Pylori Eradication In Patients Research Articles

Morphological Characteristics of Early Gastric Neoplasms Detected After Helicobacter pylori Eradication

Previous morphological studies indicated that the eradication of Helicobacter pylori (H. pylori) made gastric neoplasms endoscopically indistinct through the flattening and covering of tumors with a non-neoplastic epithelium (NE). To validate these alterations. We reviewed and compared the endoscopic and histological findings of early gastric carcinomas and high-grade dysplasias resected endoscopically from H. pylori-infected and H. pylori-eradicated patients. The extent of NE covering a tumor was expressed as the histological length ratio of NE to the tumor. Tumor morphology was compared before and after therapies in patients who received H. pylori eradication treatments during the period from tumor discovery to endoscopic resection. NE-covered ratios were higher in the 59 tumors detected after the eradication of H. pylori than in the 152 tumors detected during the infection (median 8 vs. 0%, respectively), whereas the frequency at which an elevated morphology and whitish discoloration of a tumor were observed was less (14 vs. 56%, and 14 vs. 43%, respectively). These were also independent characteristics for tumors detected after the eradication of H. pylori. Two elevated tumors showing whitish discoloration out of 16 tumors became endoscopically indistinct following H. pylori eradication treatments through the flattening of tumors and muting of the discoloration. The eradication of H. pylori promoted covering with NE, the flattening of tumors, and muting of the whitish discoloration, which may make a subset of tumors, potentially including whitish elevated neoplasms, indistinct.

A study on healing of peptic ulcer disease after eradication of helicobacter pylori infection

There is intimate connection between peptic ulcer & Helicobacter pylori infection. But some uncertainties still surround the relationship between status of H. pylori infection and extent & time required for ulcer healing. This prospective observational study was carried out in the department of Gastroenterology, BSMMU, Dhaka from January 2007 to January 2008 to determine whether the successful eradication of H. pylori leads to adequate ulcer healing. To see the pattern of endoscopic findings in patients still having H. pylori infection after standard triple therapy for H. pylori were also a objective. Eighty nine consecutive patients, aged 15-60 years and of both genders, coming to the gastroenterology outpatient department with the symptoms suggestive of peptic ulcer disease and dyspepsia were included and H. pylori status was defined as positive if both rapid urease test & histopathology were positive. As found in this study, H. pylori was associated with 90% of duodenal ulcers and 80% of gastric ulcers. H. pylori eradication rate was 69%. Healing rate of duodenal ulcer and gastric ulcer after standard triple therapy for 14 days were 80% and 78% respectively. Adequate ulcer healing was achieved in this study despite relatively low eradication rate. Follow-up for additional period is required for recurrence of ulcer in 84 patients whose peptic ulcer disease had resolved but could not attain H. pylori eradication and H. pylori eradicated patients who are still having ulcer at endoscopy DOI: http://dx.doi.org/10.3329/bmj.v43i2.21388 Bangladesh Med J. 2014 May; 43 (2): 84-89

Preneoplastic Conditions in the Stomach: Always a Point of No Return

Gastric atrophy (GA) and intestinal metaplasia are defined preneoplastic conditions of the stomach, whereas Helicobacter pylori gastritis by itself represents a risk condition for gastric cancer (GC) development. After H. pylori eradication, an overall reduction of GC incidence has been shown. However, this effect is lost once H. pylori gastritis has evolved to severe GA. On the other hand, only up to 5% of patients with severe GA may develop intestinal-type GC, and therefore the so-called ‘point of no return' may not be appropriate to define the condition of all patients carrying preneoplastic changes in the gastric mucosa. Patients with the highest risk for GC are those who have already had GC that was cured by endoscopic resection. Prospective trials on the effect of H. pylori eradication in this high-risk group of patients showed inconsistent results, probably because of the inclusion of patients with and without baseline severe GA. Severe fundic GA determined by means of histology or serology represents the condition with the highest risk for metachronous neoplastic lesions in the stomach. In the present review, we focus on the effects of H. pylori eradication in patients with severe atrophy in terms of GC prevention.

Does H. pylori Eradication Therapy Benefit Patients With Hepatic Encephalopathy?

