Histological Gastritis Research Articles

Histological characteristics of gastric mucosa prior to Helicobacter pylori eradication may predict gastric cancer

Objective. Although Helicobacter pylori (H. pylori) eradication has been shown to inhibit gastric cancer, it does not completely suppress it. Therefore, risk factors of gastric cancer development following H. pylori eradication were examined. Material and methods. A total of 2355 patients (1501 males and 824 females) underwent successful eradication of H. pylori. Endoscopic atrophy, histological gastritis, atrophy, intestinal metaplasia (IM), and operative link for gastritis assessment (OLGA) staging were subsequently evaluated. Results. Following eradication, 33/2355 patients (25 males and 8 females) developed gastric cancer. Compared to a nongastric cancer group that was matched according to gender and age, the incidence of endoscopic atrophy (3.52 ± 1.45 vs. 4.85 ± 1.18, p < 0.001), histological atrophy at the greater curvature of the antrum (1.42 ± 0.80 vs. 1.95 ± 0.86, p = 0.0059), inflammation (2.05 ± 0.59 vs. 2.33 ± 0.66, p = 0.031), IM at the greater curvature of the corpus (0.06 ± 0.30 vs. 0.24 ± 0.54, p = 0.029), the ratio of OLGA-stage 0–II/III, IV (13/8 vs. 55/11, p = 0.038) were significantly higher for the gastric cancer group. Multivariate analysis also showed the highest odds ratio (6.26, 95% confidence interval or CI, 1.28–30.60, p = 0.023) for IM at the greater curvature of the corpus. Conclusions. Severe endoscopical atrophy, OLGA staging, histological atrophy at the antrum, inflammation, and particularly IM at the corpus, were identified as risk factors for gastric cancer development following H. pylori eradication. Therefore, eradication should be performed before these predictors develop.

Serum Ghrelin; A New Surrogate Marker of Gastric Mucosal Alterations in Upper Gastrointestinal Carcinogenesis

BackgroundA few studies have indicated inverse relationships between serum ghrelin and gastric and esophageal cancers but those associations have been restricted to specific populations, including smokers and overweight individuals. We examined the association between ghrelin and gastroesophageal cancers and atrophic gastritis in a population-based setting.MethodsIn total 220 gastroesophageal cancers, comprising non-cardia and cardia gastric cancer, esophageal adenocarcinoma, esophageal squamous cell carcinoma (SCC) and age and gender-matched controls were recruited. Serum ghrelin, pepsinogen I/II ratio (PGI/II) and anti-H.pylori IgG antibodies were measured. Relationships between ghrelin and gastroesophageal cancers, after adjustment for PGI/II ratio, H.pylori status and smoking, were tested using logistic regression. Furthermore, in 125 endoscopically normal volunteers, with and without histological atrophic gastritis, the relationship with ghrelin was compared.ResultsSerum ghrelin (lowest vs. highest quintile) was inversely associated with gastric cancer: OR (95% CI) 8.71 (1.70–44.59) for cardia and 6.58 (1.26–34.46) for non-cardia cancer. Lower serum ghrelin was also associated with esophageal SCC: OR (95% CI) 5.69 (1.36–23.78), but not with esophageal adenocarcinoma. A similar association was observed between gastric cancer (cardia and non-cardia) and esophageal SCC when serum ghrelin was analysed as a continuous scaled variable. In endoscopically-normal volunteers, extensive atrophic gastritis was associated with low serum ghrelin [OR (95% CI) 0.25 (0.10–0.64)].ConclusionInverse associations between ghrelin and some gastroesophageal cancers suggest a potential role for serum ghrelin as a biomarker of upper gastrointestinal cancers and atrophic gastritis. In areas with a high incidence of gastric and/or esophageal cancer, screening might be more effectively targeted to individuals with low serum ghrelin in addition to the PGI/II ratio.

Neglected role of hookah and opium in gastric carcinogenesis: a cohort study on risk factors and attributable fractions.

