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Helicobacter pylori (H. pylori) is a major cause of peptic ulcer disease (PUD), which needs effective eradication of the organism to heal ulcers and prevent a recurrence. In recent years, increasing resistance of H. pylori to clarithromycin and amoxicillin have decreased peptic ulcer cure rate following treatment with standard triple therapy worldwide. The addition of probiotics with standard triple therapy has shown excellent efficacy in H. pylori eradication and has appeared to be an alternative treatment strategy. This study aimed to assess the efficacy of standard triple therapy plus probiotics for H. pylori eradication and ulcer healing compared to standard triple therapy alone. This double-blind, randomized placebo-controlled clinical trial included 158 with endoscopically proven H. pylori-positive PUD who were randomly allocated equally into two groups; Group A was treated with standard triple therapy plus probiotics, and Group B was treated with standard triple therapy plus placebo for 14 days. The outcome was evaluated at the end of treatment (14th day) (symptoms plus adverse events) and after 60 days of treatment completion (H. pylori eradication and ulcer healing). One hundred forty four (144) study subjects (73 in Group A and 71 in Group B) completed the study. Significantly higher H. pylori eradication rate (82.2%vs. 67.6%, p=0.043) and ulcer healing rate (92.3% vs. 60.0%, p=0.049) were observed in the standard triple therapy plus probiotic group than the standard triple therapy plus placebo group. Early relief of epigastric pain was also seen among patients getting probiotics than the placebo in addition to standard triple therapy (42.3% vs. 15.1%, p<0.001).The addition of probiotics significantly improves the H. pylori eradication rate and ulcer healing rate among the patients getting standard triple therapy. Further large-scale, multi-center studies are needed to recommend routine use of probiotics with standard triple therapy for H. pylori eradication.

Peptic ulcers, recognized for their erosive impact on the gastrointestinal mucosa, present a considerable challenge in gastroenterology. Epidemiological insights underscore the global prevalence of peptic ulcers, affecting 5-10+% of individuals, with a yearly incidence of 0.3 to 1.9 cases per thousand. Recent decades have witnessed a decline in complications, attributed to improved diagnostics and therapeutic advancements. The review deepens into H. pylori -associated and NSAID-induced ulcers, emphasizing their distinct prevalence in developing and industrialized nations, respectively. Despite advancements, managing peptic ulcers remains challenging, notably in H. pylori -infected individuals facing recurrence and the rise of antibiotic resistance. The pathophysiology unravels the delicate balance between protective and destructive factors, including the intricate molecular mechanisms involving inflammatory mediators such as TNF-α, ILs, and prostaglandins. Genetic and ethnic factors, rare contributors, and recent molecular insights further enhance our understanding of peptic ulcer development. Diagnostic approaches are pivotal, with upper gastrointestinal endoscopy standing as the gold standard. Current treatment strategies focus on H. pylori eradication, NSAID discontinuation, and proton pump inhibitors. Surgical options become imperative for refractory cases, emphasizing a comprehensive approach. Advances include tailored H. pylori regimens, the emergence of vonoprazan, and ongoing vaccine development. Challenges persist, primarily in antibiotic resistance, side effects of acid suppressants, and translating natural compounds into standardized therapies. Promising avenues include the potential H. pylori vaccine and the exploration of natural compounds, with monoterpenes showing therapeutic promise. This review serves as a compass, guiding healthcare professionals, researchers, and policymakers through the intricate landscape of peptic ulcer management., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

Competing Interests: The authors declare that they have no conflict of interest.

Background: Helicobacter pylori (H. pylori) was discovered 40 years ago and has set a milestone in human medicine. The discovery led to rejection of the dogma of the acidic stomach as a sterile organ and requested to rewrite the chapters on gastric pathophysiology and gastroduodenal diseases., Summary: Over a period of 40 years following the discovery, more than 50,000 articles can be retrieved in PubMed as of today and illustrate the amount and the intensity of research around the role of this bacterium. H. pylori emerged as cause of chronic gastritis and principal cause of peptic ulcer disease (PUD). Eradication of H. pylori became standard of care in management in PUD. The importance of this was highlighted in 2005 with the Nobel Prize in Medicine awarded to Barry Marshall and Robin Warren. H. pylori became eventually recognized for its oncogenic potential in the stomach and as the main risk factor for gastric cancer development., Key Messages: H. pylori gastritis is defined as infectious disease and requires therapy in all infected individuals. Strategies of gastric cancer prevention and development of therapies to overcome the increasing antibiotic resistance are main targets in clinical research of today., (© 2024 S. Karger AG, Basel.)