Ammonia is considered to play a central role in the pathogenesis of (minimal) hepatic encephalopathy ((M)HE). Bacterial urease activity is the regulatory enzyme, and bacteria colonizing the colon were originally assumed to be the main source of urease activity. Current concepts of the pathogenesis of (M)HE focus, among other things, on ammonia, which is generated both by urease activity of intestinal bacteria and by Helicobacter pylori in the stomach. : The aim of this study was to provide a systematic review of the role of H. pylori in the pathogenesis of HE. A systematic review was conducted following the recommendations in the Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) statement with a database search in PubMed, Scopus, and the Cochrane Database for all original contributions published from January 1950 to December 2013. As search terms in title and abstract, the following combinations were used: hepatic encephalopathy AND Helicobacter pylori, HE AND Helicobacter pylori, MHE AND Helicobacter pylori, hyperammonemia AND Helicobacter pylori, and minimal hepatic encephalopathy AND Helicobacter pylori, with a language restriction to English and German. Observational studies revealed conflicting results concerning a possible role of H. pylori infection in the pathogenesis of HE. Thirteen prospective clinical trials assessed the effect of H. pylori eradication in patients with HE and liver cirrhosis. Seven of these showed a beneficial effect of eradication therapy on (M)HE. All of these studies were highly diverse in design and methodology. Eradication therapy in H. pylori-positive cirrhotic patients may have a beneficial influence on hyperammonemia and (M)HE, but evidence from well-designed clinical studies is weak.

Helicobacter pylori infection & immune thrombocytopenic purpura in children and adolescents: A randomized controlled trial

Helicobacter pylori and immune thrombocytopenic purpura (ITP) association is not well established in chronic ITP (cITP) in children, although the cure of thrombocytopenia in approximately half of H. pylori eradicated adult patients has been described. The aim of this study was to investigate the effect of H. pylori eradication on platelet (PLT) recovery in cITP children and adolescents through a randomized, controlled trial. A total of 85 children (mean age 11.4 years) with cITP were prospectively enrolled. Diagnosis of H. pylori was established by two locally validated tests, 13C-urea breath test and monoclonal stool antigen test. Twenty-two infected patients were identified, and randomly allocated into two groups: H. pylori treatment group (n = 11) and the non-intervention control group (n = 11). The control group was offered treatment if the thrombocytopenia persisted after the follow-up. At baseline, there were no differences regarding age, sex, duration of disease, and PLT count between groups. Sixty three of 85 patients were uninfected. PLT response was classified as complete response: PLT > 150 × 109 l−1; partial response: PLT 50–150 × 109 l−1, or an increase of 20–30 × 109 l−1; no response: PLT < 50 × 109 l−1 or an increase of <20 × 109 l−1 after at least 6 months of follow-up. Complete response was observed in 60.0% (6/10, one excluded) H. pylori eradicated patients vs. 18.2% (2/11) in non-eradicated patients (p = 0.08; OR = 6.75) after 6–9 months of follow-up. Among uninfected patients, only 13.8% (8/58) presented complete response. Two non-treated controls were treated after 6–12 months of follow-up, and PLT response was observed in 61.5% (8/13) of H. pylori eradicated patients, and in 19.0% (11/58) of uninfected patients (p = 0.004). Cytotoxin associated gene A and vacuolating cytotoxin gene A IgG antibodies were present in almost all infected patients. Therefore, the study suggests that H. pylori eradication plays a role in the management of H. pylori infected cITP children and adolescents.

Comparison of half-dose and full-dose triple therapy regimens for Helicobacter pylori eradication in patients with end-stage renal disease.

The aim of this study was to compare the half-dose and full-dose triple therapy regimens for Helicobacter pylori (Hp) eradication in patients with end-stage renal disease. H. Pylori is one the most important causes of dyspepsia in patients with end-stage renal disease (ESRD). Sixty-six patients with ESRD were enrolled in the study with Hp infection and peptic disease with a need of Hp eradication. Patients were randomly assigned to full-dose (A=35 patients) or half-dose group (B=31 patients). Patients received clarithromycin 500 mg, amoxicillin 1000 mg and omeprazole 20 mg twice daily in group A and clarithromycin 250 mg and amoxicillin 500 mg twice daily and omeprazole 20 mg once daily in group B for two weeks. Patients provided stool samples 4 weeks of completing study to assess the success of Hp eradication by Hp-specific stool antigen. Finally, the rate of eradication and complications were compared between two groups. The successful Hp eradication was achieved in 26 patients (74%) in group A and in 22 patients (74%) in group B. The difference between 2 groups was not statistically significant (p=0.973) (per protocol analysis). Half-dose triple-therapy with clarithromycin, amoxicillin and omeprazole is as effective as full-dose triple-therapy to eradicate the Hp in patients with ESRD. According to lower toxicity level, complications and cost in half-dose regimen in this subset of patients, this protocol is advised.