A recent study showed an association between hookah/opium use and gastric cancer but no study has investigated the relationship with gastric precancerous lesions. We examined the association between hookah/opium and gastric precancerous lesions and subsequent gastric cancer. In a population-based cohort study, 928 randomly selected, healthy, Helicobacter pylori-infected subjects in Ardabil Province, Iran, were followed for 10 years. The association between baseline precancerous lesions and lifestyle risk factors (including hookah/opium) was analyzed using logistic regression and presented as odds ratios (ORs) and 95% confidence intervals (CIs). We also calculated hazard ratios (HRs) and 95% CIs for the associations of lifestyle risk factors and endoscopic and histological parameters with incident gastric cancers using Cox regression models. Additionally, the proportion of cancers attributable to modifiable risk factors was calculated. During 9,096 person-years of follow-up, 36 new cases of gastric cancer were observed (incidence rate: 3.96/1,000 persons-years). Opium consumption was strongly associated with baseline antral (OR: 3.2; 95% CI: 1.2-9.1) and body intestinal metaplasia (OR: 7.3; 95% CI: 2.5-21.5). Opium (HR: 3.2; 95% CI: 1.4-7.7), hookah (HR: 3.4; 95% CI: 1.7-7.1) and cigarette use (HR: 3.2; 95% CI: 1.4-7.5), as well as high salt intake, family history of gastric cancer, gastric ulcer and histological atrophic gastritis and intestinal metaplasia of body were associated with higher risk of gastric cancer. The fraction of cancers attributable jointly to high salt, low fruit intake, smoking (including hookah) and opium was 93% (95% CI: 83-98). Hookah and opium use are risk factors for gastric cancer as well as for precancerous lesions. Hookah, opium, cigarette and high salt intake are important modifiable risk factors in this high-incidence gastric cancer area.

Sa1673 Histological Gastritis in the Antrum Diagnosed With Endoscopic Magnification Combined With Spraying of 5% Acetic Acid and “Flexible Spectral Imaging Colour Enhancement” (FICE). Preliminary Study

Sa1673 Histological Gastritis in the Antrum Diagnosed With Endoscopic Magnification Combined With Spraying of 5% Acetic Acid and “Flexible Spectral Imaging Colour Enhancement” (FICE). Preliminary Study

101 Ornithine Decarboxylase Disrupts Host Immune Tolerance in Helicobacter pylori Infection by Attenuating Macrophage Production of TGF-β and Nitric Oxide

Background: Helicobacter pylori (Hp) infection results in a Th1/Th17 polarized inflammatory response. We have reported that expression of ornithine decarboxylase (ODC), the ratelimiting enzyme for polyamine synthesis, is increased in macrophages (Macs) in mouse and human Hp gastritis tissues, and that inhibition of ODC reduces gastritis and Hp colonization in mice. Our aim was to determine if ODC impairs host tolerance induced by Macs and promotes STAT1-mediated Th1/Th17 adaptive immune responses to Hp. Methods: Wild type (WT) and ODC+/C57BL/6 mice were infected with Hp SS1 for 4 months. We measured in gastric tissues: Hp colonization by qPCR, histological inflammation (0-12), TGFβ by Western blotting, and cytokines by Luminex assay. TGFβ in gastric Macs (GMacs) was measured by qPCR and immunofluorescencemicroscopy. Splenic Macs (SMacs) were isolated and activated with French-pressed Hp lysates (HPL); levels of TGFβ mRNA and nitric oxide (NO) production were measured by qPCR and Griess assay, respectively. Splenocytes, or co-culture of splenocytes depleted of Macs (SMacs-) with SMacs were activated with HPL for 48 h ± anti-TGF-β neutralizing antibody or the iNOS inhibitor 1400W, and IFNγ, IL17, IL-10, pSTAT1, and pSTAT3 were analyzed in CD4+ cells by flow cytometry. Results: In Hp-infected ODC+/versus WT mice, there was decreased histological gastritis (from 5.8 ± 0.3 to 3.2 ± 0.2; p , 0.05) and Hp colonization was reduced by 2 log orders ( p , 0.05). In SMacs from ODC+/-vs. WT mice, ex vivo activation with HPL increased TGFβ mRNA levels by 10-fold (p , 0.01) and NO production (from 6.2 ± 0.4 to 15.3 ± 0.9 μM; p , 0.01), but there was no difference in IL-10 expression. In HPL-stimulated splenocytes, IFNγ+ and IL-17+cells were increased in WT mice, but IL-10+ cells were increased in ODC+/mice. Pretreatment of splenocytes with anti-TGFβ antibody or 1400W before ex vivo activation increased IFN-γ+ and IL-17+, but not IL-10+ cells in ODC+/mice (Table 1). When WT SMacs were co-cultured with WT or ODC+/SMacs-, upon ex vivo stimulation there were increased IFN-γ+ cells, but when ODC+/SMacs were co-cultured with WT or ODC+/SMacs-, this did not occur. Pretreatment with anti-TGFβ or 1400W in the co-culture of ODC+/-SMacs with WT or ODC+/SMacsincreased IFN-γ+ cells (Table 2). In stomach tissue lysates from ODC+/vs. WT mice, IFN-γ and IL-17 levels were decreased, while IL-10 was increased. TGF-β mRNA and protein expression was increased in stomach tissues and in GMacs of ODC+/mice. In these studies, the pSTAT1/pSTAT3 ratio was decreased when IFN-γ and IL-17 were decreased and IL-10 was increased. Conclusions: During Hp infection, ODC inhibits TGF-β and NO production by Macs that impairs host immune tolerance manifested as a skewed adaptive (Th1/Th17) response, inappropriate inflammation, and persistent Hp colonization. Table 1

