Pylori Eradication Treatment Research Articles

Inhibition of caspase‐8 activity caused by overexpression of bcl10 contributes to the pathogenesis of high‐grade MALT lymphoma

Mucosa-associated lymphoid tissue (MALT) lymphoma comprises approximately 8% of all non-Hodgkin lymphomas and is the most common lymphoma in the gastro-intestinal tract. It is caused by genetic abnormalities or bacterial infections/chronic inflammation. B-cell lymphoma/leukemia 10 (BCL10) overexpression and nuclear expression have been associated with high-grade MALT lymphomas with genetic abnormalities that are unresponsive to Helicobacter pylori eradication treatment. To explore the molecular mechanism of BCL10 overexpression on the pathogenesis and malignant phenotype of MALT lymphoma, we generated EµSR-BCL10 transgenic mice. By generation of heterozygous and homozygous EuSR-BCL10 mice and showing BCL10 expression levels in these mice, we quantitatively examined relation of MZ B cell expansion and inhibition of caspase-8 activity with BCL10 protein level. We also investigated API2 and caspase-8 expression by Western blot and their interaction with BCL10 by co-immunoprecipitation. MZ B-cell expansion is directly related to BCL10 protein level in a dose-dependent manner. The activity of caspases-8 and -3, but not caspase-9, was inhibited with increasing of BCL10 protein level. Expanded MZ B cells showed selective survival under stimulation of anti-immunoglobulin M, but not dexamethasone, γ-irradiation, or anti-CD95, implying that overexpressed BCL10 exerts anti-apoptotic effects through B-cell antigen receptor (BCR) pathway. Overexpressed BCL10 protein co-immunoprecipitated with caspase-8 and API2 protein, suggesting an in vivo interaction of them. Our data demonstrate a novel effect of overexpressed BCL10 in the pathogenesis of high-grade MALT lymphoma by increasing expression of API2 and it then forming a protein complex with BCL10/caspase-8 leading to caspase-8 activity suppression.

Helicobacter pylori Eradication Rates in Children Upon Susceptibility Testing Based on Noninvasive Stool Polymerase Chain Reaction Versus Gastric Tissue Culture

In children with clarithromycin-resistant Helicobacter pylori, clarithromycin-containing therapies often fail. The present study aimed to assess the outcome of tailored therapy upon noninvasive versus invasive H pylori susceptibility testing. A retrospective cohort study was conducted in a pediatric outpatient clinic located in a region where H pylori clarithromycin resistance is highly prevalent. Between June 2007 and September 2009, 96 infected children (mean age 10.8 years), naïve to H pylori eradication treatment, were prescribed triple eradication therapies. These therapies were individually tailored upon susceptibility testing performed either noninvasively using stool polymerase chain reaction (stool PCR group) or invasively using endoscopy, biopsy, and culturing of gastric biopsies (gastric biopsy group). Eradication was defined by negative results upon noninvasive testing including stool PCR at least 5 weeks after the end of treatment. H pylori was eradicated in 43 of 55 stool PCR group versus 30 of 41 gastric biopsy group children (78.2% vs 73.2%, P = 0.63). Of those H pylori strains with pretherapeutic clarithromycin susceptibility, 78.8% were eradicated in the stool PCR group and 69.2% in the gastric biopsy group (P = 0.41) following clarithromycin-containing therapy; clarithromycin resistance was acquired by 4.1% of strains in the former group versus 12% in the latter (P = 0.33). Stool PCR is as effective as the invasive approach of H pylori susceptibility testing for targeting resistance-guided eradication treatments in children. Furthermore, stool PCR is a useful tool for tracking the emergence of clarithromycin resistance following eradication treatment.

Can Helicobacter pylori‐associated dyspepsia be categorized as functional dyspepsia?