Helicobacter pylori and Systemic Disease.

Helicobacter pylori and Systemic Disease.

CYP2C19 polymorphism influences Helicobacter pylori eradication.

The known factors that have contributed to the decline of Helicobacter pylori (H. pylori) eradication rate include antibiotic resistance, poor compliance, high gastric acidity, high bacterial load, and cytochrome P450 2C19 (CYP2C19) polymorphism. Proton pump inhibitor (PPI) is important in the eradication regimen. The principal enzyme implicated in the metabolism of PPIs is CYP2C19. The effects of PPI depend on metabolic enzyme, cytochrome P450 enzymes, and CYP2C19 with genetic differences in the activity of this enzyme (the homozygous EM, heterozygous EM (HetEM), and poor metabolizer). The frequency of the CYP2C19 polymorphism is highly varied among different ethnic populations. The CYP2C19 genotype is a cardinal factor of H. pylori eradication in patients taking omeprazole- based or lansoprazole-based triple therapies. In contrast, the CYP2C19 polymorphism has no significant effect on the rabeprazole-based or esomeprazole-based triple therapies. The efficacy of levofloxacin-based rescue triple therapy might be also affected by the CYP2C19 polymorphism, but CYP2C19 genotypes did not show obvious impact on other levofloxacin-based rescue therapies. Choice of different PPIs and/or increasing doses of PPIs should be individualized based on the pharmacogenetics background of each patient and pharmacological profile of each drug. Other possible factors influencing gastric acid secretion (e.g., IL-1β- 511 polymorphism) would be also under consideration.

Quadruple and Phytomedicine-based Therapies in Helicobacter pylori Infection: A Randomized Comparative Trial

Purpose:Helicobacter pylori is strongly associated with the development of gastrointestinal disorders. Emerging antibiotic resistance of modern therapies has created a major problem, particularly in developing countries. A clinical trial was conducted to evaluate the efficacy of current quadruple and phytomedicine-based (mixture of anti-H. pylori components) therapies for the eradication of H. pylori infection and the relief of symptoms in the high H. pylori-prevalence country of Pakistan. Methods: One hundred seventy-six H. pylori-positive patients (males: 97; females: 79; mean age: 36±12 years) were enrolled in this study and divided into two groups according to treatment regimens. Quadruple therapy with omeprazole (20 mg bid), amoxicillin (1 g bid), metronidazole (500 mg bid), and bismuth compound (400 mg bid) was prescribed for 7 days, and phytomedicine-based formulation (pylorex plus 500 mg tablet contains 150 mg Curcuma longa rhizomes, 150 mg Mallotus phillipenensis fruits powder, 100 mg Glycyrrhiza glabra roots, and 100 mg Zingiber officinale rhizomes) twice daily was prescribed for 15 days. C13 urea breath and stool antigen (HpSAg) tests were performed at baseline and after treatment. The gastrointestinal (GI) symptoms (abdominal pain, regurgitation, heartburn, indigestion and flatulence, nausea, vomiting and belching) were evaluated by questioners, using a scoring system (absent: 0, mild: 1, moderate: 2, severe: 3). Results:H. pylori was eradicated in 56 out of 90 patients (62.2%) by quadruple therapy and in 48 out of 86 patients (55.8%) by pylorex plus therapy. The eradication rate of pylorex plus therapy was comparable to that of quadruple therapy. However, pylorex plus therapy have significantly ameliorated GI symptoms not only in H. pylori-eradicated patients from baseline (median 8; IQR 6-10) to 1 month after treatment (median 3; IQR 2-6), but also in non-eradicated patients from baseline (median 9; IQR 7-10) to 1 month after treatment (median 4; IQR 2-6). Whereas, quadruple therapy only relieved GI symptoms in H. pylori-eradicated patients from baseline (median 9; IQR 6-10) to 1 month after treatment (median 4; IQR 3-7), while lesser improvement in non-eradicated patients from baseline (median 9; IQR 6-10) to 1 month after treatment (median 8; IQR 5-10). Conclusion: Current quadruple and alternate therapies yielded poor eradication rates (<70%) in a developing country, but the later produced marked symptomatic improvement in both H. pylori-eradicated and non-eradicated patients, which might also be promising in functional dyspepsia by dual effects.