Effect of Eradication on Functional Dyspepsia

Background/AimsThis study evaluated the effect of Helicobacter pylori eradication on functional dyspepsia (FD), and the relationship between the changes of histological gastritis and FD symptom responses.MethodsA total of 213 FD patients diagnosed by Rome III criteria were consecutively enrolled. H. pylori tests and gastritis grade by the Sydney system were performed before and 1 year after the proton pump based-eradication therapy for 7 days. Serum levels of pepsinogen, and genetic polymorphisms IL-6, IL-8 and IL-10 were investigated.ResultsTotal of 91 patients completed the 1 year follow-up. When the response rate of dyspepsia was compared at 1 year between the non-eradicated group (n = 24) and eradicated group (n = 67), each group showed complete response of 62.5% and 62.7%; satisfactory response (≥ 50%) of 0.0% and 19.4%; partial response (< 50%) of 12.5% and 11.9%; and refractory response of 25.0% and 6.0%, respectively (P = 0.015). In addition, the responder group (complete + satisfactory response) at 1 year showed improvement of activity and chronic inflammation in both the antrum and corpus (all P < 0.001). Multivariate analysis showed that H. pylori eradication (OR, 5.81; 95% CI, 1.07-31.59) and symptom improvement at 3 month (OR, 28.90; 95% CI, 5.29-157.82) were associated with the improvement of dyspepsia at 1 year. Among the successfully eradicated FD patients (n = 67), male (P = 0.013) and higher initial BMI (P = 0.016) were associated with the improvement of dyspepsia at 1 year.ConclusionsH. pylori eradication improved FD symptoms, as well as gastritis at 1 year, suggesting that inflammation mediates FD.

The prevalence of helicobacter pylori and gastritis in Oman

ABSTRACT Background and objectives: Helicobacter pylori (H. pylori) are considered to be the most common human infectious agents leading to gastritis, ulcer and probably stomach cancer. The aim of this study was to evaluate the prevalence of H. pylori infection and histologic gastritis in Oman using endoscopy biopsy of the stomach. Methods: A total of 366 stomach biopsies (171 males and 195 females) were histologically analyzed at Sultan Qaboos University Hospital, Muscat, Sultanate of Oman, between 2007 and 2010, using haematoxylin and eosin, Giemsa and Alcian blue / periodic acid-Schiff stains. Results: Out of 366 cases, 110 (30.1%) were positive for H. pylori infection. Out of 110, 76 cases were associated with active chronic gastritis, 32 cases with chronic gastritis and one case each with gastric carcinoma and normal histological features. The maximum number of H. pylori organisms was found among young (26 – 44 years) and middle age (45 – 59 years) groups, 34.5% and 30.9%, respectively. H. pylori was present in 36.9% females and in 22.2% of males. 40.9% of H. pylori was found in the gastric antrum site, and the gastric cardia was free of H. pylori. Conclusion: H. pylori associated active chronic gastritis is the most common form of stomach diseases encountered in this study. In addition, female, young and middle age group and gastric antrum had the highest frequency of H. pylori organisms. J Dig Endosc 2013;4(2):29-32)

