Helicobacter Pylori Density Research Articles

The Relation between Helicobacter Pylori Density and Gastritis Severity

<em>Helicobacter Pylori</em> affects many individuals in developing countries. Inflammation caused by <em>Helicobacter Pylori</em> differs depending on the virulence factors, density and host tissue response of the bacteria. This study is intended to investigate the relation between density of <em>Helicobacter Pylori</em> colonization in gastric mucosa in biopsy specimens and gastric mucosal inflammation severity.

Expression of Alpha Methylacyl CoA Racemase (AMACR) in Gastric Adenocarcinoma and Its Correlation with Helicobacter pylori Infection.

Gastric cancer develops in a multistep progression and is determined by genetic and environmental factors. Over-expression of Alpha Methylacyl CoA Racemase (AMACR) is useful in diagnosis of prostate cancer. There is plenty of genetic alteration that occurs in gastric adenocarcinoma. The present study was planned to determine if AMACR can be used as a diagnostic marker in gastric adenocarcinoma similar to prostate cancer. To study the expression of AMACR in gastric adenocarcinoma and correlate its expression with density of Helicobacter pylori. This cross-sectional, prospective study was conducted from August 2013-2015. Fifty gastric cancer biopsies were taken. Adjacent biopsy from normal/reactive mucosa was also taken from 21 cases. Samples were stained with H&E for morphological details, Loeffler's methylene blue for Helicobacter pylori and immunohistochemistry (IHC) was done to check for the expression of AMACR proteins. Statistical analysis was done using chi square test, Spearman's correlation coefficient and Fisher's exact test. The p-value ≤ 0.05 was taken as critical level of significance. Overexpression of AMACR was observed in 88.89% of intestinal type and 78.05% of diffuse type adenocarcinoma. AMACR expression was significantly less in adjacent reactive/dysplastic mucosa. Helicobacter pylori were seen in 8/9 (88.89%) and 35/41(85.36%) cases of intestinal adenocarcinoma and diffuse adenocarcinoma respectively. When grades of Helicobacter pylori were compared with the positivity of AMACR, no significant association and correlation was found. The expression of AMACR in neoplastic tissue was significantly higher as compared to adjacent dysplastic, reactive or normal tissue. Thus, IHC for AMACR can be used for differentiating the cases of reactive atypia from early neoplastic lesions similar to its role in prostatic tissue. Helicobacter pylori does not affect the expression of AMACR in neoplastic gastric lesions.

The association between Helicobacter pylori gastritis and lymphoid aggregates, lymphoid follicles and intestinal metaplasia in gastric mucosa of children.

The aim of the study was to determine the topographic prevalence of lymphoid follicles, lymphoid aggregates, gastric glandular atrophy and intestinal metaplasia among children with chronic abdominal pain. The association between these lesions and age, type of gastritis and Helicobacter pylori density was also assessed. A total of 358 patients (mean age: 10, 18 ± 3, 26 years; male : female ratio: 0.92) with chronic abdominal pain who had upper gastrointestinal endoscopy were included in the study. The endoscopic and histopathological findings were documented. The prevalence of lymphoid follicles, lymphoid aggregates, atrophy and intestinal metaplasia according to the type of gastritis and their relation with H. pylori density were determined. H. pylori was detected in 214 (59.8%) patients. H. pylori- positive patients were found to be significantly older than H. pylori-negative patients (P < 0.01). The endoscopy revealed that the most common finding observed was antral nodularity in H. pylori-positive patients and normal mucosal appearance in H. pylori-negative patients. Panmucosal gastritis both in the corpus and antrum and the prevalence of lymphoid follicles and lymphoid aggregates were more frequent in the H. pylori-positive group (P < 0.01). None of the patients had atrophy, whereas 11 patients had intestinal metaplasia. Although positive correlation was obtained between lymphoid lesions and H. pylori density, no significant relation was established between intestinal metaplasia, lymphoid lesions and H. pylori density. Lymphoid follicles and lymphoid aggregates in gastric mucosa involving both antrum and corpus significantly correlated with H. pylori infection, H. pylori density and type of gastritis in children.