Do we need to eradicate Helicobacter pylori in patients with GORD?

Eradication of Helicobacter pylori should not be avoided because of complicated reflux symptoms. Previously, although H. pylori eradication in patients with GORD was considered to induce unfavourable effects that worsen reflux symptoms, recent reports indicates that it can have favourable consequences by reducing symptoms and therefore improving quality of life, especially in GORD patients without severe corpus atrophy or severe hiatal herniation.

Randomised clinical trial: the effects ofHelicobacter pylorieradication on glandular atrophy and intestinal metaplasia after subtotal gastrectomy for gastric cancer

Helicobacter pylori eradication is recommended for early gastric cancer (GC) patients after resection. To evaluate whether H. pylori eradication improves glandular atrophy and intestinal metaplasia (IM) in GC patients undergoing subtotal gastrectomy. This randomised, double-blind trial was performed in tertiary care setting. Distal GC patients with H. pylori infection were randomised to receive proton pump inhibitor-based triple therapy or placebo. The histology was evaluated using the updated Sydney system before and at 36months after surgery. The endpoints were the comparison of atrophy and IM score changes between the allocated groups and according to final H. pylori status. Overall, 190 patients were randomised to the treatment and placebo groups. For lesser curvature of the corpus, mean atrophy and IM scores did not differ between the treatment and placebo groups. However, the H. pylori-eradicated patients had significantly lower mean scores than the H. pylori-persistent patients regarding atrophy (0.55±0.95 vs. 1.05±1.10 respectively; P=0.0046) and IM (0.66±0.99 vs. 1.05±1.16 respectively; P=0.0284). The percentage change from baseline was more marked in the H. pylori-negative than in the H. pylori-positive groups (-58.6% vs. -11.0% for atrophy and -60.5% vs. -35.6% for IM respectively). For greater curvature, mean atrophy score was lower in the H. pylori-negative group than in the H. pylori-positive group (0.14±0.50 vs. 0.41±0.75 respectively; P=0.0281). The percentage change was -36.4% vs. 86.3%. Helicobacter pylori eradication in GC patients is beneficial, as reflected by lower scores of atrophy and IM at 36months after subtotal gastrectomy. (ClinicalTrials.gov number, NCT01002443).

The Korean Perspective of Helicobacter pylori Infection: Lessons from Japan Policy to Prevent Gastric Cancer

The guideline of the Korean College of Helicobacter and Upper Gastrointestinal Research group for Helicobacter pylori infection was first produced in 1998. Definite indication for H. pylori eradication is early gastric cancer in addition to the previous indications of peptic ulcer (PUD) including scar lesion and marginal zone B cell lymphoma (MALT type). Though treatment regimen was similar, Japan government declared the inclusion of H. pylori eradication in patients with H. pylori-associated chronic gastritis, suggesting the treatment guideline is quite different between Korea and Japan from February 21, 2013. The prime rationale of Japanese extended treatment guideline for H. pylori infection was based on the drastic intention to prevent gastric cancer according to their beliefs that H. pylori eradication can decrease gastric cancer incidence as well as mortality. In this review, the discrepancy in treatment guideline between Korea and Japan will be explained.