Peptic ulcer disease is a common cause of epigastric pain typically related to Helicobacter pylori infection or NSAID use that can lead to serious consequences including upper GI bleed or perforation if undiagnosed. Diagnostic strategies vary depending on age and treatment is dependent on etiology., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Introduction: Functional dyspepsia (FD), although commoner than organic dyspepsia (OD) in-hospital studies, community data, particularly from rural areas, are lacking. We performed a rural community study in Bangladesh with the primary aims to evaluate (i) the prevalence of uninvestigated dyspepsia (UD), FD, and OD and (ii) the risk factors for UD., Methods: This house-to-house survey was performed using a translated-validated enhanced Asian Rome III questionnaire and endoscopy with Helicobacter pylori tests, including genotyping., Results: Of 3,351/3,559 responders ([94.15%], age 40.41 ± 16.05 years, female 1924 [57.4%]), 547 (16.3%) had UD (female 346 [18%] vs male 201 [14%]; P = 0.002); 201 (6%), 88 (2.6%), and 258 (7.7%) had postprandial distress (PDS), epigastric pain syndromes (EPS) and PDS-EPS overlap, respectively. On multivariate analysis, age >50 years (adjusted odds ratio [AOR] 1.34 [1.07-1.68]), female sex (AOR 1.42 [1.17-1.74]), being married (AOR 1.57 [1.21-2.07]), lower family income (AOR 1.79 [1.43-2.26]), nonsteroidal anti-inflammatory drug use (AOR 7.05 [2.11-23.55]), previous acute gastroenteritis (AOR 5.42 [1.83-16]), and psychological distress (AOR 5.02 [2.87-8.76]) were risk factors for UD. Of 346/547 (63.25%) undergoing endoscopy, 232 (67.05%) and 114 (32.95%) had FD and OD (peptic ulcers [PU] 99 [28.61%] and erosive esophagitis 13 [3.76%]). About 53% of FD subjects had EPS-PDS overlap, 32% had PDS, and only 15% had EPS. H. pylori was detected in 266/342 (78%) dyspeptics (FD 173/230 [75.2%], vs OD 92/114 [82.1%], P = 0.169)., Discussion: Sixteen percent, 11% and 5% of rural Bangladeshi Asian adults had UD, FD, and PU, respectively. One-third of UD subjects had OD, mostly PU.JOURNAL/cltg/04.03/01720094-202104000-00016/inline-graphic1/v/2021-04-15T161418Z/r/image-tiff., (Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.)

Prevalence of H. pylori (HP) is declining, whereas reflux disease and the proportion of non-steroidal antiinflammatory drugs (NSAR) to HP-induced ulcers increase. Eradication heals HP-ulcer disease, interrupts cancerous progression and can improve dyspeptic symptoms. NSAR-ulcers heal under proton pump inhibitor (PPI) therapy but tend to recur after reexposition. Anticoagulants and antiplatlet agents increase the risk additionally. PPI reduces NSAR-ulcer recurrence. Reflux patients with severe inflammation and complications often need long-term therapy. Barrett’s esophagus patients are at risk of esophageal adenocarcinoma.

The ideal treatment regimen for the eradication Helicobacter pylori infection has yet to be identified. Probiotics, particularly Lactobacillus, Bifidobacterium and Saccharomyces, have been suggested as adjuncts to antibiotics for the treatment of H. pylori. There is in vitro evidence that probiotics dampen the Th1 response triggered by H. pylori, attenuate H. pylori associated hypochlorhydria and secrete bacteriocidal metabolites. Probiotics interact with the innate host immune system through adherence to the gastric epithelium and secretion of bacterial adhesins. In prospective human studies, probiotic monotherapy effectively decrease H. pylori density (expired (13)CO2) by 2.0%-64.0%. Probiotic monotherapy has also been shown to eradicate H. pylori in up to 32.5%, although subsequent recrudescence is likely. Eleven meta-analyses have evaluated the efficacy of probiotics as adjuvants to antibiotics for the eradication of H. pylori. The addition of a probiotic increased treatment efficacy, OR 1.12-2.07. This benefit is probably strain-specific and may only be significant with relatively ineffective antibiotic regimens. The pooled prevalence of adverse effects was 12.9%-31.5% among subjects receiving adjuvant probiotics, compared with 24.3%-45.9% among controls. Diarrhea in particular was significantly reduced in subjects receiving adjuvant probiotics, compared with controls (OR 0.16-0.47). A reduction in adverse events other than diarrhea is variable. Despite the apparent benefit on efficacy and side effects conferred by probiotics, the optimal probiotic species, dose and treatment duration has yet to be determined. Further studies are needed to identify the probiotic, antibiotic and patient factors which might predict benefit from probiotic supplementation., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Data on the role of dental plaque in the transmission of Helicobactor pylori have varied. Furthermore, there has been few reports on the relationship between dental plaque control and H. pylori infection of gastric mucosa. The purpose of this study was to elucidate this potential relationship., Methods: The 13C urea breath test was conducted on 56 subjects who received dental plaque control and 51 subjects who did not., Results: The prevalence of H. pylori in the gastric mucosa was 19.64% in patients who received dental plaque control, which was significantly lower than in those without dental plaque control (84.31%)., Conclusion: Long-term professional dental plaque control was associated with less gastric reinfection by H. pylori, suggesting that dental plaque control may help to prevent H. pylori-induced gastric disease or reinfection.