Evidence for an association between H. pylori and functional dyspepsia (FD) is uncertain. In the present review, we focused the special relevance of H. pylori infection to the development dyspepsia from the aspects of pathogenesis, clinical efficacy of eradication of H. pylori in the West and in the East. Although clinical trials conducted to evaluate the efficacy of H. pylori eradication treatment for FD, including non-ulcer dyspepsia (NUD), have yielded conflicting results, it is quite clear that H. pylori eradication treatment is effective at least in a subset of FD patients. In contrast to the previous results obtained in studies of Western populations, the result of a double-blind, randomized, placebo-controlled trial conducted in a Singapore suggests that patients with FD could benefit from H. pylori eradication therapy, with as much as a 13-fold increase in the chance of symptom resolution. Especially in Asia, H. pylori should not be overlooked when considering the pathophysiology of FD. H. pylori-associated dyspepsia might be dealt as a different disease entity from FD.

The Role of Helicobacter pylori in Patients with Hypothyroidism in Whom Could Not be Achieved Normal Thyrotropin Levels Despite Treatment with High Doses of Thyroxine

Helicobacter pylori infection is a most frequent cause of chronic gastritis. H. pylori may decrease absorption of oral thyroxine by decreasing gastric acid secretion in the stomach. In this study, we aimed to investigate the change in thyroid function tests of the cases after H. pylori eradication who were not responding to high doses of thyroxine treatment before H. pylori eradication. Hypothyroid cases who were not responding to high doses of thyroxine among the ones presented to Endocrinology and Gastroenterohepatology Clinics of Sisli Etfal Training and Research Hospital between 2009 and 2010 were included in the study. Thyroid function tests were performed two times in all cases before and after H. pylori eradication. Duodenal, antral and corporal biopsies, and jejunal aspirates and biopsies were taken during upper gastrointestinal system endoscopies performed in all patients. Cases without intestinal pathology were included in the study. Serum thyrotropin (TSH), free T3, and free T4 values before H. pylori eradication were 30.5 ± 28.8 IU/mL, 2.64 ± 0.56 pg/mL, and 0.92 ± 0.32 ng/mL, respectively, and after eradication were found to be 4.2 ± 10.6 IU/mL, 3.02 ± 0.61 pg/mL, and 1.3 ± 0.34 ng/mL, respectively (p values <.001, .002, and <.001, respectively). After H. pylori eradication treatment, TSH decreased in all of the cases, factitious thyrotoxicosis developed in % 21 of these cases. In hypothyroid cases, H. pylori gastritis may be responsible for an inadequate response to the treatment. H. pylori eradication in the cases receiving high doses of thyroxine has a risk for thyrotoxicosis.

Applicability of a rapid stool antigen test, using monoclonal antibody to catalase, for the management of Helicobacter pylori infection

Most monoclonal antibody-based stool antigen tests are of the "send-out" format. Rapid Testmate pylori antigen (Rapid TPAg) uses monoclonal antibody and is an "in-the-office" test. The aim of this study was to examine the usefulness of Rapid TPAg for the management of H. pylori infection. One-hundred and two consecutive patients who received H. pylori eradication therapy underwent both urea breath test (UBT) and Rapid TPAg at 5-6 weeks after finishing the eradication therapy. Stool samples were maintained at -20, 5, 25, and 40°C and subjected to Rapid TPAg after 1-7 days. Stool samples were also tested by enzyme immunoassay (EIA) to quantify antigenicity. The agreement between Rapid TPAg and UBT in the evaluation of the results of H. pylori eradication treatment was 94.1%. The overall accuracy of Rapid TPAg and UBT to determine H. pylori eradication was 98.0 and 96.0%, respectively. The results of Rapid TPAg were not altered after storage of samples at -20 to 40°C for 7 days. Antigenicity quantified by EIA did not decrease significantly after 7 days. Rapid TPAg is a useful diagnostic test for immediate and accurate determination of the results of H. pylori eradication therapy. The antigenicity of stool sample suspensions was preserved for 7 days in the collection devices.