Serum Prohepcidin Levels Are Lower in Patients with Atrophic Gastritis

Background/Aim. Hepcidin, an iron regulatory hormone, is increased in response to inflammation and some infections. We investigated the relationships among serum prohepcidin, iron status, Helicobacter pylori infection status, and the presence of gastric mucosal atrophy. Methods. Seventy subjects undergoing esophagogastroduodenoscopy underwent multiple gastric biopsies, and the possibility of H. pylori infection and the degree of endoscopic and histologic gastritis were investigated. In all subjects, serum prohepcidin and iron parameters were evaluated. Results. No correlations were observed between serum prohepcidin levels and the other markers of anemia, such as hemoglobin, serum iron, ferritin, and total iron binding capacity. Serum prohepcidin levels were not significantly different between the H. pylori-positive group and the H. pylori-negative group. Serum prohepcidin levels in atrophic gastritis patients were significantly lower than those in subjects without atrophic gastritis irrespective of H. pylori infection. Conclusion. Serum prohepcidin levels were not altered by H. pylori infection. Serum prohepcidin levels decrease in patients with atrophic gastritis, irrespective of H. pylori infection. It suggests that hepcidin may decrease due to gastric atrophy, a condition that causes a loss of hepcidin-producing parietal cells. Further investigations with a larger number of patients are necessary to substantiate this point.

Gastrokine 1 Expression in the Human Gastric Mucosa Is Closely Associated with the Degree of Gastritis and DNA Methylation

PurposeGastrokine 1 plays an important role in gastric mucosal defense. Additionally, the Gastrokine 1-miR-185-DNMT1 axis has been shown to suppress gastric carcinogenesis through regulation of epigenetic alteration. Here, we investigated the effects of Gastrokine 1 on DNA methylation and gastritis.Materials and MethodsExpression of Gastrokine 1, DNMT1, EZH2, and c-Myc proteins, and the presence of Helicobacter pylori CagA protein were determined in 55 non-neoplastic gastric mucosal tissue samples by western blot analysis. The CpG island methylation phenotype was also examined using six markers (p16, hMLH1, CDH1, MINT1, MINT2 and MINT31) by methylation-specific polymerase chain reaction. Histological gastritis was assessed according to the updated Sydney classification system.ResultsReduced Gastrokine 1 expression was found in 20 of the 55 (36.4%) gastric mucosal tissue samples and was closely associated with miR-185 expression. The Gastrokine 1 expression level was inversely correlated with that of DNMT1, EZH2, and c-Myc, and closely associated with the degree of gastritis. The H. pylori CagA protein was detected in 26 of the 55 (47.3%) gastric mucosal tissues and was positively associated with the expression of DNMT1, EZH2, and c-Myc. In addition, 30 (54.5%) and 23 (41.9%) of the gastric mucosal tissues could be classified as CpG island methylation phenotype-low and CpG island methylation phenotype-high, respectively. Reduced expression of Gastrokine 1 and miR-185, and increased expression of DNMT1, EZH2, and c-Myc were detected in the CpG island methylation phenotype-high gastric mucosa.ConclusionsGastrokine 1 has a crucial role in gastric inflammation and DNA methylation in gastric mucosa.