Objectives: There have been no reported data on the medical care cost of idiopathic peptic ulcer disease (PUD) compared with H. pylori (+) and/or NSAID (+) cases although H. pylori-negative idiopathic ulcers are increasing. The aim of this study was to investigate the direct medical care costs of PUD based on whether it was H. pylori infection/from NSAIDs or idiopathic., Material and Methods: One hundred and seventy three patients with PUD comprising H. pylori and/or NSAID use-associated PUD (n = 145) and idiopathic PUD (n = 28) were prospectively enrolled in this study. The direct medical care costs were analyzed retrospectively for the patients with PUD during a one-year follow-up period., Results: The recurrence rate within one year was significantly higher in idiopathic PUD than H. pylori and/or NSAID-associated PUD (p = 0.002). Direct medical care costs of idiopathic PUD ($2483.8) were higher than in patients with H. pylori and/or NSAID-associated PUD ($1751.8) resulting from longer duration of medication and higher proportion of endoscopic hemostasis and hospitalization., Conclusions: More clinical research is needed to improve outcome and reduce recurrence rate and medical care costs of idiopathic PUD.

Background/purpose: Peptic ulcer disease (PUD) in children is relatively rare as compared with adults. This study aimed to assess the etiology, clinical and histological characteristics, and treatment of PUD in children., Methods: All children aged < 18 years with an endoscopic diagnosis of PUD were enrolled in a tertiary referral center. The demographic data, clinical, endoscopic, and histological findings were compared between patients with different causes of PUD., Results: From 1234 endoscopic examinations, 67 (5.4%) children (median age, 11.4 years) with gastric ulcer (GU; n=27) or duodenal ulcer (DU; n=40) were included. Thirty-two (47.7%) of them had Helicobacter pylori infection and 11 (16.5%) had previous use of non-steroidal anti-inflammatory drugs (NSAIDs). Non-H. pylori, non-NSAID PUD was found in 24 (35.8%) patients. Children with H. pylori-related PUD had a significantly higher mean age, antral chronic inflammatory score, rate of familial PUD, and presence of DU and nodular gastritis than those with NSAID-related and non-H. pylori, non-NSAID PUD (p < 0.01). In contrast, children with NSAID-related PUD had a higher rate of upper gastrointestinal bleeding, associated with acute febrile disease, than those with H. pylori-related and non-H. pylori, non-NSAID PUD (p < 0.05). All but two patients with non-H. pylori, non-NSAID PUD were disease free after H. pylori eradication and proton pump inhibitor treatment for 1-2 months., Conclusion: In children, H. pylori-related PUD is associated with familial peptic ulcer and the presence of DU. However, short-term NSAID use is correlated highly with GU. The outcome of childhood PUD is good.

This guideline updates a prior consensus recommendation of the German Society for Digestive and Metabolic Diseases (DGVS) from 1996. It was developed by an interdisciplinary cooperation with representatives of the German Society for Hygiene and Microbiology, the Society for Pediatric Gastroenterology and Nutrition (GPGE), and the German Society for Rheumatology. The guideline is methodologically based on recommendations of the Association of the Scientific Medical Societies in Germany (AWMF) for providing a systematic evidence-based S 3 level consensus guideline and has also implemented grading criteria according to the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) process. Clinical applicability of study results as well as specifics for Germany in terms of epidemiology, antibiotic resistance status, diagnostics, and therapy were taken into account.

Background: Helicobacter pylori-associated diseases and gastroduodenal ulcer disease are common conditions of major clinical and economic importance. There is thus a need for a guideline that incorporates the scientific knowledge gained in recent years and that takes specific aspects of the situation in Germany into account with regard to epidemiology, resistance status, diagnostic evaluation, and treatment., Methods: This level-S3 consensus guideline was developed in accordance with the recommendations of the Association of Scientific Medical Societies in Germany (Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften, AWMF). It was commissioned by the German Association for Digestive and Metabolic Diseases (Deutsche Gesellschaft für Verdauungs- und Stoffwechselkrankheiten, DGVS) and prepared in cooperation with other scientific societies. After search terms were compiled, a systematic, IT-supported literature search was performed in the PubMed and Cochrane databases. The search was restricted to articles that appeared in German or English from 2000 onward., Results: H. pylori infection can be accurately diagnosed either non-invasively (with a (13)C-urea breath test or a stool antigen test) or invasively (with a rapid urease test, by histology, or by culture). Gastric and duodenal ulcer and gastric MALT lymphoma are absolute indications for eradication therapy; relative indications include functional dyspepsia, the prevention of gastric cancer in persons at risk, the initiation of long-term treatment with non-steroidal anti-inflammatory drugs (NSAID), and the prior occurrence of gastroduodenal complications with the use of either NSAID or acetylsalicylic acid (ASA). First-line therapy consists of a proton-pump inhibitor (PPI) and clarithromycin combined with either metronidazole or amoxicillin, given for at least one week., Conclusion: This guideline enables the structured, evidence-based diagnosis and treatment of H. pylori infection and associated conditions, as well as of gastroduodenal ulcer disease.