Endoscopic Diagnosis of Open-Type Atrophic Gastritis Is Related to the Histological Diagnosis of Intestinal Metaplasia and Cdx2 Expression

Long-term Helicobacter pylori infection results in atrophic gastritis and intestinal metaplasia (IM) with Cdx2 expression. We have tried to determine if there was a link between endoscopic and histological diagnosis of IM based on the status of aberrant Cdx2 expression. One hundred and one subjects agreed to upper gastrointestinal endoscopic examination, with biopsy sampling for histology, Giemsa, and Cdx2 immunohistochemical staining before and after the treatment. On endoscopic examination, atrophic gastritis was defined as discoloration with blood vessel transparency, and was classified as either closed or open. Metaplastic gastritis was defined by the presence of whitish patches, whitish plaques, and/or homogeneous whitish discoloration. Histologic analysis was performed to determine H. pylori density, intensity of acute polymorphonuclear cell infiltrates and chronic mononuclear infiltrates, gastric atrophy, and IM as demonstrated using immunohistochemistry for cdx2. Cdx2 protein expression (P=0.018) and the prevalence of histologically detected IM (P=0.011) were higher in cases of endoscopically diagnosed open-type atrophic gastritis and metaplastic gastritis than in closed-type atrophic gastritis and nonatrophic/nonmetaplastic cases. The degree of activity (P=0.006) and inflammation (P=0.007) improved significantly after four weeks of successful H. pylori eradication treatment, whereas the degree of atrophy, metaplasia, and Cdx2 expression did not. Unlike endoscopic diagnosis of closed-type atrophic gastritis, that of open-type atrophic gastritis is highly correlated with the histological diagnosis of IM and Cdx2 expression. Endoscopically diagnosed open-type atrophic gastritis and endoscopically diagnosed metaplastic gastritis have similar histological features, which suggests that a high percentage of IM cases are diagnosed as open-type atrophic gastritis by endoscopic examination.

Capsaicin-sensitive afferentation represents an indifferent defensive pathway from eradication in patients withH. pylorigastritis

To study the role of capsaicin-sensitive afferent nerves in Helicobacter pylori (H. pylori) positive chronic gastritis before and after eradication. Gastric biopsy samples were obtained from corpus and antrum mucosa of 20 healthy human subjects and 18 patients with H. pylori positive chronic gastritis (n = 18) before and after eradication. Traditional gastric mucosal histology (and Warthin-Starry silver impregnation) and special histochemical examinations were carried out. Immunohistochemistry for capsaicin receptor (TRVP1), calcitonin gene-related peptide (CGRP) and substance P (SP) were carried out by the labeled polymer immunohistological method (Lab Vision Co., USA) using polyclonal rabbit and rat monoclonal antibodies (Abcam Ltd., UK). Eradication treatment was successful in 16 patients (89%). Seven patients (7/18, 39%) remained with moderate complaints, meanwhile 11 patients (11/28, 61%) had no complaints. At histological evaluation, normal gastric mucosa was detected in 4 patients after eradication treatment (4/18, 22%), and moderate chronic gastritis could be seen in 14 (14/18, 78%) patients. Positive immuno-staining for capsaicin receptor was seen in 35% (7/20) of controls, 89% (16/18, P < 0.001) in patients before and 72% (13/18, P < 0.03) after eradication. CGRP was positive in 40% (8/20) of controls, and in 100% (18/18, P < 0.001) of patients before and in 100% (18/18, P < 0.001) after eradication. The immune-staining of gastric mucosa for substance-P was positive in 25% (5/20) of healthy controls, and in 5.5% (3/18, P > 0.05) of patients before and in 0% of patients (0/18, P > 0.05) after H. pylori eradication. Distibution of TRVP1 and CGRP is altered during the development of H. pylori positive chronic gastritis. The immune-staining for TRVP1, CGRP and SP rwemained unchanged before and after H. pylori eradication treatment. The capsaicin-sensitive afferentation is an independent from the eradication treatment. The 6 wk time period might not be enough time for the restituion of chronic H. pylori positive chronic gastritis. The H. pylori infection might not represent the main pathological factor in the development of chronic gastritis.