Intra- and Interobserver Reproducibility of Grading ofHelicobacter pyloriGastritis According to the Updated Sydney System

Aims. To study the intra- and interobserver reproducibility of Sydney System amongst pathologists in Cameroon as Sydney System gradation has not gained enough confidence in African pathologists. Methods. We performed a descriptive study including 100 patients who benefited from gastric biopsy by endoscopy. These biopsy specimens were stained with hematein and eosin and modified Giemsa, and read independently using the same microscope by two pathologists with four years experience and no experience with the updated Sydney System. Gastritis was graded according to the updated Sydney System. Levels of intra- and interobserver reproducibility were assessed using the unweighted kappa coefficient. Results. The intraobserver reproducibility of gradation of Helicobacter pylori density, activity, chronic inflammation, atrophy, and intestinal metaplasia showed respective values of kappa: 0.63, 0.34, 0.61, 0.48, and 0.82 for one observer against 0.42, 0.005, 0.41, 0.31, and 0.72 for the other. Interobserver reproducibility kappa values were, respectively, 0.41, 0.18, 0.57, 0.58, and 0.82. Conclusion. Results are encouraging but experience in the updated Sydney System should be improved. The later should be introduced as a means to grade and classify gastritis in Cameroon and African countries.

Mide Biyopsilerinde Sydney Sınıflamasına Göre Histolojik Değerlendirme ve Yaş Gruplarına Göre Kronik Gastritde Mukozal Histolojik Bulguların Karşılaştırılması

The aim of this study is to evaluate the materials of gastric biopsies in cases diagnosed as chronic gastritis according to the Sydney system and to compare the parameters according to age groups. The Sydney system of gastritis has five main histological features of changes in gastric mucosa graded (chronic inflammation, neutrophil activity, glandular atrophy, intestinal metaplasia and Helicobacter pylori density) In our study, we evaluated 63 patients under 31 years, 177 patients between the ages of 31-60 and 187 patients over 61 years, who were diagnosed as having chronic gastritis by endoscopic biopsy. In 31-60 age group, the localization of Helicobacter pylori was often the antrum. In contrast, in the under 31 years of age group, Helicobacter pylori infection were found to be in the form of the distribution pangastrit. Acute inflammation in the under31 years group was found to be significantly higher than other age groups. In over 61years group, high incidence of atrophy was found. In our study, we detected the rate in atrophy and intestinal metaplasia with Helicobacter pylori is independently increased with age.

Expression of CD25highRegulatory T Cells and PD-1 in Gastric Infiltrating CD4+T Lymphocytes in Patients with Helicobacter pylori Infection

We observed by flow cytometry that the frequency of both gastric infiltrating Tregs and PD-1-positive CD4 T cells is correlated with the density of Helicobacter pylori, suggesting that cellular immunity against this pathogen is inhibited.

The significance of E266K polymorphism in the NOD1 gene on Helicobacter Pylori infection: an effective force on pathogenesis?

The severity of Helicobacter pylori-related diseases varies greatly among infected individuals and seems to be influenced by both host and bacterial factors. Infection with a cytotoxin-associated gene pathogenicity island (Cag PAI)-positive H. Pylori strain causes a higher grade of gastric mucosal inflammation than an infection caused by a negative strain. Furthermore, such an infection is associated with severe atrophic gastritis and gastric adenocarcinoma. NOD1 protein is a cytosolic pattern recognition receptor that responds to peptidoglycan delivered by H. Pylori cag pathogenicity island. The aim of this study is to investigate whether the presence of the NOD1 G796A polymorphism has any influence on the clinical outcomes of Cag PAI-positive H. Pylori. Both Helicobacter pylori and CagA-positive 150 patients were considered eligible for the study. In this selected group, NOD1 G796A was detected by using polymerase chain reaction/restriction fragment length polymorphism. Activity and severity of gastritis, atrophy, intestinal metaplasia and Helicobacter pylori density were assessed in body and antral biopsies. Also post-therapy controls for predicting Helicobacter pylori persistence were done. The correlations of these parameters were determined by SPSS 15 packet program for statistical analysis. Of the 150 CagA-positive patients, 57 had (38%) heterozygote (GA), and 29 had (19.3%) homozygote (AA) mutant variants of NOD1. The other 64 patients had (42.7%) wild-type DNA(GG). NOD1 796A allele carriers had higher risk for antral atrophy (OR = 13.35, 95% CI = 5.12-34.82) and antral intestinal metaplasia (OR = 2.71, 95% CI = 1.26-5.80). Carriage of the single nucleotide polymorphism of NOD1 G796A proved to be a significant risk factor for the Helicobacter pylori therapy failure (OR = 4.62, 95% CI = 1.67-12.79). Our results suggest that carriage of the NOD1 G796A mutation increases the susceptibility of gastric epithelial cells for intestinal metaplasia and atrophy when infected by CagA-positive Helicobacter pylori strains. Additionally, it increases the ratio of eradication failure.