Background & Aims: Helicobacter pylori (H pylori) is a risk factor for gastric cancer. We investigated whether early H pylori eradication is associated with gastric cancer risk in patients with peptic ulcer diseases., Methods: This nationwide cohort study was based on the Taiwan National Health Insurance Database (NHID), which provided data on 80,255 patients who were hospitalized for the first time between 1997 and 2004 with a primary diagnosis of peptic ulcer diseases and received H pylori eradication therapy. The patient population was divided into early (within 1 year) and late (after 1 year) eradication cohorts; standardized incidence ratios (SIRs) and hazards ratios (HRs) were determined., Results: There was no significant difference in gastric cancer risk between patients who received early H pylori eradication and the general population (SIR, 1.05; 95% confidence interval [CI]: 0.96-1.14), but late eradication was associated with an increased risk (SIR, 1.36; 95% CI: 1.24-1.49). In gastric ulcer patients who received early eradication, SIRs of gastric cancer decreased from 1.60 at 3-4 years to 1.05 at 7-10 years after hospitalization; the SIRs decreased from 0.57 to 0.33 for duodenal ulcer patients over the same period. Among patients who received late eradication, SIRs decreased from 2.14 to 1.32 for those with gastric ulcers and from 0.90 to 0.66 for those with duodenal ulcers. Early H pylori eradication (HR, 0.77) and frequent aspirin or nonsteroidal anti-inflammatory drug use (HR, 0.65) were independent protective factors for gastric cancer., Conclusions: Early H pylori eradication is associated with decreased risk of gastric cancer in patients with peptic ulcer diseases.

Recent studies indicate that oxidative stress caused by Helicobacter pylori and insufficient host antioxidant defense could play important role in pathogenesis of gastrointestinal ulcerations. By specific monoclonal antibodies we have detected weak presence of the major lipid peroxidation bioactive marker 4-hydroxynonenal (HNE) in healthy human gastric mucosa, which strongly increased in case of H. pylori-associated peptic ulcer. Considering physiological presence of HNE on one hand, and high prevalence of H. pylori associated disorders on the other, evaluation of oxidative stress after treatment is important. Therefore, in current study immunohistochemical accumulation and distribution of HNE-protein adducts in gastric mucosa was evaluated with 21 patients having H. pylori-associated duodenal peptic ulcer (DPU) before and one month after eradication of H. pylori. Although dramatic decrease in histological manifestations of inflammation was demonstrated after eradication of H. pylori, initially high immunopositivity for the HNE-protein adducts remained elevated in antrum and even increased in stomach corpus. The observed accumulation and redistribution to higher grades of HNE-immunopositivity in nuclei of glandular cells in gastric corpus indicate augmentation of oxidative stress after treatment and open possibilities for adjuvant antioxidant treatments to protect gastric mucosa from progressive oxidative stress after eradication of H. pylori infection.

This guideline updates a prior concensus recommendation of the German Society for Digestive and Metabolic Diseases (DGVS) from 1996. It was developed by an interdisciplinary cooperation with representatives of the German Society for Microbiology, the Society for Pediatric Gastro-enterology and Nutrition (GPGE) and the German Society for Rheumatology. The guideline is methodologically based on recommendations of the Association of the Scientific Medical Societies in Germany (AWMF) for providing a systematic evidence-based consensus guideline of S3 level and has also implemented grading criteria according to GRADE (Grading of Recommendations Assessment, Development and Evaluation). Clinical applicability of study results as well as specifics for Germany in terms of epidemiology, antibiotic resistance status, diagnostics and therapy were taken into account., (Georg Thieme Verlag KG Stuttgart, New York.)

Background: The incidence of peptic ulcer disease was expected to decrease following the introduction of acid inhibitors and Helicobacter pylori eradication., Aim: To analyse possible changes in the incidence of bleeding peptic ulcer, treatment and mortality over time., Methods: Residents of Malmö hospitalized for bleeding gastric or duodenal ulcer disease during 1987-2004 were identified in hospital databases (n = 1610). The material was divided into 6-year periods to identify changes over time. All patients who had been submitted to emergency surgery (n = 137) were reviewed., Results: The incidence rate for bleeding gastric or duodenal ulcers decreased by one half in males and by one-third in females and emergency operations decreased significantly (9.2%, 7.5% and 5.7% during the three time periods, respectively (P < 0.05). The post-operative mortality tended to decrease (9.7, 2.4 and 3.7%, respectively) and the 30-day mortality rates in the whole material were 1.2%, 3.6% and 3.4% during the different time periods., Conclusion: The incidence of bleeding gastric and duodenal ulcer disease has decreased markedly. Operative treatment has been replaced by endoscopic treatment. The bleeding ulcer-related mortality was less than 4% and has not changed over time.