The Effect of Probiotics forHelicobacter pylori

Background/Aims: Helicobacter pylori (H. pylori) infection is a major cause of chronic gastritis and peptic ulcer and a risk factor of gastric malignancy. Antibiotics based H. pylori eradication treatment is 90% effective, however, it is expensive and causes side effects and antibiotics resistance. Probiotics could present a low-cost, alternative solution to prevent or decrease H. pylori colonization. Materials and Methods: Eligible articles were indentified by researches of electronic databases. Results: In vitro studies demonstrated an inhibitory activity of probiotics on H. pylori growth and that this effect is extremely strain specific. The probiotics seem to be efficacious for the prevention of antibiotics associated side effects and might be of help for the prevention of H. pylori complications by decreasing H. pylori density and gastritis, and for the prevention of H. pylori colonization or re-infection by inhibiting adhesion to gastric epithelial cells. There was no significant evidence that probiotics may increase the H. pylori eradication rate. Conclusion: Probiotics could be an accessory treatment for H. pylori related gastric diseases, but more researches will be needed. (The Korean Journal of Helicobacter and Upper Gastrointestinal Research 2011;11:26-36)

Changes in gastric mucosal patterns seen by magnifying NBI during H. pylori eradication

Magnifying narrow-band imaging (NBI) endoscopy visualizes superficial gastric mucosal and capillary patterns. We aimed to investigate changes in gastric mucosal patterns seen by magnifying NBI endoscopy after Helicobacter pylori eradication. Gastric mucosal patterns in non-pathological gastric corpus were observed by magnifying NBI endoscopy before and 12 weeks after H. pylori eradication in thirty patients. By using paired photographs of each case, changes in NBI mucosal patterns during H. pylori eradication were judged in a consensus manner by three blinded endoscopists. At 12 weeks after H. pylori eradication, 20 of 24 subjects who had been successfully treated showed remarkable changes in gastric mucosal patterns (sensitivity 83.3%, specificity 100%). In the specimens from these subjects, the patterns of enlarged or elongated pits were improved to small oval or pinhole-like round pits, and the density of fine irregular vessels was decreased. Histological assessment showed alleviation of chronic inflammation in all subjects (p < 0.0001), while such a change was not observed for four subjects showing severe gastric atrophy and intestinal metaplasia. When the subjects were divided according to the presence of severe gastric atrophy, the diagnostic efficacy of magnifying NBI for predicting the results of H. pylori eradication was excellent in subjects without severe gastric atrophy and intestinal metaplasia (sensitivity and specificity, 100%). However, no change in the NBI mucosal pattern was observed in subjects with severe gastric atrophy and intestinal metaplasia, regardless of the H. pylori eradication result. At least in subjects without severe gastric atrophy or intestinal metaplasia, successful H. pylori eradication treatment shows improvements in gastric mucosal patterns with the use of magnifying NBI endoscopy early after successful treatment.

Glycosylation of mucins present in gastric juice: the effect of helicobacter pylori eradication treatment

It is suggested that gastric mucins, and in particular some specific glycan structures that can act as carbohydrate receptors, are involved in the interactions with Helicobacter pylori adhesins. The main aim of our study was to evaluate glycosylation pattern of glycoproteins of gastric juice before and at the end of eradication therapy. Gastric juices were taken from 13 clinical patients and subjected to analysis. Pooled fractions of the void volume obtained after gel filtration were subjected to ELISA tests. To assess the relative amounts of carbohydrate structures, lectins and monoclonal antibodies were used. Changes in the level of MUC 1 and MUC 5AC mucins and of carbohydrate structures, which are suggested to be receptors for Helicobacter pylori adhesins, were observed by the end of the eradication treatment. Our results support the idea about the involvement of MUC 5AC and MUC 1 with some specific sugar structures in the mechanism of Helicobacter pylori infection.

Clinical Trial Report: Eradication of Helicobacter pylori Reduces the Risk for Subsequent Gastric Cancer