Helicobacter pylori -Negative Gastritis: Prevalence and Risk Factors

Recent studies using histology alone in select patients have suggested that Helicobacter pylori-negative gastritis may be common. The objective of this study was to investigate the prevalence of H. pylori among individuals with histologic gastritis. Subjects between 40 and 80 years underwent elective esophagogastroduodenoscopy at a VA Medical Center. Gastric biopsies were mapped from seven prespecified sites (two antrum, four corpus, and one cardia) and graded by two gastrointestinal pathologists, using the Updated Sydney System. H. pylori-negative required four criteria: negative triple staining at all seven gastric sites, negative H. pylori culture, negative IgG H. pylori serology, and no previous treatment for H. pylori. Data regarding tobacco smoking, alcohol drinking, nonsteroidal anti-inflammatory drug, and proton pump inhibitor (PPI) use were obtained by questionnaire. Of the 491 individuals enrolled, 40.7% (200) had gastritis of at least grade 2 in at least one biopsy site or grade 1 in at least two sites. Forty-one (20.5%) had H. pylori-negative gastritis; most (30 or 73.2%) had chronic gastritis, five (12.2%) had active gastritis, and six (14.6%) had both. H. pylori-negative gastritis was approximately equally distributed in the antrum, corpus, and both antrum and corpus. Past and current PPI use was more frequent in H. pylori-negative vs. H. pylori-positive gastritis (68.2% and 53.8%; P=0.06). We used multiple methods to define non-H. pylori gastritis and found it in 21% of patients with histologic gastritis. While PPI use is a potential risk factor, the cause or implications of this entity are not known.

Bile Acid Promotes Intestinal Metaplasia and Gastric Carcinogenesis

Bile acid and Helicobacter pylori (H. pylori) are important toxic factors for gastric mucosal injury. We examined the role of bile acid in promoting histologic gastritis and gastric carcinoma in Japanese patients. A total of 767 patients (452 men, mean age 51.1 years) were studied. Gastric juice was collected by gastro-endoscopic examination, and the bile acid concentration was examined by enzymatic method. The grade of histologic gastritis was evaluated by gastric biopsies, and the relationship between the bile acid concentration and the gastritis score was examined. The occurrence of gastric cancer was examined by a retrospective cohort study. CDX2/CINC1 expression in RGM-1 cells was evaluated by real-time PCR. In H. pylori-positive patients, we found significant positive correlation between the bile acid concentration and the grades of atrophy/intestinal metaplasia (P < 0.01). However, we found significant negative associations between the bile acid concentrations and the histologic scores of mononuclear cell/neutrophil infiltrations (P < 0.01). Patients with a high concentration of bile acid developed gastric cancer more frequently than those with a low concentration (P < 0.05). Cholic acid treatment significantly increased CDX2 expression in RGM-1 cells. CINC1 expression in RGM-1 cell was significantly induced by coculture with H. pylori, and the induction was reduced by glycochenodeoxycholic acid treatment. The bile acid in gastric juice contributes to the progression of histologic atrophy and intestinal metaplasia without inflammatory cell infiltration, followed by carcinogenesis in H. pylori-positive patients. Bile acid promotes intestinal metaplasia and gastric carcinogenesis without inflammatory cell infiltration.

Synergistic effect of IL-1β and TNF-α polymorphisms on the H. pylori-related gastric pre-malignant condition.

We investigated the effect of IL-1β and TNF-α polymorphisms, and its synergistic effect with age, gender and H. pylori status on the gastric pre-malignant condition. IL-1β-31(T>C) and -511(C>T) and TNF-α-857 (C>T) polymorphisms were genotyped in 123 cancer free subjects. Degree of histological gastritis in both antrum and corpus, and extension of endoscopic gastric atrophy were also evaluated. Significant associations were found between degrees of mononuclear cell infiltration (p=0.007) and atrophy (p=0.01) in the antrum with IL-1β-31(T>C) polymorphism, and degree of endoscopic gastric atrophy with both IL-1β-31(T>C), -511(C>T) polymorphisms (p=0.03, 0.04, respectively). When subjects were divided into the 3 groups according to the histological severity of gastric mucosal atrophy: the non-atrophic gastritis (NA) group (atrophy score=0 and metaplasia score=0), the severe atrophic gastritis (SA) group (atrophy score>=2 or metaplasia score>=2), and the mild atrophic gastritis (MA) group (all others), synergistic effect was found between numbers of IL-1β-31C, IL-1β-511T variant alleles with co-factors on the development of gastric atrophy in the antrum (gender + H. pylori + number of IL-1β-31C allele: p=0.001, age + gender + H. pylori + number of IL-1β-31C allele: p=0.0008, gender + H. pylori + number of IL-1β-511T allele: p=0.016, age + gender + H. pylori + number of IL-1β-511T allele: p=0.013), while such association was found for TNF-α-857 T allele in the antrum and all genotypes in the corpus. IL-1β-31C, IL-1β-511T variant alleles may accelerate gastric mucosal inflammation and atrophy, not only by themselves, but also through the interaction with co-factors.