Background: An increase in the prevalence of precancerous lesions and atrophic changes in the gastric mucosa has been reported as long-term consequences of vagotomy-induced acid suppression. This study was designed to describe the long-term changes in the gastric mucosa caused by vagotomy and Helicobacter pylori infection., Methods: Seventy-nine patients with vagotomized peptic ulcers, 70 nonoperated patients with peptic ulcers, and 85 matched community control subjects were randomly selected to participate in an upper endoscopic study. Biopsy specimens were taken from predestined locations of the gastric mucosa., Results: Mean follow-up time for the vagotomized patients was 17.3 (range, 6-28) years and 12.7 (range, 10-17) years for the medically treated peptic ulcer patients. In H. pylori-positive subjects, severe atrophic changes in the distal gastric mucosa (prepylorus and angulus) was found in 30% (95% confidence interval (CI), 19-43) of the vagotomized patients and in 43% (95% CI, 29-58) of medically treated patients with peptic ulcers, and in 32% (95% CI, 20-46) of the community control subjects. Severe intestinal metaplasia was not found more frequently in vagotomized peptic ulcer patients compared with medically treated patients with peptic ulcers (p = 0.5). The histological picture of the age-matched community control subjects did not differ significantly from the patients with peptic ulcers when corrected for presence of H. pylori infection., Conclusions: This study lends no support to theories of increased premalignant changes in the gastric mucosa of vagotomized patients. H. pylori infection rather than long-term acid suppression seems to be the explanation of the gastric mucosal changes seen after vagotomy.

Peptic ulcer disease remains a common problem and it most frequently due to the presence of an Helicobacter pylori infection or use of non-steroidal anti-inflammatory drugs (NSAIDs). Dyspepsia is neither sensitive or specific for diagnosing peptic ulcer disease. The approach to patients with dyspepsia is to arrive at a definitive diagnosis without unnecessary exposure to invasive or costly diagnostic procedures. Non-invasive testing is preferred with endoscopy being reserved for those with alarm markers or above a specified age (e.g., 55 years in Western countries). Patients negative for H. pylori infection should receive an empiric trial of acid suppression for 4 to 8 weeks and if beneficial it can be continued.

Aim: To compare the effects of treatment of H pylori-infected individuals with the effects of treatment of individuals as well as all H pylori-infected family members., Methods: H pylori-positive patients with similar demographic specifications were prospectively randomized with respect to treatment, with a triple regimen of either patients and all H pylori-positive family members living togetherI (group I) or patients only (group II). Nine months after treatment, all patients were assessed for H pylori positivity., Results: There were 70 H pylori-positive patients in each group; patients in groups I and II lived with 175 and 190 H pylori-positive relatives, respectively. Age, sex and H pylori positivity rate were similar in both groups of relatives. Nine months after 14 d standard triple therapy, H pylori positivity was 7.1% in group I patients and 38.6% in group II patients [P < 0.01, OR = 8.61 95% confidence interval (CI): 2.91-22.84]., Conclusion: The present results indicate bad environmental hygienic conditions and close intra-familial relationships are important in H pylori contamination. These findings indicate all family members of H pylori-positive individuals should be assessed for H pylori positivity, particularly in developing countries where H pylori prevalence is high; they also suggest patients, their spouses and all H pylori-positive family members of H pylori-positive individuals should be treated for H pylori infection.

Background/aims: The increasing trend of antibiotic resistance emphasizes the need for the assessment of eradication rate of first and second-line therapy for Helicobacter pylori (H. pylori) infection. The reinfection rate depends on the geographical, national, or socioeconomic status of the patients. The aim of this study was to evaluate the recent 5-year changes of eradication rates and the reinfection rates after the successful eradication of Helicobacter pylori infection for 3-years follow-up in Bucheon, Korea., Methods: From February 2001 to August 2006, 3,267 patients with H. pylori-positive peptic ulcer disease received the first-line therapy for 7 days. The 317 patients who failed to the first-line therapy received the second-line therapy for 7 days. The 167 patients with 3-years follow-up after the successful eradication were included. 13C-urea breath tests or rapid urease tests and histologies were assessed to determine the H. pylori status after the eradication., Results: The eradication rate of first-line therapy was 83.7% in 2001, 83.4% in 2002, 83.7% in 2003, 85.9% in 2004, 87.2% in 2005, and 81.8% in 2006 by per protocol analysis (PP), respectively. The eradication rate of second-line therapy was 80.0% in 2002, 86.8% in 2003, 89.7% in 2004, 98.0% in 2005, and 78.8% in 2006 by PP. The cumulative reinfection rate was 6.0%. The annual reinfection rate was 2.0%. The recurrence rate of peptic ulcer was 17.2% in the patients without reinfection and 50% with reinfection., Conclusions: The eradication rate for H. pylori have not changed in the recent 5-years. The annual reinfection rate was low. The successful eradication of H. pylori was effective for preventing the recurrence of peptic ulcers.

Treatment of peptic ulcer disease has undergone a radical change due to the discovery of its main cause, the Helicobacter pylori infection. The management of the chronic infection is now the primary aim. Treatment of peptic ulcer essentially consists of eradicating H. pylori. A current problem is the resistance developed by H. pylori to the antibiotics used in eradication regimen. Ulcers that are induced by nonsteroidal antirheumatic (NSAR) agents and acetylsalicylic acid are gaining in importance. Optimized inhibition of acid secretion with proton pump inhibitors has made it possible to both prevent and cure ulcers in the stomach and duodenum caused by NSAR agents.

The author presents an objective, evidence-based analysis of the main conceptions of the infectious theory of peptic ulcer (PU), critically discussing such postulates as "no Helicobacter pylori (HB), no PU", "HP is a pathogen that presents the main cause of PU", "a good HP is a dead HP", "HP eradication leads to complete recovery from PU", etc. The article presents original author's concepts on interrelations between HP infection and the human organism, and the pathogenesis of HP-associated PU. The consequences of the practical realization of the recommendations of Maastrich Consensus on HP eradication are discussed. The data of the author's studies dedicated to the ways of increasing the effectiveness of treatment of HP-associated PU, based on the author's conception of its pathogenesis, are adduced.

Helicobacter pylori causes acute on chronic gastritis and is responsible for most peptic ulcers and gastric cancer. However, recent papers have suggested that it may protect against gastro-oesophageal reflux, Barrett's oesophagus and oesophageal cancer. Furthermore, the rapid increase in gastro-oesophageal reflux disease, Barrett's oesophagus and adenocarcinoma of the oesophagus in the developed world has been attributed by some to the falling prevalence of H. pylori. These considerations have led to the suggestion that H. pylori infection should not necessarily be treated, especially in patients with gastro-oesophageal reflux disease. Conversely, data from prospective randomized studies have shown that H. pylori eradication does not cause gastro-oesophageal reflux disease in patients with duodenal ulcer or in the normal population, nor does it worsen the outcome of pre-existing gastro-oesophageal reflux disease. Therefore, although H. pylori is negatively associated with gastro-oesophageal reflux disease, its eradication does not induce the disease. A hypothesis is presented suggesting that the increased prevalence of gastro-oesophageal reflux disease is a result of rising acid secretion in the general population, which, in turn, is a consequence of the increased linear height (a predictor of acid secretion). The greater acid secretion could also explain the decline in the prevalence of H. pylori and perhaps account for the inverse relationship between H. pylori and gastro-oesophageal reflux disease. These considerations are explored in discussing whether H. pylori infection should be treated in infected patients presenting with gastro-oesophageal reflux disease.

Significant advances continue to be made in the area of gastritis and ulcer disease. Studies to identify the most appropriate use of capsule endoscopy have now confirmed that it is superior to other methods for identifying small-bowel mucosal pathology and sites of obscure gastrointestinal bleeding. It has increasingly been recognized that the complications of ulcer disease are secondary to the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and to interactions between NSAIDs and Helicobacter pylori. Effective prophylaxis for NSAID ulcers in H. pylori-negative individuals continues to be a challenge, as it has become clear that conclusions from studies focusing on "endoscopic ulcers" in patients whose H. pylori status was unknown provided a false sense of security. The concept of multifocal atrophic gastritis has been challenged. The precursor lesion to gastric cancer now appears to be a sheet of pseudopyloric metaplasia advancing into the gastric body with islands of intestinal metaplasia embedded within it. Multifactorial models such as those proposed for understanding periodontal disease, including the organism, environmental factors, and host factors, appear particularly applicable to understanding the pathogenesis of H. pylori-associated gastric cancer.

We aimed to determine if successful or failed eradication of Helicobacter pylori with triple therapy causes any difference in gastric mucosal histology. Japanese H. pylori-positive patients with a healed peptic ulcer received high (n = 112) or low (n = 113) doses of triple therapy (omeprazole, amoxicillin and clarithromycin) for 1 week. Biopsies from the greater curvature of the central antrum and upper corpus were taken 6 weeks and 30 weeks after treatment completion, and gastric mucosal histology compared between successful (n = 171) and failed (n = 34) eradication groups. Morphological variables of gastritis were graded according to the updated Sydney System. Successful eradication therapy was defined as improvement in inflammation, neutrophil activity and atrophy; failed eradication therapy as improvement in inflammation and neutrophil activity only. Gastric mucosal atrophy gradually improved (in addition to improvements in inflammation and neutrophil activity) with successful eradication of H. pylori infection.