Curr Gastroenterol Rep (2010) 12:427–430 DOI 10.1007/s11894-010-0138-8 CLINICAL TRIAL REPORT Clinical Trial Report: Eradication of Helicobacter pylori Reduces the Risk for Subsequent Gastric Cancer Joseph R. Pisegna & Bijal Surti & David R. Scott Published online: 22 September 2010 # The Author(s) 2010. This article is published with open access at Springerlink.com Fuccio L, Zagari RM, Eusebi LH, et al.: Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer? Ann Intern Med 2009, 151:121– Aims The study’s purpose is to examine whether eradication of H. pylori infection can reduce the risk for the development of gastric cancer. Rating Methods •Of importance. The authors examined the results of seven studies that met inclusion criteria by using relevant clinical trials. Relevant trials were identified through searching PubMed, Embase, Google Scholar, and the Cochrane Library. To be eligible to include subjects in this analysis, the randomized clinical trials were required to compare an eradication treatment group to an untreated group and to provide an analysis of the number of gastric cancers occurring during follow-up evaluation. Introduction Helicobacter pylori is a carcinogen and has been associated with the development of gastric cancer. The hypothesis to be tested in this meta-analysis is to determine whether eradication of this organism is associated with a long-term reduction in the risk for development of gastric cancer. Results A total of seven studies were considered adequate to meet the inclusion criteria. One of the studies was excluded after further analysis. Overall, 27 of 3388 (1.1%) treated patients in the H. pylori antibiotic treatment group were identified as having gastric cancer, compared to 56 of 3307 (1.7%) in those subjects who did not undergo treatment. The authors identified the relative risk for gastric cancer as 0.65 (95% CI, 0.43–0.98). J. R. Pisegna : B. Surti : D. R. Scott CURE: Digestive Diseases Research Center, VA Greater Los Angeles Healthcare System, Los Angeles, CA 90073, USA J. R. Pisegna : B. Surti : D. R. Scott Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90073, USA J. R. Pisegna (*) Division of Gastroenterology and Hepatology, VA Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA e-mail: jpisegna@ucla.edu Discussion The authors conclude that eradication of H. pylori reduces gastric cancer risk.

The Evolution of Helicobacter pylori Antibiotics Resistance Over 10 Years in Beijing, China

To evaluate Helicobacter pylori antibiotics resistance evolution from 2000 to 2009 to amoxicillin, clarithromycin, metronidazole, tetracycline, levofloxacin and moxifloxacin in Beijing, China. A total of 374 H. pylori strains isolated from 374 subjects who had undergone upper gastrointestinal endoscopy from 2000 to 2009 were collected and examined by E-test method for antibiotics susceptibility. The average antibiotics resistance rates were 0.3% (amoxicillin), 37.2% (clarithromycin), 63.9% (metronidazole), 1.2% (tetracycline), 50.3% (levofloxacin) and 61.9% (moxifloxacin). Overall resistance to clarithromycin, metronidazole, and fluoroquinolone increased annually (from 14.8 to 65.4%, 38.9 to 78.8%, and 27.1 to 63.5%, in 2000 or 2006-2007 to 2009, respectively). The secondary resistance rates were much higher than primary rates to these antibiotics, which also increased annually in recent 10 years. The trend of clarithromycin, metronidazole, and fluoroquinolone resistance of H. pylori increased over time and the resistance to amoxicillin and tetracycline was infrequent and stable in Beijing. Clarithromycin, metronidazole, and fluoroquinolone should be used with caution for H. pylori eradication treatment.

Treatment of Helicobacter pylori Infection 2010

It is accepted that the success of Helicobacter pylori eradication treatment using standard triple therapy is declining. Resistance, particularly to clarithromycin, has been shown in numerous countries to be rising to a level where the use of standard triple therapy in its current form may no longer be justified. The two major factors influencing resistance are prior exposure to the antibiotic and compliance with therapy. Regimes based on bismuth and levofloxacin, which had previously been mainly second-line options, are now emerging as superior first-line options. Trials of sequential and concomitant therapies are also showing the usefulness of these treatments in different populations. Options for third and subsequent line therapies include furazolidone and rifabutin-based regimes. Susceptibility testing should be performed to maintain accurate data on resistance levels, and has also clinical utility in difficult to eradicate cases. None of these, however, will be successful unless compliance is improved upon. If compliance is assured and eradication confirmation pursued, it has been repeatedly illustrated that near full eradication is achievable.