The aspirin cardiovascular/gastrointestinal risk calculator ‐ a tool to aid clinicians in practice

Assessment of both GI and CV risks vs. the benefits of low-dose aspirin for individual patients can be difficult in clinical practice. To develop a tool to estimate CV and GI risks to facilitate the clinical decision-making process. We constructed risk-ratio estimations and determined the incidence of CV events and upper GI complications according to the presence of different risk factors. For upper GI complications we assumed a baseline incidence of 1 case/1000-persons-year, a twofold increased risk with low-dose aspirin, and estimated a 60% GI risk reduction with proton pump inhibitors (PPI) co-therapy and a 60% risk reduction with H. pylori eradication in patients with a history of peptic ulcer. The calculator can be found at http://www.asariskcalculator.com. In patients with low CV risk the number of GI complications induced by low-dose aspirin may be greater than the number of CV events prevented. In patients with high CV risk, low-dose aspirin is recommended, but the number of GI complications induced may still overcome the CV events saved. The use of PPI reduces the number of complication events induced by low-dose aspirin, but the number of CV events saved may still be offset by the number of GI complications induced in patients at very high GI risk. There are many clinical situations where the number of potential upper GI complications induced by low-dose aspirin may exceed the number of potentially prevented CV events. A risk calculator should guide physicians in choosing appropriate therapy and maximise the aspirin benefit.

Helicobacter pylori infection in functional dyspepsia

Functional dyspepsia is the most common reason for patients to experience chronic epigastric pain or discomfort. The causes of functional dyspepsia are multifactorial but Helicobacter pylori infection is one likely candidate. Infection with this bacterial pathogen clearly results in chronic mucosal inflammation in the stomach and duodenum, which, in turn, might lead to abnormalities in gastroduodenal motility and sensitivity. Chronic gastritis might also affect a variety of endocrine functions of the stomach including the production of the gastrointestinal hormones and neurotransmitters somatostatin, gastrin and ghrelin. Although these abnormalities might generate symptoms in some patients with functional dyspepsia, the clinical evidence needs to be critically evaluated before this hypothesis can be confirmed. A Cochrane review reported that eradication of H. pylori in these patients had a small but statistically significant long-term effect on symptom relief when compared with placebo, lasting at least 12 months after 1 week of eradication therapy. The efficacy of eradication therapy was seen in all symptom subtypes of functional dyspepsia, but was more marked in Asian than Western patients. This evidence has led to alterations in most of the major guidelines throughout the world, which now recommend H. pylori eradication in patients with functional dyspepsia if they test positive for this bacterium.

Extra-Intestinal Manifestation ofHelicobacter pyloriInfection: Allergic Diseases Including Asthma, Atopy and Idiopathic Urticaria

Helicobacter pylori (H. pylori) infection is known to be negatively associated with allergic diseases including asthma in epidemiologic studies, mainly from the western countries. Bronchial asthma and allergic diseases are initiated by T-cells producing T-helper type 2 (Th2) cytokines (e.g. interleukin-4 (IL-4) and IL-5), which is inhibited by Th1 responses. H. pylori infection appears to inhibit Th2 responses, as well as to drive Th1 inflammation, and recent studies using experimental models of allergic airway disease elucidated a direct link between H. pylori infection and suppression of allergic airway disease through the induction of regulatory T cells. H. pylori has been implicated as a factor in idiopathic urticaria. Its eradication, however, has been shown conflicting results only. Therefore, routine H. pylori eradication for patients with chronic urticaria is not recommended. In Korea, prevalence of H. pylori infection shows a decreasing trend, and studies on association of H. pylori infection with asthma is warranting in the population. (Korean J Med 2013;84:774-780)

Does Helicobacter pylori treatment improve the symptoms of globus hystericus?

Globus hystericus is a feeling of tension in the throat, irrelevant of swallowing, persisting for at least 12 weeks. Since the cause of globus hystericus is not fully described, the treatment is controversial. We aimed in this study to determine the symptoms of gastroesophageal reflux disease, upper gastrointestinal endoscopic findings, prevalence of Helicobacter pylori,and post-treatment symptoms (symptoms of gastroesophageal reflux and/or Helicobacter pylori) in patients with a diagnosis of globus hystericus. One hundred twenty three patients were recruited from the archives of the Department of Gastroenterology and Endoscopy at Celal Bayar University Medical School between January 2009 and August 2010. Helicobacter pylori was positive in 75 (60%) of 123 patients with globus hystericus. Helicobacter pylori (+) patients had significantly more heartburn, regurgitation, and inlet patch in upper esophagus than Helicobacter pylori (-) patients. Significantly more Helicobacter pylori (-) patients had normal endoscopy findings when compared to Helicobacter pylori (+) patients. While 27 (50%) of Helicobacter pylori-eradicated patients had regressing globus symptoms, 12 (17.3%) of them did not have any regression in globus symptoms. Improvement in symptoms showed a positive correlation with Helicobacter pylori eradication (p=0.001). Helicobacter pylori rate among cases with globus sensation was similar to values in the general population. Helicobacter pylori eradication was found to decrease globus symptoms.