Long‐term Follow‐up Helicobacter Pylori Reinfection Rate and Its Associated Factors in Korea

The reinfection rate of Helicobacter pylori has been reported to be low in developed countries but high in developing countries. The aim of this study is to evaluate the long-term reinfection rate of H. pylori and to investigate its associated risk factors in South Korea. During 2003-2010, H. pylori-positive 970 patients received standard proton pump inhibitor (PPI)-based triple eradication therapy, and follow-up H. pylori tests were performed with (13) C urea breath test or invasive tests (Giemsa histology, CLO test, and culture) 4 weeks after completion of treatment. A total of 331 patients who were maintained an H. pylori-eradicated state at 1 year after eradication were divided into two groups according to reinfection. For the evaluation of risk factors of reinfection, gender, age, smoking, alcohol, income, education, gastrointestinal symptoms, clinical diagnosis, histologic atrophic gastritis or intestinal metaplasia, and clarithromycin resistance were analyzed. The follow-up period was 18-95 months (mean: 37.1 months), and H. pylori reappeared in 36 of 331 patients (10.9%), resulting in the annual reinfection rate of 3.51% per year. Multivariate analysis showed that male gender (HR 2.28; 95% CI, 1.05-5.00, p = .037) and low monthly family income (≤5000$ vs >5000$) (HR 3.54; 95% CI, 1.08-11.67, p = .038) were associated with H. pylori reinfection. This long-term reinfection rate of H. pylori stayed rather low (3.51% per year), and male and low income determined the reinfection, factors already known to be important for H. pylori infection.

High Expression of Gastrin Receptor Protein in Injured Mucosa of Helicobacter pylori-Positive Gastritis

Gastrin is a growth factor for the gastric epithelial cells. However, it is unknown how gastric receptor (GR) expression is regulated in the gastric mucosa. We studied GR expression using a newly raised antibody and investigated the relationship between GR expression and gastritis. Gastric receptor expression in 63 human gastric mucosa was studied. Helicobacter pylori infection and histological gastritis status were evaluated in gastric biopsy samples. In gastric ulcer cases, additional biopsy specimens were taken from injured mucosa. Fasting sera were collected and serum gastrin level evaluated. MKN-28 cells were cultured at various pH conditions, and the change in GR expression was determined. Gastric receptor expression was detected in the foveolar epithelium of the gastric mucosa, and its expression was stronger in patients infected with H. pylori. In particular, higher expression was detected in regenerating injured mucosa. There was no association between gastritis score/serum gastrin level and GR expression in H. pylori-positive cases. In MKN-28 cells, GR protein expression was lower in neutral conditions than in acidic or alkaline conditions. Gastric mucosal injury with H. pylori infection destroys the pH barrier on the foveolar epithelium and may induce GR expression through pH changes.

