Successful Helicobacter Pylori Eradication Research Articles

Culture and Successful Eradication of Helicobacter pylori from Heterotopic Gastric Mucosa

Helicobacter pylori colonizes the gastric mucosa of humans and can cause chronic gastritis, peptic ulcer disease, gastric cancer or mucosa-associated-lymphoid tissue (MALT) lymphoma. Here, we report the case of a 61-year-old male patient who presented with tickle of the throat, globus sensation and heartburn. In an esophagogastroduodenoscopy subpharyngeal localized heterotopic gastric mucosa (HGM), reflux esophagitis and a chronic gastritis were diagnosed. HGM and stomach were H. pylori positive as proven by culture and histopathological examination. After eradication therapy with a proton pump inhibitor (PPI), amoxicillin and clarithromycin followed by PPI treatment, the patient reported clinical improvement and the histopathological changes in the HGM due to H. pylori infection improved, too. This case report demonstrates that culture and susceptibility testing of H. pylori using established protocols succeeds not only from tissue samples of the stomach but also from heterotopic gastric mucosa. Eradication therapy may not only improve typical H. pylori associated discomforts of the stomach but also extragastric signs and symptoms of H. pylori infection.

Early Development of Refl ux Esophagitis after Successful Helicobacter Pylori Eradication in Superfi cial Gastritis

The relationship between gastroesophageal reflux disease (GERD) and Helicobacter pylori (H. pylori) eradication is still debated. Recently, we had a patient of GERD who had developed it shortly after H. pylori eradication therapy. A 72-year-old man was diagnosed by endoscopy as suffering from severe superficial gastritis in the stomach body. A rapid urease test showed H. pylori infection. He was then started on proton pump inhibitor (PPI) based therapy for two weeks eradicating H.pylori. After completion of H. pylori eradication, he complained of a heart-burn sensation. Follow-up endoscopy showed reflux esophagitis, of grade B according to the Los Angeles classification. Since the patient had developed GERD after completion of the triple therapy, their suggests that H. pylori eradication must have triggered the development of de novo GERD after a short period of time.

Stress-induced hemorrhagic gastric ulcer after successful Helicobacter pylori eradication: two case reports.

IntroductionHelicobacter pylori infection is a major cause of gastric ulcers, and Helicobacter pylori eradication drastically reduces ulcer recurrence. It has been reported, however, that severe physical stress is closely associated with gastric ulceration even in Helicobacter pylori -negative patients.Case presentationWe report the cases of a 47-year-old Japanese man and a 69-year-old Japanese man who developed psychological stress-induced hemorrhagic gastric ulcers, in both of whom Helicobacter pylori had been successfully eradicated.ConclusionOur cases strongly suggest that not only physical but also psychological stress is still an important pathogenic factor for peptic ulceration and accordingly that physicians should pay attention to the possible presence of psychological stress in the management of patients with peptic ulcers.

Clinicopathological Analysis of Early-Stage Gastric Cancers Detected After Successful Eradication of Helicobacter pylori

The results of a randomized controlled study and meta-analysis study have recently proved that Helicobacter pylori eradication has a preventive effect against the development of metachronous and primary gastric cancer. However, gastric cancer is sometimes detected after successful eradication. There is a lack of study about gastric cancers in eradicated patients. To clarify the characteristics of gastric cancers detected after H. pylori eradication, we analyzed the clinicopathological features of these cancers. The subjects were 18 early-stage gastric cancer specimens resected from 17 patients who had received successful eradication of H. pylori from February 1995 to March 2009. The control group consisted of 36 specimens from noneradicated patients with persistent H. pylori infection who were matched with the subjects in age, sex, and depth of invasion. Clinicopathological features and mucin phenotypes of gastric cancer were clinically and immunohistologically evaluated. The average diameter of gastric cancer was smaller and Ki-67 index was lower in the eradication group. The morphological distribution of depression types was significantly lower in the control group. Immunohistochemical phenotyping revealed that 72.2% of the lesions in the eradicated group were complete gastric type or gastric predominant mixed type, whereas the percentages of gastric type and intestinal type in the control group were similar. Our findings indicate that the clinicopathological characteristics of gastric cancers detected after H. pylori eradication are different from those of gastric cancers in patients with persistent H. pylori infection. H. pylori eradication may suppress intestinalization during the development of gastric cancer.