Relationship among Oxidative DNA Damage, Gastric Mucosal Density and the Relevance of cagA, vacA and iceA Genotypes of Helicobacter pylori

The aim of this study was to evaluate the relationship among oxidative DNA damage, density of Helicobacter pylori and the relevance of cagA, vacA and iceA genotypes of H. pylori. Gastric epithelial cells were isolated from 24 uninfected patients, 42 H. pylori infected patients with gastritis, and 61 patients with gastric cancer. Oxidative DNA damage was analyzed by the Comet assay, the density of H. pylori was measured by real-time polymerase chain reaction (PCR), and allelic variants of cagA, vacA and iceA were identified using the PCR. Infected patients by Helicobacter pylori cagA(+), vacAs1 m1 and iceA1 genotype showed higher levels of oxidative DNA damage than infected patients with H. pylori cagA(-), vacAs2 m2 and iceA2 genotypes and uninfected patients. Density of H. pylori did not influence oxidative DNA damage. Our results indicate that H. pylori genotype is more relevant than density for oxidative DNA damage.

The roles of Helicobacter pylori and pattern of gastritis in the pathogenesis of reflux esophagitis

Comparing the infection rates and density of Helicobacter pylori (H. pylori) and the patterns of gastritis in reflux esophagitis (RE) and non-erosive reflux disease (NERD) patients to investigate the role of H. pylori in the pathogenesis of RE. Two hundred and twenty-three out-patients with typical gastroesophageal reflux symptoms who consecutively visited the hospital underwent ambulatory 24-hour pH monitoring and gastroscopy, and biopsy of the gastric mucosa. RE and NERD were diagnosed based on the presentation of endoscopy. Gastritis was divided into four different patterns: chronic non-atrophic antritis (CNAA); chronic non-atrophic pan-gastritis (CNAG); chronic atrophic antritis (CAA); and chronic atrophic pan-gastritis (CAG). H. pylori infection was evaluated by Warthin-Starry staining. DeMeester score > or = 15 was considered as pathological acid reflux. Sixty-two patients (27.8%) were found to have RE, 161 (72.2%) were found to have NERD. Totally, 67 patients had H. pylori infection (30.0%). There was no significant difference in H. pylori infection rate between the RE and NERD groups (25.8% vs. 31.5%, P > 0.05). 45 of the 223 patients were diagnosed as with CNAA (20.2%), 88 (39.5%) with CNAG, 65 (29.2%) with CAA, and 25 (11.2%) with CAG. The CAG rates in the RE and NERD groups were 6.5% and 13.0% respectively (P > 0.05). There were no differences in abnormal pH monitoring rate and DeMeester score among the different patterns of gastritis. In the sixty-seven H. pylori-positive GERD patients, the 24 h pH monitoring positive rate of the moderate-severe H. pylori colonization density group was 46.4%, significantly higher than that of the mild H. pylori colonization density group (73.5%, P < 0.05); and the mean intra-gastric pH value during 24 hours of the moderate-severe H. pylori colonization density group was 2.3 +/- 0.8, significantly higher than that of the mild H. pylori colonization density group (2.0 +/- 1.1, P < 0.05). H. pylori infection is associated with the pattern of gastritis, but shows no relationship to the incidence of RE. High density of H. pylori colonization in gastric corpus may reduce the esophageal acid exposure. Diffuse atrophic gastritis may protect the patients from RE.

The role of mast cells and eosinophils in chronic gastritis

The role of mast cells and eosinophils in influencing the pathology of chronic gastritis remains unclear. We attempted to study the relationship between endoscopy and the mast cell and eosinophil infiltrate. We also studied the role of gene polymorphisms, Helicobacter pylori density and the CagA antibody status in influencing the mast cell and eosinophil infiltrate. One hundred and twenty consecutive patients were studied. Endoscopic evaluation was done and 3 antral biopsies were taken from each patient and were assessed for eosinophilic and mast cell infiltration, H. pylori density and the density of the other inflammatory cells as per the revised Sydney system. Cytokine gene polymorphisms (IL-1beta, IL-1RA and TNF-alpha) were done on the DNA extracted from the peripheral blood by PCR-RFLP. ELISA was done on the patients' serum for the anti-CagA antibody titres. Nodularity is strongly associated with the presence and density of eosinophils on biopsy (P < 0.05). Eosinophil density is strongly associated with the density of H. pylori, neutrophils, lymphocytes, plasma cells, atrophy, ulceration, foveolitis and lymphoid follicles. The mast cell density is not associated with any of the other histopathological variables. Gene polymorphisms and the CagA antibody titres have no relationship to the mast cell and eosinophil density. Eighty-one patients showed positive anti-CagA antibody titres but there was no association with the eosinophilic or the mast cell infiltrate. It is likely that eosinophilic infiltration is influenced by the H. pylori density but the CagA protein has no role to play in influencing the grade of the eosinophilic infiltrate in the Indian context. Cytokine gene proinflammatory polymorphisms have no role to play in influencing the eosinophilic or the mast cell response. It is likely that other mediators are involved in the inflammatory cell responses.

