Helicobacter pylori eradication in patients with peptic ulcer disease: clinical consequences and financial implications

We assessed clinical consequences and financial implicationsof Helicobacter pylori eradication in 175 patients with pepticulceration, of whom 106 had been free from H. pylori infectionfor a mean of 3.2 years, while 69 remained infected. We usedquarterly questionnaires to examine consumption of ulcer-healingmedication and antacids. In the 106 successfully treated patients,gastrointestinal haemorrhage as a complication of peptic ulcercomplications during the 344 patient years after eradication(0.003 per patient year) was 18-fold lower than during the 912patient years before eradication (0.056 per patient year). Ofthe H. pylori-negative patients, 12–18% used ulcer-healingmedication during any one of the three-month periods of thesurvey, compared with 34–51 % of the patients with residualH. pylori infection. The average cost of the ulcer-healing drugsconsumed by the H. pylori-negative patients was £30.59during the 12 months of the survey, compared with £99.05for H. pylori-positive patients. Consumption of antacids wasalso lower in the H. pylori-negative group. Successful eradicationof H. pylori significantly reduced the annual cost of ulcer-healingdrugs consumed by the patients with ulcer disease. Maintenanceof ulcer remission following successful eradication of H. pylorialso significantly reduced ulcer complications.     

Guidelines for the management of Helicobacter pylori--Maastricht III-2005 and Japanese guidelines

The guidelines on the management of Helicobacter pylori were updated at the European Helicobacter study group third Maastricht consensus conference in March 2005. Especially, this conference emphasis on the management of non ulcer dyspepsia, GERD, and the patients who use non steroidal anti-inflammatory drug. Eradication of H. pylori is recommended in patients with peptic ulcer, low grade MALT lymphoma, atrophic gastritis, unexplained iron deficiency anemia, chronic idiopathic thrombocytopenic purpura and first degree relatives of patients with gastric cancer. H. pylori eradication is less effective than proton pomp inhibitor(PPI) treatment in preventing ulcer recurrence in long term NSAIDs users. This meeting also emphasized on the relationship between H. pylori and gastric cancer. The guideline concluded that H. pylori eradication has the potential to reduce the risk of gastric cancer development. Japanese guideline in 2003 does not mention the effect of eradication for prevention of gastric cancer. The H. pylori eradication and new strategy should be desirable for global strategy of gastric cancer prevention.     

Reinfection or recrudescence after apparently successful eradication of Helicobacter pylori infection: implications for treatment of patients with duodenal ulcer disease

Helicobacter pyloris is considered to be aetiologically implicatedin gastritis and peptic ulceration, since if H. pyloris infectioncan be eradicated the risk of subsequent ulcer relapse is markedlyreduced. The rate of ‘reinfection’ following treatment rangesfrom 0% to 45%, but its origin remains controversial (reappearanceof uneradicated original infection or a fresh infection). Todistinguish temporary suppression of H. pylori from fresh infectionwe conducted a retrospective analysis of the criteria used toestablish eradication of the original infection in 304 patients.We used the [¹⁴C]urea breath test, in which an integrated areaunder the curve (AUC) value of < 40 in 2 h is consideredto indicate eradication of H. pylori in patients tested 1 monthafter treatment. The results suggest that relapsed infection with H. pylori usuallyrepresents recrudescence of the original infection rather thana fresh infection; there was a higher relapse rate in patientswith a breath test AUC > 20 < 40, compared with thosewith an AUC < 20. All ‘reinfections’ occurredwithin 24 months of the original treatment. ‘Reinfection’was uncommon in patients receiving powerful therapeutic regimens(e.g. triple therapy) compared with those receiving monotherapyor relatively ineffective dual therapy combinations. In patientswhose urea breath test remains negative 12 months after treatmentthe subsequent reinfection rate is only 0.44%/ year. This supportsthe strategy of eradicating H. pylori infection from suitablepeptic ulcer patients.     

Serum IL-8 as a possible marker for determining the status of<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in patients with untreated and treated peptic ulcer

Failure to eradicateHelicobacter pylori can lead to peptic ulcer recurrence and gastric malignancy. Therefore, the objective of this study was to develop a noninvasive method for determining whetherH pylori infection was eradicated with antibiotic-based triple therapy. A total of 17 patients with duodenal ulcer (DU) and 17 with gastric ulcer (GU) were evaluated both before and after treatment. Outcomes included serum levels of interleukin-8 (IL-8), pepsinogen I, and gastrin, and the Wilcoxon signed rank test was used to test significance. Changes in these parameters were also correlated with disease status. In those patients where both GU and DU healing occurred as a result of treatment, most showed an increase in serum IL-8 and a decrease in serum pepsinogen. Serum gastrin levels were not significantly changed in either group. Posttreatment increases in serum IL-8 were seen in 15 of 17 (88%) recovered DU patients and 14 of 17 (82%) recovered GU patients (P < .05 for each). Posttreatment decreases in pepsinogen I were found in 15 of 17 DU and 15 of 17 GU patients (P < .05 for each). These preliminary findings suggest that an increase in serum IL-8 and possibly a decrease in pepsinogen I may be useful in identifying the successful eradication ofH pylori infection in patients with peptic ulcer treated with antibiotics. A more systematic analysis of these putative diagnostic markers is now warranted.     