The Role of Abdominal CT Scan as Follow-up after Complete Remission with Successful Helicobacter pylori Eradication in Patients with H. pylori-Positive Stage IE1 Gastric MALT Lymphoma

Eradication of Helicobacter pylori with antibiotics is the established initial treatment of patients with localized gastric mucosa-associated lymphoid tissue (MALT) lymphoma. However, there are few reports on follow-up modalities to identify sustained remission in patients who achieve complete remission (CR). We therefore investigated the role of abdominal computed tomography (CT) as follow-up after CR with H. pylori eradication. We retrospectively analyzed 122 patients with H. pylori-positive stage I(E1) gastric MALT lymphoma who achieved CR with successful H. pylori eradication. The median follow-up after CR was 35 months (range 3-140 months). At a median of 17 months (range 12-21 months) after CR, 7 of 122 patients (5.7%) experienced lymphoma recurrence, all cases of which were confined to the gastric mucosa and were detectable only by endoscopy with multiple biopsies. At the time of recurrence, four of seven patients showed re-infection by H. pylori. Eradication therapy was successful in these patients, resulting in both bacterial eradication and tumor regression. Three patients who experienced histologic recurrence without H. pylori re-infection were observed by a watch and wait strategy and again achieved CR. None of the patients with H. pylori-positive stage I(E1) gastric MALT lymphoma who experienced tumor recurrence after CR with successful H. pylori eradication showed recurrence at extragastric sites, including lymph nodes without gastric mucosal lesion. These findings indicate that endoscopic biopsies without abdominal CT scans are sufficient to detect recurrence in these patients.

The long-term risk of gastric cancer after the successful eradication of Helicobacter pylori

We previously reported that eradication of Helicobacter pylori reduced the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient group to investigate the occurrence and clinical features of gastric cancers that developed after cure of the infection. Prospective post-eradication evaluations were conducted on 1674 consecutive patients who had received successful H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosal atrophy, and H. pylori infection. After confirmation of cure of the infection, follow-up endoscopy was performed yearly. The patients were followed for up to 14.1 years (a mean of 5.6 years). During the follow-up, gastric cancer developed in 28 of the 1674 patients as long as 13.7 years after the cure of H. pylori infection. The risk of developing gastric cancer was 0.30% per year. Histologically, 16 of the gastric cancers were the intestinal type and 12 were the diffuse type; the risk of each cancer type was 0.17 and 0.13% per year, respectively. There was no significant inflammatory cell infiltration in the background gastric mucosa at the time the cancers were recognized. There is a risk of developing gastric cancer of both the intestinal and diffuse types even after the cure of H. pylori infection and extinction of gastric inflammation. It is important to inform patients about the risk of gastric cancer after eradication therapy and offer them surveillance endoscopy.

PREDICTIVE VALUE OF ENDOSCOPY AND ENDOSCOPIC ULTRASONOGRAPHY FOR REGRESSION OF GASTRIC DIFFUSE LARGE B‐CELL LYMPHOMAS AFTER HELICOBACTER PYLORI ERADICATION

Some gastric diffuse large B-cell lymphomas have been reported to regress completely after the successful eradication of Helicobacter pylori. The aim of this study was to investigate the clinical characteristics of gastric diffuse large B-cell lymphomas without any detectable mucosa-associated lymphoid tissue (MALT) lymphoma that went into complete remission after successful H. pylori eradication. We examined the effect of H. pylori eradication in 15 H. pylori-positive gastric diffuse large B-cell lymphoma patients without any evidence of an associated MALT lymphoma (clinical stage I by the Lugano classification) by endoscopic examination including biopsies, endoscopic ultrasonography, computed tomography, and bone marrow aspiration. H. pylori eradication was successful in all the patients and complete remission was achieved in four patients whose clinical stage was I. By endoscopic examination, these gastric lesions appeared to be superficial. The depth by endoscopic ultrasonography was restricted to the mucosa in two patients and to the shallow portion of the submucosa in the other two patients. All four patients remained in complete remission for 7-100 months. In gastric diffuse large B-cell lymphomas without a concomitant MALT lymphoma but associated with H. pylori infection, only superficial cases and lesions limited to the shallow portion of the submucosa regressed completely after successful H. pylori eradication. The endoscopic appearance and the rating of the depth of invasion by endosonography are both valuable for predicting the efficacy of H. pylori eradication in treating gastric diffuse large B-cell lymphomas.

Predictors of long-term outcome of functional dyspepsia and duodenal ulcer after successful Helicobacter pylori eradication – a 7-year follow-up study

To investigate the course of dyspeptic symptoms, predictors of symptom relief and use of antidyspeptic drugs in patients with duodenal ulcer disease and functional dyspepsia 6-7 years after successful Helicobacter pylori eradication. Patients with H. pylori-positive duodenal ulcer or functional dyspepsia, included in a prospective, randomized study from January 1996 to June 1997, and successfully treated with standard triple therapy, were eligible. After 6-7 years, case histories of 142 patients were retrieved and patients were interviewed by telephone. They were asked about the presence of dyspeptic symptoms and health care needs during the last week and over the last 6-7 years. Predictive factors of complete long-term relief of symptoms have been evaluated. Of the 114 eligible patients, 104 (49 with duodenal ulcer and 55 with functional dyspepsia) were included in the study. The mean duration of follow up was 6.6+/-0.5 years. Complete relief of dyspeptic symptoms was reported, in this period, by 49.0% of duodenal ulcer patients and 36.4% of patients with functional dyspepsia (P=0.271). Persistence of symptoms within 3 months of H. pylori eradication and female sex were predictive of persistence of symptoms in the following 6-7 years, in patients with functional dyspepsia. In turn, approximately 50% of the patients with complete symptom remission, within 6 months of H. pylori eradication, later became symptomatic. Since the end of the H. pylori eradication trial, 26.9% of patients were still using or had used antidyspeptic drugs; patients with functional dyspepsia having used them more frequently than duodenal ulcer patients (36.4 vs. 16.3%; P=0.037). In clinical practice, long-term symptomatic benefit, in duodenal ulcer patients, after H. pylori eradication, is similar to that in patients with functional dyspepsia. Early evaluation of symptoms after successful H. pylori eradication may be predictive of outcome in dyspeptic patients. Most symptomatic patients did not seek antidyspeptic drugs. Use of antisecretory medications was, however, greater in patients with functional dyspepsia than in duodenal ulcer patients.

Effects of CYP2C19 and MDR1 genotype on the eradication rate of Helicobacter pylori infection by triple therapy with pantoprazole, amoxycillin and clarithromycin

CYP2C19 polymorphism plays an important role in the metabolism of proton pump inhibitors. The multidrug resistance (MDR)1 genotype is associated with the successful eradication of Helicobacter pylori. The aim of the present study was to investigate the effects of CYP2C19 and MDR1 genotypes on the eradication rate of H. pylori using a pantoprazole-based triple therapy. A total of 210 patients infected with H. pylori were treated with 40 mg pantoprazole, 500 mg clarithromycin and 1000 mg amoxicillin twice daily for 7 days. The CYP2C19 genotype was determined with polymerase chain reaction (PCR)-restriction fragment length polymorphism analysis. The MDR1 C3435T polymorphism was identified by PCR-based allele-specific amplification (PCR-ASA). Of the 210 patients who completed the study, 174 (82.9%, 95.0% confidence interval [CI], 77.8-88.0%) achieved successful eradication after the first cycle of therapy. The eradication rates for H. pylori were 86.7%, 81.1% and 82.1% in the homozygous extensive, heterozygous extensive and poor metabolizer groups, respectively (P = 0.65). Moreover, the cure rates in the CC, CT, and TT groups were 82.7%, 84.4% and 76.9%, respectively (P = 0.66). Multiple logistic regression analysis revealed that endoscopic diagnosis was a significant independent risk factor for treatment failure. The eradication rates of H. pylori by pantoprazole, amoxicillin and clarithromycin were not significantly different among the CYP2C19 and MDR1 genotypes. Hence, the cure rate of H. pylori in the Korean population was no different for the CYP2C19 and MDR1 genotypes.

Predictive Factors for Metachronous Gastric Cancer in High-Risk Patients after Successful Helicobacter pylori Eradication

Background:Helicobacter pylori eradication following endoscopic mucosal resection of early gastric cancer reduces the risk of metachronous gastric cancer. Aim: To identify subgroups of differing cancer risk after endoscopic mucosal resection of early gastric cancer. Methods: Histological assessment of antral and corpus tissue was done by the updated Sydney Classification and serum pepsinogen I and II levels were measured using ELISA kits. Infected patients were treated with a 7-day regimen consisting of amoxicillin, clarithromycin and a proton pump inhibitor. Results: 100 patients were enrolled; in 80 patients H. pylori was successfully eradicated and they were followed up for more than 2 years (median observation period 33 months). Metachronous gastric cancers developed in 9 patients after successful eradication. All cases were men. The frequency of severe atrophy assessed by histology (100 vs. 53.2%, p = 0.03) was higher and pepsinogen I/II ratio before eradication was significantly lower in the group that developed cancer compared to the group that did not. Pepsinogen I <25 ng/ml was significantly associated with development of a new lesion. Conclusions: The cancer risk after eradication correlated with the severity of corpus atrophy. It should be possible to identify subgroups requiring intensive and less intensive surveillance after eradication.

Entzündliche Magenerkrankungen und Helicobacter pylori – State of the Art – Risikofaktoren für ein Magenkarzinom

Gerade weil das Magenkarzinom auf der Liste der tumorbedingten Todesfälle auf den Plätzen 4 (Frauen) bzw. 5 (Männer) rangiert, ist es wichtig, Patienten mit hohem Risiko zu erkennen und modifizierbare Risikofaktoren zu verändern. An erster Stelle steht hierbei die Diagnostik und Therapie entzündlicher Magenerkrankungen, die oft auf dem Boden einer Helicobacter–pylori–Infektion entstehen. Denn besteht beispielsweise eine korpusdominante Helicobacter–Gastritis, steigt das Risiko der Betroffenen im Vergleich zur Allgemeinbevölkerung fast um das 40–fache. Grundlage einer korrekten Gastritis–Diagnose auf der Basis der aktuellen Sydney–Klassifikation ist eine suffizient ausgeführte Routinebiopsie, die zusätzlich auch Informationen zu Grad, Aktivität, Metaplasie, Atrophie und Topografie der Gastritis liefert. Empfohlen sind jeweils 2 Antrum– und 2 Korpusbiopsien und eine Angulusbiopsie, gefärbt in der Regel mit Hämatoxylin–Eosin. Bestätigt sich die Diagnose 'Helicobacter–Gastritis', ist eine 7–tägige französische Tripeltherapie angezeigt, die – nach erfolgreicher Eradikation von Helicobacter pylori – das Risiko für ein Magenkarzinom signifikant senken kann.

Association of Inflammatory Cytokine Gene Polymorphisms with Platelet Recovery in Idiopathic Thrombocytopenic Purpura Patients after the Eradication of Helicobacter pylori

Background: Idiopathic thrombocytopenic purpura (ITP) is associated with the cytokine response and dysregulation of the cytokine network. Gene polymorphisms of proinflammatory cytokines are associated with several diseases including ITP. Recently, the successful eradication of Helicobacter pylori has been reported to improve the platelet counts in some patients with ITP. The aim of this study was to elucidate the relationship between cytokine gene polymorphisms and platelet recovery in ITP patients after the eradication of H. pylori. Materials and Methods: Gastric H. pylori infection was confirmed using a culture method or specific IgG antibodies against H. pylori in the serum. Thirty-six adult H. pylori-positive ITP patients received antibiotic therapy for H. pylori. The response to treatment was defined as complete response (CR) if the platelet count was above 150 × 10³/µl and partial response (PR) if the platelet count increased by more than 50 × 10³/µl above the pretreatment count. Genomic DNA was extracted from peripheral blood and polymorphisms in IL-1B (–31, –511), IL-1RN (long or short), TNFA (–308) and TNFB (+252) were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: Of the 36 ITP patients, twenty patients (responders) exhibited a platelet response after successful H. pylori eradication therapy, but the other patients (nonresponders) did not. There were no statistical differences in the frequencies of polymorphisms in IL-1B, IL-1RN and TNFA genes between responders and nonresponders. In contrast, the frequency of responders in ITP patients with the TNFB G/G or G/A genotype was significantly higher (69.6%) than that with the TNFB A/A genotype (30.8%). Conclusion: The TNFB (+252) G/G or G/A genotype may therefore be a good predictor of platelet recovery in ITP patients after the eradication of H. pylori.

Gastroesophageal reflux disease after Helicobacter pylori eradication in gastric ulcer patients: A one-year follow-up study

The aim of this study was to evaluate the course of gastroesophageal reflux disease in gastric ulcer patients after successful Helicobacter pylori eradication (group A), in patients with persistent infection after attempt to eradicate Helicobacter pylori (group B), and in control group without Helicobacter pylori eradication treatment (group C). Gastric ulcer patients (n=88) were assigned either to the group receiving Helicobacter pylori eradication treatment (54 patients) or to the control group (34 patients; omeprazole treatment for 4 weeks) and were followed up for 1-year or until gastric ulcer relapsed. Gastroesophageal reflux disease was diagnosed in patients who had erosive esophagitis and/or without esophagitis if they experienced heartburn and/or regurgitation at least 2 times a week and it was associated with impairment of daily activities (Genval consensus). The study was completed by 69 patients: 25 in group A, 19 in group B, and 25 in group C. At the beginning and at the end of the follow-up, gastroesophageal reflux disease was diagnosed in 10 (40%) and 9 (36%) group A patients, respectively (P>0.05); in 12 (63%) and 8 (42%) group B patients, respectively (P>0.05); and in 9 (36%) and 5 (20%) group C patients, respectively (P>0.05). At the beginning and at the end of the follow-up, reflux esophagitis was found in 3 (12%) and 5 (20%) group A patients, respectively (P>0.05); in 5 (26%) and 5 (26%) group B patients (P>0.05); in 4 (16%) and 3 (12%) group C patients (P>0.05). There was no statistically significant difference regarding the development of gastroesophageal reflux disease in gastric ulcer patients after Helicobacter pylori eradication, in the patients with persistent infection after attempt to eradicate, and in the control group without Helicobacter pylori eradication treatment.

Secretion of epidermal growth factor in saliva of duodenal ulcer patients; an association with Helicobacter pylori eradication and erosive esophagitis

Erosive esophagitis frequently develops after successful Helicobacter pylori eradication. Since salivary secretion of epidermal growth factor (EGF) plays a crucial role in the pathogenesis of gastroesophageal reflux disease, the current study objective was to find out whether erosive esophagitis development after Helicobacter pylori eradication is associated with the secretion of EGF in saliva. A total of 115 H. pylori infected patients (positive results of CLO-test, histology and serology) with a duodenal ulcer were recruited for the study. Gastroscopic examinations and saliva collections were performed twice, prior to H. pylori eradication and one year after its cessation. The salivary EGF was determined using a radioimmunological method. Salivary EGF secretion was lower in H. pylori infected subjects with erosive esophagitis than without (0.82+/-0.66 vs 1.70+/-3.49 ng/min, p=0.021). However, a year after successful H. pylori eradication, salivary EGF did not differ between the groups (2.17+/-2.06 vs 1.79+/-2.06 ng/min); the lack of difference was due to high peptide secretion in patients who developed erosive esophagitis after eradication. Erosive esophagitis development following H. pylori eradication is not the result of decreased salivary EGF secretion.