Mucin Phenotype and Background Mucosa of Intramucosal Differentiated-Type Adenocarcinoma of the Stomach

Objectives: Gastric carcinomas have been divided into differentiated (intestinal) and undifferentiated (diffuse) types. Recently, classification studies based on mucin expression have revealed that some differentiated-type carcinomas are of a gastric phenotype. In this study, we investigated the clinicopathological features of differentiated-type adenocarcinomas and evaluated the background mucosa of the stomach based on mucin expression by the tumors. Methods: Seventy-six intramucosal differentiated-type adenocarcinomas of the stomach were evaluated macroscopically and histologically. The mucin expression of tumor cells was examined by immunohistochemical staining with monoclonal antibodies against human gastric mucin (45M1), class III mucin (HIK1083), small intestinal mucinous antigen (SIMA-4D3), and MUC2 (Ccp58). Tumors were classified by phenotype as gastric (G-type), intestinal (I-type), mixed (M-type), or null (N-type). Not only the clinicopathological features but also the background mucosa of the stomach of G-type and I-type carcinomas were compared histologically and serologically. Results: Seventeen tumors (22.4%) were classified as G-type, 31 (40.8%) as I-type, 22 (28.9%) as M-type, and 6 (7.9%) as N-type. The frequencies of elevated type tumors and papillary adenocarcinomas and the ratio of moderately/well-differentiated adenocarcinomas were higher in G-type than in I-type carcinomas. The scores for glandular atrophy and intestinal metaplasia were higher and the scores for chronic inflammation, polymorphonuclear neutrophil activity, and the density of Helicobacter pylori were lower in G-type than in I-type tumors. The serum level of pepsinogen I and the pepsinogen I/II ratio were significantly lower in G-type than in I-type tumors. Conclusions: G-type carcinoma is the predominant phenotype of papillary adenocarcinoma. The background mucosa of G-type carcinoma is associated with glandular atrophy and intestinal metaplasia, whereas that of I-type carcinoma is associated with active and chronic inflammation induced by H. pylori infection.

'Cardiac-type' (mucinous) mucosa and carditis are both associated with Helicobacter pylori-related gastritis.

Adenocarcinoma of the gastro-oesophageal junction is rapidly increasing in incidence and there is much interest in precursor lesions. The aetiology of inflammation of the gastric cardia (carditis) and the concept of the cardia as a native zone of mucinous gastric glands are disputed. To investigate the relationship between the type of cardiac mucosa and carditis with various histological and clinical parameters. Ninety-eight sets of gastric biopsies (cardia, corpus, incisura and antrum) were obtained prospectively in young patients (median age 40 years) who presented to the outpatient clinic with symptoms of gastro-oesophageal reflux (n = 25) or other upper gastrointestinal symptoms. Patients with neoplasia or Barrett's oesophagus were excluded. The presence (n = 19) or absence of oesophagitis at endoscopy was recorded. The degree of inflammation, Helicobacter pylori density, intestinal metaplasia and atrophy were scored according to the Sydney classification and the type of cardiac mucosa (oxyntic or mucinous) was noted. We found that carditis and mucinous-type cardiac mucosa were strongly associated with H. pylori-related gastritis (P = 0.00019 and P = 0.006, respectively) but not with clinical or endoscopic gastro-oesophageal reflux. Mucinous mucosa in the cardia was only seen in 17% of biopsies. H. pylori-related gastritis is associated with mucinous-type cardiac mucosa as well as with carditis. The former strongly points to expansion of mucinous cardiac mucosa in H. pylori gastritis. This probably represents metaplasia of oxyntic to mucinous mucosa and raises the possibility of a role in carcinogenesis of the gastro-oesophageal junction.