Quadruple therapy with ecabet sodium,omeprazole, amoxicillin and metronidazole is effective for eradication of Helicobacter pylori after failure of first‐line therapy (KDOG0201 Study)

Background and object: An antiulcer agent, ecabet sodium, is active against Helicobacter pylori. The aim of the present study was to clinically examine whether eradication therapy, which includes ecabet sodium, is effective in eradication of H. pylori after failure of first‐line therapy. Methods: Patients with peptic ulcer who failed with first‐line triple eradication therapy containing clarithromycin received quadruple therapy with omeprazole (20 mg, twice daily), amoxicillin (750 mg, twice daily), metronidazole (500 mg, twice daily) and ecabet sodium (1000 mg, twice daily) for 14 days. Eradication of H. pylori was judged by ¹³C‐urea breath test 8 weeks later. Results: Fifty‐two patients (36 men and 16 women) were included. Their mean age was 51·4 years (range 28–73). One patient dropped out because of diarrhoea. The eradication rate was 98·0% (50/51) according to the per‐protocol analysis and 96·2% (50/52) according to the intention‐to‐treat analysis. Side effects occurred in seven patients, but none were serious. Conclusions: Quadruple therapy including ecabet sodium is useful as second‐line eradication treatment for H. pylori.     

Performances diagnostiques du test rapide à l’uréase dans la détection de l’infection à Helicobacter pylori en période hémorragique

Introduction

The rapid urease test is considered one of the primary diagnostics of Helicobacter pylori infection among patients undergoing upper endoscopy and thanks to its high sensitivity and specificity, cost and reproducibility compared with the histological study. However, many studies suggest that the sensitivity of rapid urease test decreased significantly in patients with bleeding peptic ulcer. The aim of our study is to evaluate the diagnostic performance of rapid urease test in the diagnosis of H. pylori infection in peptic ulcer during bleeding complication.

Materials and methods

Our work is a prospective study on patients hospitalized for bleeding peptic ulcer, conducted at the hepatogastroenterology unit of University Hospital Hassan II over a period of two years and three months. All patients included in the study have benefited from antral biopsies with search of H. pylori infection in rapid urease test (CLOtest) and histology.

Results

One hundred and sixteen patients with bleeding peptic ulcer were admitted during this period. The sensitivity of rapid urease test was 72% with a negative predictive value of 30%, specificity of 88% and positive predictive value of 97%. The presence of blood in the stomach and the consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) were the major factors that decrease the sensitivity of this rapid test.

Conclusion

The rapid urease test is a test commonly used in practice for the diagnosis of H. pylori infection. Acute bleeding may be responsible for many false negatives due to the presence of blood in stomach and NSAIDs.     

Role of Helicobacter pylori in cirrhotic patients with dyspepsia: a 13C-urea breath test study

The role ofHelicobacter pylori in dyspeptic, cirrhotic patients remains unclear. This prospective outpatient study, conducted to assess the relationship of gastroduodenal disease andH. pylori as determined by the (¹³C) urea breath test, enrolled 109 consecutive cirrhotic patients with dyspepsia. All patients underwent upper-gastrointestinal endoscopy, which revealed respective prevalences of peptic ulcer, gastric ulcer, and duodenal ulcer of 41.3%, 23.9%, and 22.9%;H. pylori infection was found in 52.3%. The rate of peptic ulcer disease in theH. pylori-positive (45.6%) and -negative (36.5%) groups was not significantly different; neither was the prevalence ofH. pylori in patients with or without portal hypertensive gastropathy and with or without esophageal varices. The relationship between peptic ulcer disease andH. pylori in dyspeptic patients with cirrhosis appears to be weak. Likewise, no significant relationship was evident betweenH. pylori and portal hypertensive gastropathy or esophageal varices. This organism may not be a major pathogenetic factor in gastroduodenal diseases in dyspeptic patients with cirrhosis.     