Most patients with minimal histological residuals of gastric MALT lymphoma after successful eradication of Helicobacter pylori can be managed safely by a watch and wait strategy: experience from a large international series

Background:Eradication of Helicobacter pylori is the established initial treatment of stage I MALT (mucosa associated lymphoid tissue) lymphoma. Patients with minimal persisting lymphoma infiltrates after successful eradication of H pylori...

Host factors contributing to the discovery of gastric cancer after successful eradication therapy of Helicobacter pylori: Preliminary report

Clinical features of patients who develop gastric cancer after successful eradication of Helicobacter pylori are still unclear. We attempted to identify host factors associated with the discovery of gastric cancer, including changes in the background gastric mucosa in patients with atrophic gastritis. We enrolled 101 patients (59 men, 42 women; mean age 56.0 years) who underwent successful eradication therapy. All patients had no neoplastic lesion in the stomach and were diagnosed with corpus atrophic gastritis histologically before the eradication therapy. After successful eradication, these patients were followed up by an annual endoscopic examination (mean follow-up time 63.2 months; range 12-157 months). Fasting sera were obtained before and after eradication therapy and the serum levels of gastrin/pepsinogens were evaluated. Gastric cancer occurred during follow-up in eight of the 101 patients (7.9%). We compared the host features between the cancer-discovered group (n = 8) and the non-discovered group (n = 93). We found no difference in gender, history of previous treatment of gastric cancer, and serum pepsinogen/gastrin levels at entry between them. The trends in alterations of serum markers did not differ between the two groups. However, gastric cancer was more frequently found in older patients (>54 years at eradication) than in others (P < 0.05). Improvement of gastric inflammation did not correlate with the discovery of gastric cancer after eradication; however, age at the time of eradication seemed to be important. Strict follow-up after eradication is needed in older patients with atrophic gastritis.

Susceptibility-Guided vs. Empiric Retreatment of Helicobacter pylori Infection After Treatment Failure

Successful eradication of Helicobacter pylori after failure of standard triple therapy is difficult because of the higher resistance to metronidazole and clarithromycin. We evaluated the efficacy of susceptibility-guided vs. empiric retreatment for H. pylori after at least one treatment failure and determined the prevalence of posttreatment antibiotic resistance. Forty-nine patients in whom at least one treatment regimen for H. pylori eradication had failed underwent gastric biopsy and culture and were retreated according to the in vitro susceptibility results. Findings were compared with those for 49 control patients referred to our center for a (13)C-urea breath test. H. pylori eradication was assessed by urea breath test at least 6 weeks after retreatment in both groups. Susceptibility-guided retreatment was associated with better eradication rates than empiric treatment. The difference remained significant in stratified and multivariate analysis. Susceptibility-guided retreatment appears to be significantly more effective than empiric retreatment in eradicating H. pylori after at least one previous treatment failure.

Rapid Development of Diffuse Large B-Cell Lymphoma After Successful Eradication of Helicobacter pylori for Gastric MALT Lymphoma

Primary low-grade mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach has a potential to transform to high-grade diffuse large B-cell lymphoma (DLBCL). However, the clonal relation between MALT lymphoma and de novo DLBCL is still controversial. We report here three patients with Helicobacter pylori (H. pylori)-positive gastric MALT lymphoma rapidly progressing to DLBCL at the same site after successful eradication of H. pylori. Although MALT lymphomas in our cases did not possess t(11; 18)(q21;q21), sequence analysis of the rearranged immunoglobulin heavy chain gene showed no clonal relation between preceding MALT lymphoma cells and de novo DLBCL cells at the same site. These findings question the scenario of direct clonal progression of low-grade MALT lymphomas without t(11; 18)(q21;q21) to DLBCL and serve as a reminder of the risk of the progression of DLBCL with a distinct clonality immediately after H. pylori eradication for low-grade MALT lymphoma.