Assessment of Helicobacter pylorieradication in patients on NSAID treatment

BackgroundIn this post-hoc analysis of a randomized, double blind, placebo controlled trial, we measured the sensitivity and specificity of Helicobacter pylori IgG-antibody titer changes, hematoxylin and eosin (H&E) stains, immunohistochemical (IHC) stains and culture results in NSAID using patients, following H. pylori eradication therapy or placebo.Methods347 NSAID using patients who were H. pylori positive on serological testing for H. pylori IgG-antibodies were randomized for H. pylori eradication therapy or placebo. Three months after randomization, gastric mucosal biopsies were taken for H. pylori culture and histological examination. At 3 and 12 months, blood samples were taken for repeated serological testing. The gold standard for H. pylori infection was based on a positive culture or both a positive histological examination and a positive serological test. Sensitivity, specificity and receiver operating curves (ROC) were calculated.ResultsH. pylori eradication therapy was successful in 91% of patients. Culture provided an overall sensitivity of 82%, and 73% after eradication, with a specificity of 100%. Histological examination with either H&E or IHC stains provided sensitivities and specificities between 93% and 100%. Adding IHC to H&E stains did not improve these results. The ROC curve for percent change in H. pylori IgG-antibody titers had good diagnostic power in identifying H. pylori negative patients, with an area under the ROC curve of 0.70 (95 % CI 0.59 to 0.79, P = 0.085) at 3 months and 0.83 (95% CI 0.76 to 0.89, P < 0.0001) at 12 months. A cut-off point of at least 21% decrease in H. pylori IgG-antibody titers at 3 months and 58% at 12 months provided a sensitivity of 64% and 87% and a specificity of 81% and 74% respectively, for successful eradication of H. pylori.ConclusionsIn NSAID using patients, following H. pylori eradication therapy or placebo, histological examination of gastric mucosal tissue biopsies provided good sensitivity and specificity ratios for evaluating success of H. pylori eradication therapy. A percentual H. pylori IgG-antibody titer change has better sensitivity and specificity than an absolute titer change or a predefined H. pylori IgG-antibody titer cut-off point for evaluating success of H. pylori eradication therapy.

Enfermedades relacionadas con la infección por Helicobacter pylori

This article summarizes the main conclusions drawn from the studies presented in Digestive Disease Week in 2012 on Helicobacter pylori infection. In developed countries, the prevalence of this infection has decreased, although it continues to be high. The prevalence in Spain is high (50%) and does not seem to be decreasing. There is an increase in antibiotic resistance, which is correlated with the frequency of prior antibiotic prescription. H. pylori eradication improves the symptoms of “epigastric pain syndrome” in functional dyspepsia. The frequency of idiopathic peptic ulcers seems to be increasing. To prevent the development of gastric cancer, eradication therapy should be administered early (before intestinal metaplasia develops). H. pylori eradication in patients undergoing early endoscopic resection of gastric cancer reduces the incidence of metachronous tumors, although endoscopic follow-up should be performed periodically. H. pylori eradication induces MALT lymphoma regression in most patients and tumoral recurrence in the long term is exceptional; radiotherapy is an excellent second-line option; a watch and wait approach to histologic recurrence after initial MALT lymphoma remission is a reasonable alternative. Idiopathic thrombocytopenic purpura is an indication for eradication therapy in children as well as adults. There are several diagnostic innovations, such as high-resolution endoscopy, narrow-band imaging, a method based on the electrochemical properties of H. pylori, and the cytosponge. Quadruple therapy with bismuth is at least as effective as standard triple therapy. The superiority of “sequential” therapy over standard triple therapy should be confirmed in distinct settings. The efficacy of “concomitant” therapy is similar –or even better– than that of “sequential” therapy, but has the advantage of being simpler. A hybrid sequential-concomitant therapy is highly effective. In patients allergic to beta-lactams, the efficacy of treatment with a proton pump inhibitor-clarithromycin-metronidazole is insufficient. When standard triple therapy fails, the second-line option of a 10-day course of levofloxacin is effective and is simpler and better tolerated than quadruple therapy. Triple therapy with levofloxacin is also a promising alternative after failure of “sequential” and “concomitant” therapy. New-generation quinolones, such as moxifloxacin and sitafloxacin, could be useful as eradication therapy, especially as rescue therapy. When two eradication therapies have failed, empirical administration of a third (e.g. levofloxacin) is a valid option. Even after three eradication therapies have failed, an empirical rescue therapy (with rifabutin) can be effective. H. pylori reinfection is highly frequent in developing countries, probably due to intrafamilial transmission.

Impact of Helicobacter pylori on the clinical course of recurrent aphthous stomatitis

Recurrent aphthous stomatitis is one of the most common lesions of oral mucosa. Helicobacter pylori is suggested as one of the etiological agents of recurrent aphthous stomatitis. Here, we conduct a study for evaluating the impact of H. pylori eradication on clinical course of recurrent aphthous stomatitis. Forty-six patients with minor aphthous lesions were enrolled. The number of RAS lesions at last 6 months and vitamin B(12) levels were recorded. All patients were detected for H. pylori with endoscopic biopsy. H. pylori was positive in 30 patients and negative in 16 patients. H. pylori-positive 30 patients received eradication therapy. Three months after therapy, patients were re-evaluated with urea breath test; 18 patients were negative (eradicated), and the remainders (12 patients) were positive (non-eradicated) for H. pylori. 6 months after eradication, vitamin B(12) levels and number of aphthous lesions at 6 months were recorded. Vitamin B(12) levels were significantly increased in H. pylori-eradicated group (P = 0.001), whereas no significant change was found in non-eradicated group (P = 0.638). Mean number of aphthous lesions (per 6 months) of H. pylori-eradicated group was significantly decreased after eradication (P = 0.0001); in the non-eradicated group, no significant change was found (P = 0.677). In Hp-positive group, number of RAS lesions and vitamin B(12) levels were negatively correlated when evaluated both before and after eradication. This study provides evidence to support the beneficial effect of H. pylori eradication in patients with recurrent aphthous stomatitis. The underlying mechanism might be the increase in vitamin B(12) levels after eradication.

Long-Term Follow-Up of 1,000 Patients Cured of Helicobacter pylori Infection Following an Episode of Peptic Ulcer Bleeding

To evaluate the effect of Helicobacter pylori (H. pylori) eradication on ulcer bleeding recurrence in a prospective, long-term study including 1,000 patients. Patients with peptic ulcer bleeding were prospectively included. Prior non-steroidal anti-inflammatory drug (NSAID) use was not considered exclusion criteria. H. pylori infection was confirmed by rapid urease test, histology, or (13)C-urea breath test. Several eradication therapies were used. Subsequently, ranitidine 150 mg o.d. was administered until eradication was confirmed by (13)C-urea breath test 8 weeks after completing therapy. Patients with therapy failure received a second, third, or fourth course of eradication therapy. Patients with eradication success did not receive maintenance anti-ulcer therapy and were controlled yearly with a repeat breath test. NSAID use was not permitted during follow-up. Thousand patients were followed up for at least 12 months, with a total of 3,253 patient-years of follow-up. Mean age 56 years, 75% males, 41% previous NSAID users. In all, 69% had duodenal ulcer, 27% gastric ulcer, and 4% pyloric ulcer. Recurrence of bleeding was demonstrated in three patients at 1 year (which occurred after NSAID use in two cases, and after H. pylori reinfection in another one), and in two more patients at 2 years (one after NSAID use and another after H. pylori reinfection). The cumulative incidence of rebleeding was 0.5% (95% confidence interval, 0.16-1.16%), and the incidence rate of rebleeding was 0.15% (0.05-0.36%) per patient-year of follow up. Peptic ulcer rebleeding virtually does not occur in patients with complicated ulcers after H. pylori eradication. Maintenance anti-ulcer (antisecretory) therapy is not necessary if eradication is achieved. However, NSAID intake or H. pylori reinfection may exceptionally cause rebleeding in H. pylori-eradicated patients.