Nigerian patients (19 with duodenal ulcer, 22 with non-ulcer dyspepsia). The vacA alleles, cagA and iceA genotypes were determined by PCR. The vacA s1,m1 and s1,m2 genotypes were found in 26.3% and 22.7%, and in 73.7% and 72.7% of H. pylori isolates from patients with duodenal ulcer and non-ulcer dyspepsia, respectively. The iceA1 genotype was present in 94.7% and 86.4% of isolates from duodenal ulcer and non-ulcer dyspepsia patients, respectively. cagA + infection was found predominantly (>90%) in Nigerian H. pylori isolates irrespective of the clinical diagnosis. In conclusion, vacA s1,m2, iceA1 and cagA + are common genotypes of H. pylori isolated from Nigerian patients. As in several other developing countries there seems to be no association between these genotypes and duodenal ulcer disease.

Helicobacter pylori causes antral gastritis and peptic ulcers and is associated with development of gastric cancer. It is unclear why only a few of the infected subjects develop duodenal ulcers whereas the majority remains asymptomatic. Both bacterial factors as well as the nature of the host immune response might be important for the outcome of disease. The aims of this thesis were to characterize the local inflammatory response in human H. pylori infection and to study the relation of the local cytokine response to gastritis and peptic ulcer disease. Furthermore, the inflammatory properties of different putative virulence factors of H. pylori were examined.The cytokine, secretory component (SC) and immunoglobulin (Ig) A expression in antral biopsies from H. pylori infected duodenal ulcer (DU) patients and asymptomatic (AS) carriers as well as from healthy volunteers was studied by immunohistochemistry. The cytokine response in DU patients as well as in AS carriers was of the T helper 1 type. Furthermore, the levels of proinflammatory cytokines were increased in the H. pylori infected subjects. The gastric epithelial cells contributed substantially to the increased expression of several of the cytokines. However, none of the studied cytokines was correlated with peptic ulcer disease since the levels in DU patients and AS carriers were comparable. Also the antibody-mediated immune response, i.e. IgA producing cells and SC, to H. pylori infection was of the same magnitude in DU patients and AS carriers. Locally produced IFNg, but not IL-4, was correlated with increased SC expression.Acute gastritis induced in healthy volunteers by aspirin treatment allowed studies of the role of inflammation in the dysregulation of gastric secretory function, which is associated with H. pylori infection. The aspirin and the chronic H. pylori-induced gastritis shared common features, i.e. increased levels of IL-1b, IL-6, and IL-8 in the antral mucosa. Antral distention normally inhibits acid secretion and gastrin release. Components of the gastric inflammation, possibly cytokines, seemed to dysregulate the acid secretion, since antral distension failed to inhibit the acid secretion after aspirin therapy. However, the inhibition of gastrin release in response to antral distension was preserved, indicating another underlying mechanism of the H. pylori associated hypergastrinemia.As a prerequisite for studies of the acute inflammatory responses to H. pylori strains and antigens the expression of different putative virulence factors of H. pylori was studied by sensitive inhibition ELISA assays using specific monoclonal antibodies. The expression of three conserved antigens varied considerably between the different strains and culture conditions tested. A model of cultured human stomach explants was modified to allow studies of cytokine responses in culture media, as measured by ELISA, to acute experimental H. pylori infection and after stimulation with different antigens. Infection as well as antigen stimulation of the explants induced strong chemokine and cytokine responses. The different H. pylori LPS preparations tested induced cytokine production of comparable levels as after inoculation with whole bacteria. Furthermore, some H. pylori strains and antigens induced particularly strong chemokine responses indicating the presence of proinflammatory H. pylori strains or antigens

Over a period of 14 years, 1246 patients had emergency gastroscopy because of upper gastrointestinal tract (UGIT) bleeding. The endoscopic findings in these patients showed duodenal ulcer disease (DUD) in 364 (29.2%) was the most common followed by esophageal varices in 302 (24.2%), erosive gastritis in 198 (15.9%), gastroesophageal reflux disease (GERD) in 156 (12.5%), gastric ulcer in 69 (5.5%), and normal (negative) endoscopy in 132 (10.6%). Only 65 (21.5%) patients with varices had active bleeding from the esophageal varices, 10 (3.3%) from the gastric varices and in 34 other patients with varices (11.3%), the bleeding was mainly from associated gastrophy. Eighty-six patients (23.6%) with DUD had active bleeding at endoscopy; 66 (80.5%) of these had ulcers showing stigmata of recent hemorrhage. Of those who had active bleeding, the source of the bleeding could not be identified in only five.

SUMMARY One hundred and twenty-five patients with duodenal ulcer disease were given continuous ranitidine therapy after initial acute healing. Cumulative remission rates indicated that 95 % of patients were ulcer-free after 1 year, 89% at 2 years, 81% at 3 years, 70% at 4 years and 60% at 5 and 6 years. Nine patients had a second recurrence after healing of the first. No patient developed an ulcer complication. These results support the view that long-term continuous ranitidine therapy prevents ulcer recurrence and complications.

Antral biopsy specimens were processed for Helicobacter pylori by Gram staining, rapid urease test (RUT) and culture from 25 patients with symptoms of duodenal ulcer, amongst whom the positivity rate was 84%. Follow up of 16 patients after appropriate therapy showed complete regression of the disease in 87.5% of cases whereas in 12.5% of cases a decrease in the extent of duodenal ulceration was noted.

The present review examines the evidence for the existence of an asymptomatic variant of duodenal ulcer disease, as well as its clinical significance and therapeutic implications. Asymptomatic duodenal ulcers have definitely been shown to occur only in patients treated with non-steroidal anti-inflammatory drugs (NSAIDs) and in patients who have previously suffered from ulcer disease, especially if the latter have been subjected to gastric surgery or are receiving long-term continuous (maintenance) treatment with drugs. It seems likely (although conclusive evidence is not yet available) that NSAID-associated asymptomatic duodenal ulcers are predisposed to haemorrhage or perforation and should therefore be healed and kept in remission. Asymptomatic duodenal ulcers discovered during maintenance treatment appear to be clinically innocuous and do not therefore indicate therapeutic failure, nor require modification of therapy.

Helicobacter pylori (formerly, Campylobacter pylori ) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H, pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended.