Helicobacter pylori Infection Significantly Increases Insulin Resistance in the Asymptomatic Japanese Population

Background: Helicobacter pylori infection has been shown to contribute to atherosclerosis and cardiovascular diseases. Insulin resistance is the pathophysiologic background of the clinical features of atherosclerosis and cardiovascular diseases. We examined the association between H. pylori infection and insulin resistance in a large Japanese population. Materials and Methods: Fifteen hundred ninety‐eight consecutive asymptomatic subjects that underwent a complete medical survey in our institute between May 2007 and July 2008 were recruited. Cases under medication for hypertension, hyperlipidemia, diabetes mellitus, hyperuricemia, or cardiovascular diseases were excluded from the study. Cases suffering from chronic renal or liver failure were also excluded. The homeostasis model assessment of insulin resistance (HOMA‐IR) score was used to quantitatively estimate insulin resistance. Visceral and subcutaneous adipose tissues (SAT) were measured by computed tomography. The association between H. pylori serostatus and HOMA‐IR score was investigated by multivariate regression analysis. Results: A total of 988 men and 119 women were eventually eligible for this cross‐sectional survey. Helicobacter pylori seropositivity was significantly higher in 99 cases with insulin resistance (HOMA‐IR ≥2.5) compared with 1008 cases without insulin resistance (HOMA‐IR <2.5) (39.4 vs 28.7%, p = .027). There was a significant association between H. pylori serostatus and HOMA‐IR score by multiple linear regression analysis (coefficients = 0.152, 95% CI = 0.058–0.246, p = .001), after adjusting for sex, age, body mass index, waist girth, visceral and subcutaneous adipose tissues, smoking status, alcohol consumption, dietary habits, and physical activity. Conclusions: Helicobacter pylori infection significantly and independently contributed to promoting insulin resistance in a large asymptomatic population.     

Micronutrients (Other than iron) and Helicobacter pylori infection: a systematic review

Background: Many micronutrients depend on a healthy stomach for absorption. Helicobacter pylori chronic gastritis may alter gastric physiology affecting homeostasis of vitamins and minerals. Objectives: Systematic review to assess whether H. pylori infection is associated with reduced micronutrient levels (other than iron) in the plasma or gastric juice and whether low micronutrient levels are modified by eradication treatment. Method: Medline was searched for relevant publications from inception to June 2010. Studies describing micronutrient levels in H. pylori‐infected and not‐infected adults and/or the effect of eradication treatment on micronutrient levels were included. Findings: Fifty‐two publications were selected: 46 investigated the association between H. pylori infection and reduced micronutrient levels and 14 the effect of eradication treatment on micronutrient levels. Sixty‐four studies investigated vitamins (23 ascorbic acid, four ß‐carotene, 21 cobalamin, 11 folate, and five α‐tocopherol) and 10 addressed minerals (one calcium, one copper, one magnesium, one phosphorus, three selenium, and three zinc). Pooled standardized mean differences in micronutrient levels showed positive associations with H. pylori infection for ascorbic acid (gastric juice, ?1.087) and cobalamin (?0.744), and a positive effect of eradication treatment, which increased ascorbic acid in the gastric juice (?1.408) and serum cobalamin (?1.910). No significant association between infection and low folate levels was observed. Meta‐analyses for other micronutrients were not performed owing to insufficient data. Conclusions: Meta‐analyses indicate that H. pylori infection is associated with reduced levels of ascorbic acid and cobalamin, supported by the positive effect of eradication treatment. For other micronutrients, further studies are needed.     

Effects of Helicobacter pylori eradication on gastroesophageal reflux disease

Background and Aims: Helicobacter pylori infection appears to be a protective factor for gastroesophageal reflux disease (GERD). However, H. pylori is associated with the subtype of esophageal carcinoma, and long‐term proton‐pump inhibition usage would cause gastric atrophy in patients with persistent H. pylori infection, which is a precancerous lesion. The relationship between H. pylori infection and GERD is still unclear. We aimed to confirm whether the eradication of H. pylori would worsen or improve symptomatic or endoscopic GERD. Methods: A systematic review of the published data was undertaken, and a meta‐analysis was performed to determine the effect of H. pylori eradication on the occurrence of symptomatic (heartburn, acid regurgitation) and endoscopically proven erosive (esophagitis) GERD in patients with or without pre‐existing GERD. Results: A total of 11 articles met the inclusion criteria and thus were included in the meta‐analysis. There was no significant difference in the frequency of symptomatic or endoscopically proven erosive GERD after the eradication between patients with H. pylori eradicated and those with persistent infection, regardless of follow‐up period, location, or the baseline disease. Conclusion: H. pylori eradication does not aggravate the clinical outcomes in terms of short‐term and long‐term posteradication occurrence of GERD. There is no association between H. pylori eradication and the development of GERD in the patients with different diseases, even those with GERD.     

Correlation Between Helicobacter pylori Infection, Gastric Inflammation and Serum Homocysteine Concentration

Background. Epidemiological studies have suggested a link between chronic Helicobacter pylori infection and ischemic heart disease but the underlying mechanism remains elusive. We hypothesized that H. pylori‐associated chronic gastritis causes impairment of absorption of vitamin cofactors that are essential in the metabolism of homocysteine and results in hyperhomocysteinemia. Materials and Methods. Forty‐nine dyspeptic patients were studied. H. pylori infection was defined by rapid urease test and histology. Fasting serum homocysteine level, which was measured by a validated commercial fluorescence polarization immunoassay, was correlated with H. pylori infection statuses and gastric histology. H. pylori‐infected patients were followed up for 24 weeks post eradication for changes in serum homocysteine concentration. Results. Univariate analyses showed that serum homocysteine level correlated with increasing age (p < .001), male sex (p = .003) and smoking habit (p = .025). There was no significant difference in serum homocysteine levels between H. pylori infected and uninfected subjects (median 10.5 vs. 10.2 µmol/l). After successful eradication of the bacterium, there was no significant reduction in homocysteine level. Moreover, there was no correlation between homocysteine level and gastric histology including H. pylori density, activity and inflammation scores, presence of atrophy or intestinal metaplasia. Conclusions. The postulated link between H. pylori infection and ischemic heart disease, if it actually exists, is unlikely to be mediated through hyper‐homocysteinemia.     

Eradication of Helicobacter pylori infection reduces the incidence of peptic ulcer disease in patients using nonsteroidal anti-inflammatory drugs: a meta-analysis

Aim: To investigate the association between use of nonsteroidal anti‐inflammatory drugs (NSAID) and Helicobacter pylori infection, interactive effect of H. pylori infection and NSAID use on the development of peptic ulcer disease (PUD), and the effect of H. pylori eradication therapy on PUD development. Material and Methods: We performed a systematic literature search in EMBASE and PubMed for relevant articles published in English between January 1989 and August 2010, with the following MeSH and/or key words: non‐steroidal anti‐inflammatory drugs, or NSAIDs, Helicobacter pylori, or H. pylori, peptic ulcer disease or PUD, and randomized‐control study or clinical trial. The meta‐analysis was conducted using the Review Manager 4.2.2. Results: In the analysis of five studies, the pooled prevalence of H. pylori infection was 74.5% and 71.1% in NSAID users and non‐NSAID users, respectively, (OR = 0.65; 95% CI: 0.35–1.20, p = .170). In the analysis of nine studies, the pooled prevalence of PUD in NSAID users was 31.2% and 17.9% in the presence and absence of H. pylori infection, respectively, (OR = 3.08; 95% CI: 1.26–7.55, p = .010). Moreover, in the analysis of seven studies, PUD developed in 6.4% and 11.8% of NSAID users with and without eradication therapy, respectively (OR = 0.50; 95% CI: 0.36–0.74, p < .001). The preventive effect of the eradication therapy was further revealed in NSAID‐naive users (OR = 0.26; 95% CI: 0.14–0.49, p < .0001) and in the Asian population (OR = 0.30; 95% CI: 0.16–0.56, p < .001). Conclusion: NSAID use is not associated with H. pylori infection in patients with PUD. PUD is more common in H. pylori positive than in negative NSAID users. Moreover, H. pylori eradication therapy reduces PUD incidence in NSAID users, especially in naive users and in the Asian population.     

Stool antigen assay to screen H. pylori infection and to assess the success of 3-Day and 7-Day eradication therapy in the patients with partial gastrectomy

Background. Even after partial gastrectomy, Helicobacter pylori may persist in the residual stomach but be less abundant in the bacterial load. H. pylori stool antigen is a reliable noninvasive tool to detect H. pylori infection in patients without gastrectomy. We thus test whether [ 1 ] the course of H. pylori eradication therapy could be diminished [ 2 ]; stool antigen can effectively detect H. pylori infection for the patients with gastrectomy. Methods. One hundred and eight patients who had undergone partial gastrectomy were enrolled to receive panendoscopy and provided stool samples for H. pylori stool antigen within 3 days after endoscopy. The H. pylori‐infected patients were then randomized to receive either a 3‐ or 7‐day triple therapy for H. pylori eradication. Six weeks later, to evaluate the success of H. pylori eradication, patients received a follow‐up endoscopy and again provided stool samples for H. pylori stool antigen. Results. Seventy out of 108 patients, proven to have H. pylori infection, were evenly randomized into 3‐day and 7‐day therapy groups. The H. pylori eradication rates were similar between the 3‐day and 7‐day triple therapy (90.9 vs. 93.8%, p > .05). Before therapy, the H. pylori stool antigen was 93% sensitive and 100% specific to detect H. pylori. After therapy, H. pylori stool antigen remain 100% sensitive and 88.3% specific to detect the failure of eradication therapy. Conclusion. H. pylori stool antigen is a highly reliable tool to screen H. pylori infection before therapy and to assess the success of eradication therapy in partial gastrectomy patients. To eradicate H. pylori infection for patients with partial gastrectomy, the duration of triple therapy can be shortened.     

Oral health status and oral hygiene practices of patients with peptic ulcer and how these affect Helicobacter pylori eradication from the stomach

Background: Helicobacter pylori eradication from the oral cavity is more difficult than from the stomach. Thus, if the bacterium survives the antibacterial therapy in the oral cavity, it would be able to re‐infect the stomach within a few weeks. Since oral health status could correspond to oral infection with H. pylori, the aim of the study was to determine whether oral health and oral hygiene practices affect the efficacy of H. pylori eradication from the stomach. Material and Methods: The study was performed in 137 patients with peptic ulcer who had undergone a 7‐day course of eradication treatment with one of two sets of drugs: 1, omeprazole, amoxicillin, and tinidazole or 2, omeprazole, clarithromycin, and tinidazole. The efficacy of H. pylori eradication from the stomach was evaluated at the second gastroscopy 4 weeks after cessation of eradication therapy by means of two methods: rapid urease test and histology. The examination of natural dentition and prosthetic restorations as well as the assessment of hygienic procedures referring to natural dentition and dentures accompanied the second gastroscopy. Results: No association was found between the efficacy of H. pylori eradication from the stomach and the number of natural teeth, decayed teeth, use of dentures, debris index, or periodontal index. However, an association between eradication success and some oral hygiene procedures were noted. Unexpectedly, in patients treated with omeprazole, amoxicillin and tinidazole, the removal of dental prosthesis for the night and brushing the natural teeth twice a day or more reduced the efficacy of H. pylori eradication from the stomach. Conclusions: Oral health and oral hygiene practices seem unlikely to increase the efficacy of H. pylori eradication from the stomach.     

Eradication of Helicobacter pylori infection improves blood pressure values in patients affected by hypertension

Background. Arterial hypertension is a risk factor for atherosclerosis of whose pathogenesis is unknown. Growing evidence underscores the causative role of endothelial dysfunction. A possible association between Helicobacter pylori infection and cardiovascular and autoimmune disorders has been found. The release of cytotoxic substances either of bacterial origin or produced by the host may represent mediators of these systemic sequelae. The aim of our study was to determine the prevalence of H. pylori infection in hypertensive patients and the effects of H. pylori eradication on blood pressure and on digestive symptoms. Materials and Methods. Seventy‐two hypertensive patients (34 male and 38 female; mean age 53 ± 12 years) and 70 normotensive controls (35 male and 35 female; mean age 52 ± 10 years) were enrolled. All patients were subjected to a first ambulatory blood pressure monitoring (ABPM) at enrollment, a ¹³C urea breath test and a test for IgG‐CagA antibodies, and completed the validated dyspepsia questionnaire. H. pylori‐positive patients were treated with triple therapy (amoxicillin, clarithromycin and ranitidine bismute citrate) for 7 days. Control of eradication was assessed by ¹³C urea breath test, and all patients underwent a second ABPM 6 months after enrollment. Results. H. pylori infection was 55% in hypertensive patients, with 90% CagA positivity, and 50% in controls, with 60% CagA positivity. At the first ABPM, blood pressure values were similar in H. pylori‐positive and ‐negative individuals; positive patients showed a significant increase in pyrosis and epigastric pain compared to negative patients. H. pylori was eradicated in 80% of patients and in 85% of controls. At the second ABPM, we found a statistically significant decrease in 24‐hour mean blood pressure values when compared to the first ABPM only in the eradicated hypertensive group. Conclusions. Our study demonstrated a significant decrease in blood pressure values, in particular in diastolic blood pressure values, after H. pylori eradication in hypertensive patients. A high prevalence of CagA positivity was found. The association between cardiovascular disease and H. pylori infection seems pronounced only in CagA‐positive patients. The possible links between hypertensive disease and H. pylori infection may involve the activation of the cytokine cascade with the release of vasoactive substances from the primary site of infection, or molecular mimicry between the CagA antigens of H. pylori and some peptides expressed by endothelial cells and smooth muscle cells.     

Interactions Among Gastric Somatostatin, Interleukin-8 and Mucosal Inflammation in Helicobacter pylori-Positive Peptic Ulcer Patients

Background. To investigate whether Helicobacter pylori infection, but not drugs, affects gastric somatostatin, interleukin‐8 (IL‐8), histological inflammation through eradication therapy, and interactions among these parameters. Methods. Twenty‐eight H. pylori‐positive patients (21 males; mean age 47.0 years) with either gastric ulcer (GU: n = 11) or duodenal ulcer (n = 17) diagnosed endoscopically were treated with dual therapy. Eradication was defined as negative microbiologic tests and ¹³C‐urea breath test. Levels of antral and gastric juice somatostatin and mucosal IL‐8 were measured by radioimmunoassay and enzyme‐linked immunosorbent assay, respectively. Histology was assessed by the Sydney system. Results. H. pylori was eradicated in 15 patients (10 males, 6 GU) out of 28 (54%). The patients’ backgrounds did not affect the eradication of H. pylori. Successes in eradication significantly increased antral and juice somatostatin contents, and dramatically decreased IL‐8 levels and histological gastritis. In contrast, persistent H. pylori infection did not affect somatostatin and histological gastritis. An inverse correlation was present between changes in somatostatin levels and histological activity. No relationship was observed in changed values between antral somatostatin and IL‐8. Conclusions. These results indicate that eradication of H. pylori, but not the drugs used, induced an increase in somatostatin levels in the antrum and gastric juice, suggesting a close relationship between H. pylori and gastric somatostatin regulation. A close correlation between an increase in gastric somatostatin levels and the normalization of histological activity was present, suggesting that certain peptide‐immune interactions in the gastric mucosa exist in H. pylori infection.     

Effect of Helicobacter pylori infection on gastric acid secretion and meal-stimulated serum gastrin in children

Background. Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal‐stimulated gastrin in relation to H. pylori infection among pediatric patients. Materials and Methods. Thirty‐six children aged 10–17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2–3 months after H. pylori eradication. Meal‐stimulated serum gastrin response was assessed before and 12 months after eradication. Results. H. pylori gastritis was typically antrum‐predominant. Acid secretion was greater in H. pylori‐positive patients with duodenal ulcer than in gastritis‐only patients or controls [mean ± standard error (SE): 6.56 ± 1.4, 3.11 ± 0.4 and 2.65 ± 0.2 mEq/10 minutes, respectively; p < .001]. Stimulated acid secretion was higher in H. pylori‐positive boys than girls (5.0 ± 0.8 vs. 2.51 ± 0.4 mEq/10 minutes, respectively; p < .05). Stimulated acid secretion pre‐ and post‐H. pylori eradication was similar (5.47 ± 0.8 vs. 4.67 ± 0.9 mEq/10 minutes, respectively; p = .21). Increased basal and meal‐stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p < .001 and peak from 544 to 133 pg/ml, p < .05). Conclusions. H. pylori infection in children is associated with a marked but reversible increase in meal‐stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection.     

Antibacterial effects of the urushiol component in the sap of the lacquer tree (Rhus verniciflua Stokes) on Helicobacter pylori

Background: Urushiol is a major component of the lacquer tree which has been used as a folk remedy for the relief of abdominal discomfort in Korea. The aim of this study was to evaluate the antibacterial effects of the urushiol on Helicobacter pylori. Materials and Methods: Monomer and 2–4 polymer urushiol were used. In the in vitro study, pH‐ and concentration‐dependent antibacterial activity of the urushiol against H. pylori were investigated. In addition, the serial morphological effects of urushiol on H. pylori were examined by electron microscopy. In vivo animal study was performed for the safety, eradication rate, and the effect on gastritis of urushiol. The expression of pro‐inflammatory cytokines was checked. Results: All strains survived within a pH 6.0–9.0. The minimal inhibitory concentrations of the extract against strains ranged 0.064–0.256 mg/mL. Urushiol caused separation of the membrane and lysis of H. pylori within 10 minutes. Urushiol (0.128 mg/mL × 7 days) did not cause complications on mice. The eradication rates were 33% in the urushiol monotherapy, 75% in the triple therapy (omeprazole + clarithromycin + metronidazole), and 100% in the urushiol + triple therapy, respectively. H. pylori‐induced gastritis was not changed by urushiol but reduced by eradication. Only the expression of interleukin‐1β in the gastric tissue was significantly increased by H. pylori infection and reduced by the urushiol and H. pylori eradication (p = .014). Conclusions: The urushiol has an antibacterial effect against H. pylori infection and can be used safely for H. pylori eradication in a mouse model.     

Inverse association between Helicobacter pylori and pediatric asthma in a high-prevalence population

Background: Helicobacter pylori‐associated disease has led to aggressive diagnostic and eradication protocols that are partially responsible for the decrease in prevalence of H. pylori carriage. Recent evidence indicates that in low‐prevalence populations, H. pylori may have protective effects on allergic diseases. The aim of this study was to explore the relationship between pediatric asthma and H. pylori infection in a population with high prevalence of H. pylori infection. Materials and Methods: A national referral laboratory was screened for all ¹³C urea breath tests performed in children aged 5–18 years between 2007 and 2008, for patient demographics and physician‐diagnosed asthma. Data concerning asthma‐associated medication usage were extracted from electronic medical records and databases. Data were analyzed using a stepwise logistic regression model. Results: During the study period, 6959 patients underwent urea breath testing (average age 12.4 ± 3.5 years). Of these, 3175/6959 (45.6%) were positive for H. pylori, and 578/6959 (8.3%) had asthma. Rates of asthma in H. pylori‐positive and H. pylori‐negative children were 7.3 and 9.1%, respectively (odds ratio 0.82; 95% confidence interval (CI) 0.69–0.98; p = .032). We also confirmed that male gender, urban residence, and age are associated with childhood asthma. Conclusions: We demonstrate an inverse association between H. pylori and pediatric asthma in a population with a high prevalence of H. pylori.     

Acid inhibitory potency of twice a day omeprazole is not affected by eradication of Helicobacter pylori in healthy volunteers

Background & Aims. The acid inhibitory effect of proton pump inhibitors is reported to be greater in the presence than in the absence of an H. pylori infection. This study was undertaken to test the hypothesis that the acid inhibitory effect of omeprazole given twice a day is greater in H. pylori infected healthy volunteers than in the same individuals following eradication because of differences in the pharmacodynamics of omeprazole, greater duodenogastric reflux, the effects of ammonia produced by the H. pylori, or lower gastric juice concentrations of selected cytokines, which may inhibit gastric acid secretion. Materials and Methods. We undertook 24‐hour pH‐metry in 12 H. pylori‐positive healthy volunteers: (1) when on no omeprazole; (2) when on omeprazole 20 mg bid for 8 days; (3) 2 months after eradication of H. pylori and when on no omeprazole; and (4) after eradication of H. pylori and when on omeprazole 20 mg twice a day. Results. In subjects given omeprazole, eradication of H. pylori reduced pH and percentage pH ≥ 3, as well as increasing the area under the H⁺ concentration‐time curve. These differences were not due to alterations in (1) gastric juice concentrations of IL‐1α, IL‐8, IL‐13, epidermal growth factor, or bile acids; (2) serum gastrin concentrations; or (3) the pharmacokinetics of omeprazole. There was no change in the difference in the H⁺ concentration‐time curve ‘without omeprazole’ minus ‘with omeprazole’, when comparing ‘after’ versus ‘before’ eradication of H. pylori. Conclusions. Eradication of H. pylori was not associated with an alteration in the acid inhibitory potency when comparing the difference in gastric acidity ‘with’ versus ‘without’ omeprazole. When the results were expressed by simply taking into account the acid measurements while on omeprazole before versus after eradication of H. pylori, the acid inhibition with omeprazole was greater in the presence than in the absence of a H. pylori infection. The clinical significance of the small difference is not clear.     

Is the recurrence of Helicobacter pylori infection after eradication therapy resultant from recrudescence or reinfection,in Japan

Background. Reinfection of Helicobacter pylori after eradication is rare in developed countries but most often occurs within 1 year. In the present study, we attempted to differentiate between reinfection and recrudescence of H. pylori strains between 6 months and 6 years after successful eradication in Japan, a country with a high prevalence of H. pylori infection. Materials and Methods. After successful eradication of H. pylori, 274 patients were followed up by endoscopy and urea breath test. In recurrent patients, H. pylori strains isolated initially and after recurrence were compared using PCR‐based restriction fragment length polymorphism (RFLP) analysis. Results. Recurrence of H. pylori occurred in 15 of 274 patients (5.5%) at 6 months after eradication and the annual recurrence rate was 2.0% per patient year (between 1 and 6 years). PCR‐based RFLP analysis of H. pylori strains isolated initially and after recurrence showed that 62.5% (at 6 months) and 100% (after 1 years) of bacteria were of different strains. Conclusion. Reinfection of H. pylori was not as rare at 6 months after eradication as reported previously, and up to 6 years after eradication, the annual reinfection rate is 2.0% per patient year in Japan.     