Role of Helicobacter pylori eradication in the prevention of peptic ulcer in NSAID users

Helicobacter pylori (H. pylori) and non-steroidal anti-inflammatory drug (NSAID) are independent risk factors for peptic ulcers and ulcer complications and they have additive or synergistic effects. A meta-analysis showed that the OR for the incidence of peptic ulcer was 61.1 in patients infected with H. pylori and also taking NSAID when compared to patients uninfected with H. pylori and not taking NSAID. H. pylori eradication may prevent NSAID-induced ulcers in NSAID naive patients. In patients receiving long-term NSAID, proton pump inhibitor(PPI) is more effective in the prevention of ulcer recurrence and bleeding. However, H. pylori eradication should be considered in patients receiving long -term PPI maintenance treatment to prevent the development of corpus gastritis and gastric atrophy.     

Helicobacter pylori: ENOUGH TO GIVE ANYONE AN ULCER!

SUMMARY Since the early 1980s, research into gastritis and peptic ulcer disease has been dominated by Helicobacter pylori. This is a small, Gram-negative spiral bacterium which inhabits the mucus layer that coats the gastric mucosa. Colonisation of the human stomach by this bacterium is worldwide and, in certain continents, virtually ubiquitous. While histological gastritis is always the result, H. pylori-positive individuals are characteristically asymptomatic. Transmission is thought to be via the faecal-oral route and infection, usually acquired in childhood, will persist unless treatment supervenes. H. pylori is the main causative agent of peptic ulceration, but its role in non-ulcer dyspepsia is less clearcut. Recently epidemiological, histological and experimental data have been described linking H. pylori to gastric neoplasia — in particular adenocarcinoma and MALT lymphoma. A variety of treatment modalities exists for the eradication of this bacterium, and for adults the recommended drug therapy is a combination course of tetracycline, bismuth and metronidazole. Currently the new combination of omeprazole and amoxycillin is suggested as second-line treatment after failed triple therapy.     

Effects of Helicobacter pylori(Hp) eradication on gastric mucosal pathophysiology in Hp-positive, NSAIDs-induced gastric ulcer

It has been suggested that the mechanisms of NSAIDs-induced peptic ulcer disease are totally different from those induced by Hp. Although a number of studies have examined the effects of Hp eradication on pathophysiology of NSAIDs-induced ulcer diseases, the results have been controversial. At present, therefore, we do not know whether Hp should be eradicated in Hp-positive NSAIDs-induced ulcer patients. Recent studies have shown that both Hp eradication and NSAIDs treatment increases gastric acid secretion, and often causes mucosal lesions in upper GI tract. Based on this back ground, we have decided to review pathophysiology of the Hp-dependent ulcer, and the NSAIDs-induced ulcer. We also discussed the merit and demerit of Hp eradication on gastric mucosal pathophysiology in Hp-positive, NSAIDs-induced ulcer.     

Treatment of Helicobacter pylori infection

Helicobacter pylori infection has been shown to be the principal cause of peptic ulcer disease and has been associated with MALT lymphoma and gastric cancer. Eradication of H. pylori has been shown to change the natural history of peptic ulcer disease by preventing relapse and to reduce health care expenditures when compared with traditional therapy. Two-drug regimens have been superceded by three-drug regimens because they are more effective in eradication. Therapies with the highest efficacy are cost-effective because failed eradication is associated with high costs.     

Geographical Pathology of Helicobacter pylori Infection: Is There More than One Gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection.

This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.     

New Therapeutic Approaches to Peptic Ulcer Disease: The Role of Helicobacter Pylori

One of the most common bacterial infections of human involves Helicobacter pylori, a spiral, gram-negative bacterium that is now thought to be a dominant factor in the development of peptic ulcer disease and may be significant in causing certain forms of gastric cancer. Almost 100% of patients with duodenal ulcer and 70 to 90% affected with gastric ulcer are infected with H. pylori. In order to achieve cure of H. pylori--induced ulcer disease, it is necesary to eradicate the bacterial infection. Mere suppression or clearance infection without eradication is associated with a >80% recurrence of the ulcer. The epidemiology, microbiology, and pathogenesis of H. pylori infections are reviewed. Diagnostic methods and optimal treatment strategies for H. pylori infections are examined. The most current diagnostic and treatment algorithms for peptic ulcer disease are discussed critically, and future directions for drug development aimed at eradication of H. pylori infection are considered.     