Helicobacter pylori is an organism that is thought to be important in the pathophysiology of ulcer disease and gastritis. Eradication of the organism is useful in the treatment of infected patients. Efficacious regimens generally include an antisecretory agent combined with two antimicrobials. The main determinant of the overall cost of treatment is the eradication of H. pylori in the microorganism. Resistance to the commonly used antibiotics can occur but it can be usually overcome with regimen changes. It is important for care physicians to clearly understand when and how to test and how to select appropriate therapy for Helicobacter pylori infection.

There appears to be a disconnect between current guidelines for Helicobacter pylori testing and treatment, and clinical practice, including physician beliefs and actual prescribing patterns. In particular, there are markedly different approaches in primary and secondary care, and country-specific differences in eradication therapy for H pylori infection. Although most physicians do not believe that H pylori causes non-ulcer dyspepsia, the majority appear to prescribe eradication. Less information is available on the management of H pylori infection and gastro-esophageal reflux disease, and more marked differences in attitudes and practice occur in this condition. Even in peptic ulcer disease, where most clinicians both in primary and in secondary care believe H pylori should be eradicated, there is often a breakdown in the translation of this belief into practice. There is also confusion in terms of treatment regimens applied for H pylori eradication. Eradication regimens are less successful in practice than in clinical trials. Furthermore, a sizable proportion of patients with peptic ulcer remain symptomatic despite cure of the ulcer diathesis, which may undermine confidence. Therapeutic confusion about what to prescribe, side effects limiting compliance, bacterial resistance, and socioeconomic factors may all impair therapeutic success with eradication therapy in practice. Unfortunately, it has been well documented that guidelines alone are likely to have little or no impact in practice. Publication in a journal is unlikely to lead to effective implementation in primary care. On the basis of available evidence, clinical behaviour is most likely changed when guidelines are developed by the peer group of clinicians for whom they were intended, are disseminated through a specific educational program, and are implemented by applying, preferably during the consultation, specific reminders.

Medical ethics are not absolute; they change according to social attitudes, technological advances and alterations in the doctor/patient relationship. The discovery of Helicobacter pylori highlighted entrenched attitudes in academia and the pharmaceutical industry that were not always appropriate. The explosion of research that followed was ethically controlled by local research ethics committees and the system of peer review and editorial responsibility. Now that effective treatments are available, the control arm in trials of new therapy should be either placebo (giving the option of effective treatment later) or a first-line treatment; mono and dual therapy should not be employed because of the risk of inducing bacterial resistance. Ethical issues that still remain include whether always to test patients for H pylori at endoscopy and what information should be given when they test positive. The most important issue is the approach of the medical profession to the high death rate carried by H pylori infection. Peptic ulcer and gastric cancer together account for a large number of deaths worldwide, and the medical profession and public health services have not yet grappled with this problem, neither advocating universal testing and treatment nor funding or research to determine whether this approach would be effective.

Background and Study Aims: Eradication of Helicobacter pylori infection can reduce the rebleeding rate of peptic ulcer bleeding in the long term. There are few data on the influence of H. pylori on the rebleeding rate in the acute phase of bleeding however. We therefore prospectively investigated the influence of H. pylori infection on the early rebleeding rate in patients who had undergone successful endoscopic hemostasis treatment for peptic ulcer bleeding., Patients and Methods: Between January 1996 and November 2000 all patients with peptic ulcer bleeding were evaluated consecutively. The diagnosis of H. pylori infection was made at index endoscopy, using histology and the rapid urease test. Bleeding activity was assessed using the Forrest classification. After successful endoscopic hemostasis all patients received omeprazole 40 mg or pantoprazole 40 mg, intravenously, twice a day for 3 days. Rebleeding episodes were recorded over 21 days following primary hemostasis., Results: 344 patients were enrolled into the study. The prevalence of H. pylori infection was 62.9 %. A total of 51 patients showed rebleeding (14.8 %), of whom 31 were H. pylori-positive (60 %). There was no statistically significant difference between the H. pylori-positive and -negative patients, however. The rebleeding rate did not differ between patients with H. pylori infection alone and patients also using nonsteroidal anti-inflammatory drugs. When stratifying patients according to activity of bleeding at index endoscopy, we were also unable to find any significant influence of H. pylori infection on the outcome of Forrest class I and IIa bleedings., Conclusion: Based on our data, it can be concluded that H. pylori infection does not affect the early rebleeding rate in patients with peptic ulcer bleeding after successful endoscopic hemostasis.