Efficacy and safety of Saccharomyces boulardii in the 14-day triple anti-Helicobacter pylori therapy: a prospective randomized placebo-controlled double-blind study

Background: Recent studies indicate a potential role of Saccharomyces boulardii in the prevention of Helicobacter pylori treatment‐related side‐effects and also in improvement of eradication rate. Our aim is to investigate the efficacy and safety of S. boulardii in the prevention of side‐effects related to H. pylori eradication. The secondary aim of the study was to define the effect of S. boulardii on the eradication success of anti‐H. pylori therapy. Materials and methods: One hundred and twenty‐four patients with H. pylori infection (male/female: 44/80, mean age: 48 ± 14.25 year) receiving 14 days of triple therapy (clarithromycin 500 mg b.i.d., amoxicillin 1000 mg b.i.d., and lansoprazole 30 mg b.i.d.) were randomly assigned to S. boulardii or placebo. Dyspeptic symptoms were recorded by using modified Glasgow Dyspepsia Questionnaire (GDQ). Side‐effect profile and tolerability were assessed using a symptom‐based questionnaire. H. pylori status was rechecked after 6 weeks after completion of eradication therapy. Results: H. pylori eradication rate, although higher in the treatment group, was statistically similar in treatment and control groups: 71% (44/62) versus 59.7% (37/62), respectively (p > .05). Nine (14.5%) patients in the treatment group and 19 (30.6%) patients in the placebo group experienced diarrhea (p < .05). Epigastric discomfort was more frequent in the control group [9 (14.5%) versus 27 (43.5%), respectively (p < .01)]. Diffuse abdominal pain, abdominal gas, taste disturbance, urticaria, nausea symptoms were similar in both groups. GDQ scores after treatment were significantly better for treatment group (mean ± SD, range: 1.38 ± 1.25 (0–5) vs. 2.22 ± 1.44 (0–6), respectively; p < .01). Conclusion: S. boulardii improved anti‐H. pylori antibiotherapy‐associated diarrhea, epigastric discomfort, and treatment tolerability. In addition, S. boulardii supplement decreased post‐treatment dyspepsia symptoms independent of H. pylori status. However, S. boulardii had no significant affect on the rate of H. pylori eradication.     

The role of abdominal CT scan as follow-up after complete remission with successful Helicobacter pylori eradication in patients with H. pylori-positive stage I(E1) gastric MALT lymphoma

Background: 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. Patients and Methods: We retrospectively analyzed 122 patients with H. pylori‐positive stage I_E1 gastric MALT lymphoma who achieved CR with successful H. pylori eradication. Results: The median follow‐up after CR was 35 months (range 3–140months). 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. Conclusions: 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.     

Are individuals with lower neutrophil oxidative burst activity more prone to Helicobacter pylori infection?

Helicobacter pylori infection has been reported to cause enhanced reactive oxygen species in the gastric mucosa. We examined the relationship between H. pylori infection and neutrophil function of peripheral blood. The subjects were 904 volunteers who participated in the Iwaki Health Promotion Project in 2005. 158 subjects who were infected with H. pylori in 2005 also participated in this project in 2006 and were categorized into two groups: the eradication group, in which H. pylori was successfully eradicated during the 12 month period, and the non‐eradication group, in which eradication was unsuccessful or the subjects did not receive eradication therapy. The laboratory assays performed were: a titre of H. pylori antibody; neutrophil counts; and oxidative burst activity (OBA) of neutrophils. Logistic regression analysis was executed, with H. pylori infection as the dependent variable and other items as the independent variables. OBA showed an inverse association with H. pylori infection in 2005. Additionally, when comparing the eradication and non‐eradication groups, the change rates of OBA between 2005 and 2006 did not show any significant difference. It was concluded that H. pylori infection does not lower OBA, but those individuals in whom OBA was lower were more prone to H. pylori infection. Copyright © 2008 John Wiley & Sons, Ltd.     