Endoscopic diagnosis of gastric mucosal activity and inflammation

Gastritis is an important pathological state that causes gastric atrophy and cancer. The Sydney System is a well-used classification for histological evaluation for gastritis. However, there is no concordance with endoscopic findings. In the present study, we tried to establish endoscopic criteria and diagnosis for the inflammation activity of gastric mucosa. A prospective multicenter study was conducted and 24 facilities participated. Two hundred and seventy patients received endoscopic examinations and 15 endoscopic features were evaluated. Biopsy specimens were taken from five points, and evaluated by a single pathologist for mononuclear cell infiltration and polymorphonuclear cell infiltration. Sensitivity, specificity, positive predictive value, negative predictive value, area under curve of receiver operating characteristics (AUC/ROC) of each endoscopic finding to histological gastritis were calculated. There was no single endoscopic finding that was highly specific for mononuclear cell infiltration and polymorphonuclear cell infiltration. In the corpus, the combination of swelling of areae gastrica by the indigo carmine contrast method (IC method) and lack of a regular arrangement of collecting venules (RAC) in angle for mononuclear cell infiltration (0.887), and the combination of swelling of areae gastrica by the IC method and diffuse redness for polymorphonuclear cell infiltration (0.851) showed the highest AUC/ROC. In the antrum, the combination of diffuse redness and visibility of a vascular pattern for mononuclear cell infiltration (0.780), and the combination of visibility of vascular pattern and swelling of areae gastrica by the IC method for polymorphonuclear cell infiltration (0.795) showed the highest AUC/ROC. Combination of endoscopic findings can improve diagnostic accuracy, and sensitivity of examination for inflammation.

Commentary: something new to consider in the treatment of Helicobacter pylori infection? Authors' reply

Dr Nseir and colleagues from Israel reported the results from their randomised, double-blinded comparison of simvastatin and placebo added to a triple regimen for Helicobacter pylori infection. Current approaches to the treatment of H. pylori infection are inadequate. This is borne out by Nseir et al. in the power calculation for their trial, as their expected cure rate with a 7-day course of a PPI, clarithromycin and amoxicillin was 65%. It is therefore reasonable to question why physicians in Israel do not treat for longer, or use alternative regimens. Nonetheless, the decision to study simvastatin as an adjunct was innovative and has produced potentially important findings. It is not immediately obvious how simvastatin might improve the performance of a standard triple therapy combination. As the authors point out, simvastatin may have anti-inflammatory effects, independent of its lipid-lowering properties. Although statins may improve histological gastritis caused by H. pylori, it is unclear whether this is through some direct effect on the bacterium or on the inflammatory response that it induces. On ITT analysis, the eradication rates were 86% for triple therapy with simvastatin, and 69% for triple therapy with placebo. It appears that the 95% confidence interval for this 17% difference is 1.9–32.1% and that the NNT is approximately 6. Given the generally excellent safety record of simvastatin, this strategy seems reasonable. Furthermore, reported adverse events for both treatment arms in this trial were infrequent, minor and comparable. However, before advocating widespread implementation, larger, confirmatory trials will be needed and a greater understanding of the mechanisms that may be behind this potentially useful effect is required.

Sa1135 Self-Expandable Metal Stents or Surgery in Colonic Obstruction: Which is Better?

Introduction: Endoscopic findings such as erythema are frequently labelled as gastritis. Some previous studies have shown reasonable concordance between endoscopy and histology findings while others demonstrate a very poor correlation. Aims: To study the positive and negative predictive values of endoscopic diagnosis of antral gastritis and gastropathy. Method: 400 consecutive patients who underwent an OGD and had at least two antral biopsies were included in the study retrospectively. The endoscopic results were then compared to the histology reports for concordance. Only endoscopic reports of antral gastritis according to the criteria described by the Sydney classification were considered ‘positive for antral gastritis'. Histologically, those reported as acute or chronic inflammation, Helicobacter-associated gastritis, chemical or reactive gastritis, hypertrophic gastropathy, eosinophilic gastritis, lymphocytic gastritis, collagenous gastritis and granulomatous gastritis were regarded as being ‘positive for antral gastritis'. Results: In total, there were 182 male patients and 218 female patients. The median age was 50.5 ± 17.2 years (range 15 to 91). The endoscopic appearance of the antrum was positive for gastritis in 51.0% (204/400) of patients and was negative in 49.0% (196/400) of patients. The percentages of patients with presence of inflammation on histology were similar in those with or without endoscopic gastritis (65.7% vs 60.7%, p=0.303). Of the 17.3% (69/400) patients who were eventually diagnosed and treated for Helicobacter-associated gastritis on biopsy, 55.1% (38/400) had endoscopic evidence of gastritis and 44.9% (31/400) of patients did not, p=0.267. The positive and negative predictive values of endoscopy in predicting histological antral gastritis were 39.3% and 65.7% respectively. Conclusion: The predictive values of the endoscopic appearance in the diagnosis of antral gastritis is extremely poor. An endoscopically non-inflamed antrum is as likely as an inflamed antrum to harbour significant pathology such as Helicobacter pylori. Hence, it is essential to obtain antral biopsies in all patients.