HELICOBACTER PYLORI AND GASTROESOPHAGEAL REFLUX DISEASE IN CHILDREN

Introduction: The role of Helicobacter pylori (HP) in gastroesophageal reflux disease (GERD) remains controversial particularly in children since there is limited published data. Previous studies in adult populations suggested that there is an increased prevalence of GERD following successful eradication of HP. These studies suggested that HP infection might protect against GERD by its propensity to produce atrophic gastritis and reduced gastric acid secretion. The objective of our study is to determine the significance of HP for GERD in the pediatric population. Methods: A retrospective analysis of 437 patients (M:F = 227:210) who underwent upper endoscopies with biopsies between January 2000 and April 2006 was conducted. The prevalence of reflux esophagitis (RE) in two groups, HP+ and HP- was reviewed. The prevalence of RE in HP+ and HP- was further analyzed based on their gender and age (0-1 yr, 1-10 yr, 10-20 yr). The mean age of the study population was 8.15 years (range 0-20 yr). Statistical analysis used Chi-square test. Results: Of 437 patients, 17 patients were HP+ and 100 patients were found to have RE with an incidence of 22.9%. The prevalence of RE in HP+ was 41.2% and in HP- was 22.1% (P = 1.31E-05). In 227 male patients, the prevalence of RE in HP+ was 40.0% and in HP- was 25.8% (P = 3.57E-05). In 210 female patients, the prevalence of RE in HP+ was 42.9% and in HP- was 18.2% (P = 1.05E-06). In the first age group (0 - 1 yr), there was 0 patients with HP +. In the second age group (1 - 10 yr), the prevalence of RE in HP+ was 50.0% and in HP- was 27.6% (P = 5.64E-11). In the third age group (10 - 20 yr), the prevalence of RE in HP+ was 33.3% and in HP- was 21.3% (P = 1.19E-02). Conclusions: Our study results suggest that there is an increased prevalence of RE in HP+ group compared with HP- group in both male and female patients in all age groups, except for infants in which there were zero patients with HP+. The findings do not support a hypothesis that HP infection may have a protective role against GERD in the pediatric population.

Helicobacter pylori Recurrence in Patients with Duodenal Ulcer: Clinical, Endoscopic, Histologic, and Genotypic Aspects. A 10‐Year Brazilian Series

Recurrence infection following successful eradication of Helicobacter pylori is usually low, except for countries with high prevalence of H. pylori. The aim of this study was to verify H. pylori recurrence rate in patients with duodenal ulcer after eradication and the possible relationship with environmental factors, histologic pattern of the mucosa and bacterial genotype. One-hundred and ninety-four patients with an active duodenal ulcer and who were successfully treated for H. pylori infection from 1990 to 1999 were studied. A questionnaire was answered about their living conditions, and a 14C-urea breath test was performed. Patients with a positive breath test underwent an upper endoscopy to investigate for possible ulcer recurrence; gastric biopsy samples were than collected for rapid urease test and for histologic assessment. H. pylori vacA and cagA genotype was determined by polymerase chain reaction in those samples with positive urease test. H. pylori infection was detected in 11 patients (recurrence rate of 5.7%) that were not associated with the type of bacterial virulence. In 10 patients the ulcer was healed and all of them were clinically asymptomatic. In eight, histology showed an intensification of gastritis. All 11 patients had adequate housing and sanitary conditions and no other risk for H. pylori recurrence was identified. The recurrence rate of H. pylori in Brazil was higher than that reported in developed countries, but lower than usually reported in developing ones. Ulcer relapse rarely occurs even in long-term follow up.