Helicobacter pylori-negative gastric cancer in South Korea: incidence and clinicopathologic characteristics

Background and Aim: It is difficult to determine the exact incidence rate of Helicobacter pylori (H. pylori) infection‐negative gastric cancer (HPIN‐GC) because H. pylori detection rates decrease with the progression of gastric atrophy and intestinal metaplasia. The aim of this study was to evaluate the incidence and clinicopathologic characteristics of HPIN‐GC in South Korea. Methods: Helicobacter pylori infection status was evaluated by histology, a rapid urease test (CLO test), culturing, serology, and history of H. pylori eradication for 627 patients with gastric cancer. Current H. pylori infection was defined as positive results from histology, the CLO test, and culturing. Previous H. pylori infection was defined as negative in all three biopsy‐based tests and positive serology or history of H. pylori eradication. Patients were considered to be negative for H. pylori infection if all results from five methods were negative. However, patients who were found to have severe gastric atrophy by the serum pepsinogen test or metaplastic gastric atrophy by histology were assumed to have had a previous H. pylori infection even if results from other tests for H. pylori infection were all negative. Results: The number of patients with gastric cancer with current or previous H. pylori infection was 439 (70.0%) and 154 (24.6%), respectively. The rate of HPIN‐GC occurrence was 5.4% (n = 34). Sex, age, Lauren type, location of the tumor, and treatment modalities were not different according to H. pylori infection status. However, HPIN‐GC had a more advanced pT classification (T3/T4; 51.9 vs 31.1%, p = .025) and a more advanced stage (more than stage I; 63 vs 41.3%, p = .027) than H. pylori‐positive gastric cancer. Conclusion: At least 5.4% cases of gastric cancer were H. pylori negative among South Korean patients. HPIN‐GC looks like to have a poorer prognosis than H. pylori‐positive cases.     

The effect of Helicobacter pylori and economic status on growth parameters and leptin, ghrelin, and insulin-like growth factor (IGF)-I concentrations in children

Background: It was suggested that gastric colonization with Helicobacter pylori (H. pylori) was associated with suboptimal nutrition and growth in childhood. Furthermore, several studies indicated a relationship between H. pylori colonization and alterations in the circulating levels of growth‐related molecules (GRM). Accordingly, in this study, we investigate the effect of H. pylori infection on GRMs and on the growth of healthy school children, taking into consideration the effect of their economic status (ES) and anthropometric indices of their parents. Methods: To acquire sociodemographic and anthropometric nutritional parameters and to detect H. pylori‐specific serum IgG antibodies and growth‐related molecules, we evaluated a total of 473 children attending four different primary and secondary schools in Istanbul. Subsequently, we assessed the effect of H. pylori on growth‐related parameters (weight for age SDS, height for age SDS, BMI SDS, TSF, and waist‐to‐hip ratio) and on GRMs (leptin, ghrelin, and insulin‐like growth factor‐1 (IGF‐1)), controlling for age, gender, family income, household crowding (HC), breastfeeding, maternal and paternal BMI SDS, and midparental height SDS with complex statistical models. Results: Of the 473 children (275 F/198 M, age 6–15 years; mean: 10.3 ± 0.1 years), 161 (34%) were H. pylori‐positive. The prevalence of H. pylori was significantly higher in lower economic status (ES) groups, in children living in crowded houses, and in older age groups. Using simple statistical models, we did not find any significant associations between H. pylori infection and the growth parameters. However, in complex models for height for age SDS and for weight for age SDS, there was a significant interaction between H. pylori infection status and ES. Whereas in H. pylori‐positive subjects, mid‐income family children were both taller and heavier than the low‐income group, there was no such an association in H. pylori‐negative subjects. Among biochemical parameters, only ghrelin levels were associated with H. pylori infection in all models. Leptin levels were associated with HC in girls, whereas none of the parameters was significantly associated with leptin levels in boys. For IGF‐1 levels, for boys, age and maternal BMI, and for girls, age and HC were significantly associated with IGF‐1 levels. Conclusion: We suggest that H. pylori may impair growth significantly only in susceptible children where unfavorable socioeconomic conditions facilitate its action, probably through mechanisms, at least in part, involving growth‐related molecules.     

Clinicopathological analysis of early-stage gastric cancers detected after successful eradication of Helicobacter pylori

Background and Aims: 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. Methods: 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. Results: 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. Conclusion: 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.