Gastric Cancer Working Group Report

Gastric cancer is the second most common cancer in Asia, more than half of the world's gastric cancer cases arise in Eastern Asia, and the majority of Asia's cases still occur in the distal part of the stomach. The etiology of gastric cancer consists of genetic susceptibility, Helicobacter pylori infection and environmental risk factors. Helicobacter pylori eradication treatment, consumption of fresh vegetables and fruits and use of aspirin and non-steroidal anti-inflammatory drugs seem to reduce the risk of gastric cancer. Screening for gastric cancer is cost-effective in countries with high incidence. Risk stratification may increase the cost-effectiveness of screening in populations at moderate risk. Endoscopic resection is curative in a subset of patients with early cancer. R0 resection with D2 lymph node dissection has produced the best survival data. Some kind of post-operative adjuvant chemotherapy including S-1 is recommended after D2 surgery. As chemotherapy for gastric cancer, fluorouracils plus platinum are the most widely accepted first-line regimens, whereas taxanes or irinotecan are mostly used in second- and third-line settings. Differences in the approval and medical insurance systems may influence the status of these regimens. Trastuzumab in combination with fluorouracils/platinum will be a standard regimen for HER2-positive gastric cancer. Many new targeting agents are currently under investigation, and Asian countries are playing important roles in investigation and development of new and better treatments for this malignancy.

One size does not fit all - time to regionalize Helicobacter pylori eradication?

Sirs, As clinicians responsible for the day to day care of patients, we want our evidence-based medicine to be quick, clean and to the point. Although the study by Molina-Infante et al. fragments the directive concerning the first line eradication therapy for patients with Helicobacter pylori (H. pylori), the authors should still be congratulated, as more important than an unambiguous treatment regimen is the desire to have one that works at the coal face. The study by Molina-Infante et al.1 highlights the regional heterogeneity of responses to various H. pylori eradication treatments. The authors point out that standard triple therapy with omeprazole, clarithromycin and amoxicillin (OCA) in the Spanish population achieved per protocol cure rates of only 66%, whilst levofloxacin-based triple therapy (OLA), and sequential therapy with either clarithromycin (OACM) or levofloxacin (OALM) achieved adequate cure rates of greater than 80%. This contrasts with our experience in Hong Kong, China, where we found that standard esomeprazole, clarithromycin and amoxicillin (ECA) comprised still the most effective empirical first line treatment for H. pylori [92.7% for ECA vs. 85.7% for esomeprazole, levofloxacin and amoxicillin(ELA)], as rates of H. pylori resistance here to amoxycillin and clarithromycin are still low.2 Molina-Infante et al. also studied the intriguing sequential therapy concept. On the basis of the rationale that initial treatment with amoxicillin lowers the gastric bacterial load, thereby amplifying the impact of the metronidazole and clarithromycin subsequently delivered,3, 4 the authors found that of the four H. pylori eradication regimens studied, the OALM achieved the highest intention to treat cure rate, but at 82.5%, falls below the >90% threshold required to be deemed a ‘good’ first treatment. This ‘average’ response to sequential therapy has also been seen in France5 and Korea,6 whilst ‘good’ responses have been reported in Italy,3, 4 Thailand7 and Taiwan.8 Given the balance of the evidence thus far, perhaps in the H. pylori realm, regionalized treatment regimens may be the way forward, as one size may no longer fit all. Declaration of personal and funding interests: None.

M1140 Helicobacter pylori Eradication Treatment is More Successful When Diagnosis is Made After Urea Breath Test Than After Rapid Urease Testing at Endoscopy in Patients With Dyspepsia

Background: This study was conducted to determine (1) whether Helicobacter pylori infection decreases in conjunction with time elapsed after gastrectomy and (2) the diagnostic efficacy of 13C urea breath test (UBT) for H pylori in patients after gastrectomy. Methods: From January 1997 to June 1998, 86 patients who had undergone gastrectomy and 180 patients with dyspepsia without gastrectomy were enrolled. A UBT for the analysis of excess 13CO2/12CO2 ratio (ECR) was obtained for each patient. Each patient also underwent endoscopy to obtain gastric biopsies for histology and H pylori culture. The presence of H pylori by either histology or culture served as the standard to test the efficacy of UBT. The 86 patients with a prior gastrectomy were categorized into 3 subgroups (I, less than 1 year; II, 1 to 3 years; III, greater than 3 years), according to the interval between surgery and UBT. The initial H pylori status of these 86 patients was determined by histologic evaluation of the resected stomach. Results: At trial initiation, the postgastrectomy group had a lower H pylori infection rate (52.3%) as compared with the dyspeptic control group (80%). The initial H pylori status among subgroups I, II, and III was similar. There was a trend for the presence of H pylori in the stomach to decrease with increasing time elapsed after surgery (I to III: 68.8%, 48.3%, 36%, respectively; p < 0.05). The maximum UBT sensitivity and specificity achieved were 82.2% and 87.8% in the gastrectomy group and 97.2% and 96.3% in the dyspeptic group, with cutoff points of 2.5 and 4.0, respectively. Conclusion: The prevalence of H pylori diminishes with time elapsed after gastrectomy. UBT for detection of H pylori is more effective in patients without prior gastrectomy than in patients who have undergone gastrectomy and is less effective than endoscopy for patients who have had a gastrectomy. (Gastrointest Endosc 2000;51:670-5.)