Pharmacogenetics of esomeprazole or rabeprazole‐based triple therapy in Helicobacter pylori eradication in Hong Kong non‐ulcer dyspepsia Chinese subjects

Objective: Our study aimed to assess the effectiveness of esomeprazole or rabeprazole in combination with amoxicillin and clarithromycin for the eradication of Helicobacter pylori in Hong Kong non‐ulcer dyspepsia (NUD) patients. Methods: A prospective clinical trial was conducted at the Alice Ho Miu ling Nethersole Hospital outpatient endoscopy center from June 2004 to December 2005. Participants received amoxicillin 1 g, clarithromycin 500 mg, and, esomeprazole 20 mg (EAC) or rabeprazole 20 mg (RAC), all given twice daily for 1 week. The H. pylori status was determined by the [¹³C] urea breath test at least 4 weeks after completion of the treatment. Mutation status of CYP2C19 in exon 4 and exon 5 associated with the poor metabolizer phenotype was determined. Results: The intention‐to‐treat eradication rates in patients treated with RAC and EAC were 77% and 84·6% respectively, and per protocol‐based eradication rates were 83·7% and 88·9% respectively. The eradication rates did not vary with CYP2C19 phenotype found. For clarithromycin‐sensitive strains, the cure rates were statistically significant regardless of CYP2C19 polymorphism (P < 0·0001). Conclusion: Triple therapy with either EAC or RAC is effective for Hong Kong Chinese NUD patients with H. pylori infection. Success eradication was related to clarithromycin resistance and not CYP2C19 genotype.     

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple Helicobacter pylori eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.     

Current state and measures of NSAIDs induced ulcer

In recent years, the incidence of Helicobacter pylori (H. pylori) infection has been decreasing and the incidence of peptic ulcer and bleeding ulcer induced by NSAIDs, especially low-dose aspirin (LDA), have been increasing. PPI and PG are useful for treatment and prevention of ulcers in patients receiving continuous administration of NSAIDs and/or LDA. H. pylori eradication is effective if performed before the start of NSAIDs administration, but a beneficial effect of H. pylori eradication performed during NSAIDs treatment cannot be expected. The incidence of ulcers is lower when administering COX-2-selective inhibitor than when administering non-selective NSAIDs, but attention must be given to cardiovascular events as side effects when administering COX-2-selective inhibitor.     

Strategy for peptic ulcer therapy in the era of H. pylori eradication therapy

The Japanese guideline for gastric ulcer therapy published 2003 has adopted a policy that eradication therapy for H. pylori as the first line therapy on ulcer patients with positive H. pylori status. For NSAID-induced gastric ulcer patients, cessation should be considered. In patients who cannot stop NSAIDs, proton-pump inhibitors or prostaglandin drugs is recommended. Similar strategy can be applied for duodenal ulcer patients. Implementation of this basic strategy in daily clinical practice, however, require further efforts to wider recognition of the new guideline for gastric ulcer therapy as well as to solve several barriers caused by discrepant health reimbursement policy.     

Time trends in the prevalence of Helicobacter pylori infection in patients with peptic ulcer disease: a single-center retrospective study in Shanghai

ObjectiveThe present study aimed to investigate the recent trends in Helicobacter pylori infection associated with peptic ulcer disease in a large population in Shanghai.MethodsWe analyzed the medical records of all patients who had undergone upper gastrointestinal endoscopy (EGD) for uninvestigated dyspepsia at Ren Ji Hospital between 2013 and 2019 to determine the prevalence of H. pylori infection in patients with peptic ulcers.ResultsPeptic ulcers were found in 40,385 of the 383,413 patients who underwent EGD during the study period. Over the 7-year study period, the annual prevalence of H. pylori among patients receiving EGD declined from 32.2% to 26.5%. H. pylori was present in 60% of ulcers and the incidence was higher (66.9%) in duodenal compared with gastric ulcers (48.5%). The proportion of H. pylori-associated gastric ulcers declined from 52.2% to 49.3% and that of H. pylori-positive duodenal ulcers declined from 70.0% to 63.9%.ConclusionThe prevalence of H. pylori-positive peptic ulcers, mainly duodenal ulcers, fell from 2013 to 2019. However, the proportion of non-H. pylori-associated peptic ulcer disease increased, especially in elderly people, possibly due to the use of nonsteroidal anti-inflammatory drugs. Further research is needed to confirm this hypothesis.     

Anti-ulcer therapy after eradication of Helicobacter pylori

Helicobacter pylori (H. pylori) infection is the cause of the frequent relapse of peptic ulcer disease. Successful eradication therapy of H. pylori is associated with a decline in the recurrence of peptic ulcer. In this paper, we discussed the significance of anti-ulcer therapy after H. pylori eradication therapy. In patients with duodenal ulcer, maintenance therapy for preventing ulcer recurrence is not necessary because the rate of ulcer recurrence after eradication therapy is very low. However, in patients with gastric ulcer, the rate of ulcer relapse and reflux esophagitis ranges between 5-10% in the Japanese population even after successful eradication therapy; therefore, maintenance therapy for 1 year may be permissible in patients with gastric ulcer even after successful eradication therapy.