Sa1133 Predictive Value of Endoscopic Diagnosis of Antral Inflamation. Correlation With Histology

Introduction: Endoscopic findings such as erythema are frequently labelled as gastritis. Some previous studies have shown reasonable concordance between endoscopy and histology findings while others demonstrate a very poor correlation. Aims: To study the positive and negative predictive values of endoscopic diagnosis of antral gastritis and gastropathy. Method: 400 consecutive patients who underwent an OGD and had at least two antral biopsies were included in the study retrospectively. The endoscopic results were then compared to the histology reports for concordance. Only endoscopic reports of antral gastritis according to the criteria described by the Sydney classification were considered ‘positive for antral gastritis'. Histologically, those reported as acute or chronic inflammation, Helicobacter-associated gastritis, chemical or reactive gastritis, hypertrophic gastropathy, eosinophilic gastritis, lymphocytic gastritis, collagenous gastritis and granulomatous gastritis were regarded as being ‘positive for antral gastritis'. Results: In total, there were 182 male patients and 218 female patients. The median age was 50.5 ± 17.2 years (range 15 to 91). The endoscopic appearance of the antrum was positive for gastritis in 51.0% (204/400) of patients and was negative in 49.0% (196/400) of patients. The percentages of patients with presence of inflammation on histology were similar in those with or without endoscopic gastritis (65.7% vs 60.7%, p=0.303). Of the 17.3% (69/400) patients who were eventually diagnosed and treated for Helicobacter-associated gastritis on biopsy, 55.1% (38/400) had endoscopic evidence of gastritis and 44.9% (31/400) of patients did not, p=0.267. The positive and negative predictive values of endoscopy in predicting histological antral gastritis were 39.3% and 65.7% respectively. Conclusion: The predictive values of the endoscopic appearance in the diagnosis of antral gastritis is extremely poor. An endoscopically non-inflamed antrum is as likely as an inflamed antrum to harbour significant pathology such as Helicobacter pylori. Hence, it is essential to obtain antral biopsies in all patients.

Expression of melanoma differentiation associated gene 5 is increased in human gastric mucosa infected with Helicobacter pylori

Helicobacter pylori infection is associated with gastroduodenal diseases. Melanoma differentiation associated gene 5 (MDA5) plays a role in antiviral host defense. We investigated the effect of H pylori infection on...

Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa

Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gastritis, peptic ulcer disease, gastric MALT lymphoma, or gastric adenocarcinoma. The bacterial and host factors that determine clinical outcome and influence the development of widely varying diseases have not been elucidated. We compared disease in Helicobacter-infected severe combined immunodeficient (SCID) mice on different genetic backgrounds with their corresponding immunocompetent partners to determine if the genetics of the host significantly impacts the innate inflammatory outcome, independent of variations in bacterial virulence factors. BALB/c SCID and C57BL/6 SCID mice developed equivalent histologic gastritis by 8 weeks of infection. Immunocompetent BALB/c mice and C57BL/6 mice developed significantly lower or higher degrees of inflammation respectively. Innate inflammation in immunodeficient mice on the C57BL/6 background remained low even in the absence of the regulatory cytokine IL-10. These results demonstrate that adaptive immunity is not required for the generation of low level inflammation in response to Helicobacter infection and that the degree of inflammation is consistent among different genetic backgrounds. Additionally, this inflammation is limited even in the absence of regulatory T cells.