Background: Helicobacter pylori infection is highly prevalent and may cause disease in 10% to 15% of infected individuals: duodenal and gastric ulcer, gastric cancer and gastric lymphoma. Guidelines for a test-and-treat policy have been published by the European H. pylori working group in Maastricht., Goals: To assess the current approach to H. pylori-related diseases, indications for testing and eradication therapy, among internists and surgeons of a University affiliated medical center., Study: A 15-items questionnaire was formulated according to the Maastricht II test-and-treat recommendation and distributed among the physicians of 6 internal medicine departments and the department of surgery. The questionnaires were completed anonymously at the department's staff meeting, under the supervision of the head of the department. All questions required a yes/no answer; the maximum possible score was 15. The relative ratio (RR) of correct answers was calculated for every question and by subgroups as follows: all participants, internists, surgeons, experts and residents in internal medicine and surgery., Results: The response rate was 68% (55 out of 80 physicians). Total score for all participants was 10.9 (RR = 0.73), significantly lower than the maximum score of 15 (RR = 1.00). The internists had significantly higher average score than the surgeons for 2 questions: causative agent in gastric cancer (p = 0.003) or gastric lymphoma (p = 0.003), 1 question about triple therapy, PPI, penicillin and azythromycin being not recommended (p = 0.022), and for 1 question of test-and-treat policy: should this strategy apply to family members of gastric cancer patients (p = 0.045). Only 56% of the internists and 21% of surgeons knew what MALToma is, and the correlation with H. pylori infection., Conclusion: Knowledge of Surgeons and Internists regarding infection and correlation with diseases or test and treat policy should be improved.

Recurrence of peptic ulcer after successful eradication of Helicobacter pylori is closely associated with reinfection. The aim of this study was to examine the recurrence of peptic ulcer and reinfection with H. pylori after successful eradication. To eradicate H. pylori infection, patients with active peptic ulcer disease were assigned to two treatment groups depending on the year of their enrollment (AM group and OAMR group). Patients in the AM group received 400 mg of cimetidine twice per day, 300 mg of amoxicillin three times per day, and 250 mg of metronidazole three times per day for 2 weeks. Patients in the OAMR group received 20 mg of omeprazole once per day, 500 mg of amoxicillin granules three times per day, 250 mg of metronidazole three times per day, and 150 mg of roxithromycin twice per day for 1 week. After endoscopy verified ulcer scarring and successful eradication of H. pylori infection, study patients were followed up monthly and did not undergo acid-suppressive therapy. Endoscopy was performed at 6-month intervals for the 1st year. After the 1st year, follow-up endoscopies were performed annually. In total, 107 patients with peptic ulcer (duodenal ulcer [DU], 65; gastric ulcer [GU], 42) were followed up for a mean period of approximately 2 years. Recurrence of infection occurred in 10 (9.3%) of 107 patients (AM group, 9; OAMR group, 1) after 210 patient-years of follow-up; the recurrence rate was 4.8% per patient-year. Recurrence of H. pylori infection was significantly higher in the AM group (23.1%) than in the OAMR group (1.5%). H. pylori infection recurred in two patients 6 months after eradication therapy, in seven 1 year after, and in one 2 years after. Thereafter, no further cases of H. pylori recurrence were observed. During follow-up periods, seven cases of ulcer recurrence were observed (DU, 4; GU, 3). The rate of peptic ulcer recurrence within 2 years after eradication therapy was significantly higher than that after more than 2 years. Four cases of ulcer recurrence (DU, 3; GU, 1) also had recurrence of H. pylori infection. One recurrent case of DU without reinfection was associated with nonsteroidal anti-inflammatory drugs. The remaining two cases of GU recurred without H. pylori reinfection. In conclusion, peptic ulcer recurrence rarely occurred (3 [2.9%] of 103) in patients cured of H. pylori infection. Reinfection after apparent successful eradication was rarely noted when a powerful therapeutic regimen in eradication was used. Therefore, to eradicate H. pylori, a highly effective therapeutic regimen should always be used.

Gastroduodenal ulcerations still account for the majority of nonvariceal gastrointestinal hemorrhage. The causative roles of Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are still being discussed, but the role of H. pylori appears less significant in the complicated ulcers, while NSAIDs are increasingly implicated. The two factors do not appear to potentiate each other, and some data suggest that H. pylori should not be eradicated in the context of an NSAID-related ulcer hemorrhage. The role of triage and risk assessment was highlighted in several of last year's publications, and increasing attention has been given to the cost aspects of peptic ulcer bleeding. There have been few comparative therapeutic trials, but several reports from Japan make a case for ethanol injection as an alternative to other injection agents. However, a randomized comparative trial is needed to further define the role of this technique. Radiological embolization techniques and minimally invasive surgery are increasingly becoming viable options in patients with complex cases, and a multidisciplinary approach is perhaps even more crucial today than ever before.