Rejuvenation of atrophic gastritis in the elderly

See article in J. Gastroenterol. Hepatol. 2010; 25: 544–547

Does Pretreatment with Lansoprazole Influence Helicobacter pylori Eradication Rate and Quality of Life?

Background/Aims: It is controversial whether pretreatment with a proton pump inhibitor (PPI) before Helicobacter pylori eradication treatment decreases the eradication rate. To determine the effects of pretreatment with lansoprazole alone, followed by an H. pylori eradication regimen (lansoprazole 30 mg, amoxicillin 750 mg and clarithromycin 200 mg twice daily for 1 week), on the eradication rate and quality of life (QoL) of the patient. Methods: Patients with H. pylori-positive peptic ulcer were randomly assigned to two groups. The patients received either lansoprazole (30 mg) once daily for 6–8 weeks before H. pylori eradication (group A), or eradication treatment and then lansoprazole (30 mg) for 6–8 weeks (group B). To assess the QoL of the patients, the Gastrointestinal Symptom Rating Scale (GSRS) questionnaire was evaluated. Results: A total of 116 patients were enrolled. The cure rates were 78.9% in group A and 78.0% in group B. In both groups, GSRS analysis showed a significant improvement of the overall GSRS score at the assessment of eradication efficacy, compared to baseline; there was no difference between the groups. Conclusion: With this H. pylori eradication regimen, there was no difference in the cure rates and QoL associated with PPI pretreatment.

Levofloxacin-based triple therapy for first-line Helicobacter pylori eradication treatment: a multi-central, randomized, controlled clinical study

To compare efficacy and tolerability of 7-day standard triple therapy versus 7-day levofloxacin-based triple therapy in first-line treatment for Helicobacter pylori (H. pylori) infection. Three hundred consecutive H.pylori positive patients were randomized to receive: clarithromycin, amoxicillin, lansoprazole (Group A: n = 150); or amoxicillin, levofloxacin, lansoprazole (Group B: n = 150). H. pylori status was rechecked by (13)C-urea breath test 4 weeks after the end of therapy. The eradication rates in intention to treat (ITT) and per protocol (PP) analyses were: Group A, 74.5% (111/149) and 78.2% (111/142); and Group B, 82.4% (122/148) and 83.0%(122/147). Although the eradication rate achieved with levofloxacin-based triple therapy was higher than that with standard therapies in either ITT or PP analysis, but no significantly difference was found between the two triple therapies. The incidence of side effects was similar among groups. A 7-day levofloxacin-based triple therapy can achieve higher H.pylori eradication rate than standard regimen. The levofloxacin-based regimen can be one effective therapy for the first-line anti-H.pylori treatment.

Treatment outcome of localizedHelicobacter pylori-negative low-grade gastric MALT lymphoma

To investigate treatment outcome of Helicobacter pylori (H. pylori)-negative low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In this study, we retrospectively reviewed the clinical outcome and clinicopathologic factors of stage IE H. pylori-negative low-grade gastric MALT lymphoma cases from August 1998 to June 2009. A total of eleven patients with H. pylori-negative low-grade gastric MALT lymphoma were enrolled in the study and received anti-H. pylori eradication treatment and/or radiotherapy or excisional therapy. Complete remission (CR) of gastric MALT lymphoma was achieved in all patients. The time to CR was 1-66 mo (median, 1 mo). Eradication therapy may be offered as an initial treatment option even in cases of localized H. pylori-negative gastric MALT lymphoma.