Density of Helicobacter pylori (Hp) organisms does not affect eradication rates in peptic ulcer disease (PUD) and non-peptic ulcer disease (NPUD)

Density of Helicobacter pylori (Hp) organisms does not affect eradication rates in peptic ulcer disease (PUD) and non-peptic ulcer disease (NPUD)

Does serum nitrite concentration reflect gastric carcinogenesis in Japanese Helicobacter pylori-infected patients?

This study investigated whether the serum nitrite concentration reflects Helicobacter pylori-induced inflammation and atrophic changes of gastric mucosa. Ninety-seven patients underwent biopsy of both antrum and fundus. Samples were analyzed by the rapid urease test and histopathological examination according to the updated Sydney system. Fasting serum samples from each subject were analyzed for specific IgG Helicobacter pylori antibodies, pepsinogen I and II concentrations, and NO2-/NO3- content. Eleven patients had H. pylori eradicated with proton pump-based triple therapy. There was a strong positive correlation between the Helicobacter pylori density in the gastric mucosa and the serum nitrite concentration, but a negative correlation existed between the atrophic grade of the gastric mucosa and both serum nitrite concentration and Helicobacter pylori density in the gastric mucosa. Serum nitrite concentrations decreased significantly after successful eradication of Helicobacter pylori. Therefore, serum nitrite concentration may be a useful marker for oxidative DNA damage and apoptosis associated with Helicobacter pylori infection.

Prevalence of Helicobacter pylori resistance to antibiotics in Northeast Italy: a multicentre study

Aims. To evaluate prevalence of primary Helicobacter pylori antibiotic resistances in Northeast Italy and to identify risk factors associated with this resistance. Materials and methods. A total of 248 patients undergoing upper gastrointestinal endoscopy were enrolled from 19 Endoscopy Units over a 6-month period. From each patient, 4 gastric biopsies were taken for histology and 2 were sent to the Central Referral Microbiological Laboratory for culture and determination of antibiotic activity against Helicobacter pylori by means of E-test. Strains were considered resistant when minimum inhibitory concentration was >8 μg/ml for metronidazole and > 1 μg/ml for clarithromycin. No cut-off value was predefined for amoxycillin. Results. Culture of Helicobacter pylori was successfully performed in 167 patients. Primary resistance to metronidazole, clarithromycin or amoxycillin was 14.9%, 1.8% and 0.%, respectively. Patients infected with Helicobacter pylori strains resistant to antibiotics were more frequently females than males (70.3% vs 41.4%), had a significantly lower coffee intake (66.6% vs 86.6%) and lower body mass index (23.7±2.6 vs 25.3±3.6) than patients with susceptible Helicobacter pylori strains. Age, smoking, alcohol use, family history of Helicobacter pylori infection, concomitant diseases and treatments, endoscopic diagnoses, Helicobacter pylori density and histological activity of chronic gastritis were not associated with antibiotic resistance. Multivariate analysis confirmed that female gender (odds ratio = 2.74, 95% confidence interval = 1.03–7.27) was the only significant risk factor associated with antibiotic resistance. Conclusions. In this population, primary Helicobacter pylori resistance to metronidazole was higher than resistance to clarithromycin, and female gender was significantly associated with this resistance. The low prevalence of resistance to metronidazole, clarithromycin and amoxycillin identified in this geographical area suggests that proton pump inhibitor-based triple regimens including these antibiotics may still be used as first line therapies against Helicobacter pylori infection.

Helicobacter pylori cag pathogenicity island is associated with enhanced interleukin-8 expression in human gastric mucosa.

In vitro studies showed that Helicobacter pylori strains carrying the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8. To evaluate the assessment of cag pathogenicity island and the expression of Interleukin-8 in the gastric mucosa of Helicobacter pylori-infected patients and correlate these data with the activity of gastritis and Helicobacter pylori density. cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dyspepsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene transcription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter pylori density were also investigated. cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia (53.8%] and in 13/13 duodenal ulcer patients (100%), (p<0.05). Interleukin-8 mRNA and protein expression in epithelial and inflammatory cells was higher in cag+ than in cag- patients (p<0.005). Gastritis activity significantly correlated with cag (p<0.05) and Interleukin-8 expression (p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression (p<0.0051. The present study demonstrates that in Helicobacter pylori-infected human gastric mucosa, cag+ infection is associated with enhanced Interleukin-8 expression, higher levels of active gastritis and bacterial density, and presence of duodenal ulcer.

A topographic study of Helicobacter pylori density, distribution and associated gastritis.

The topographic distribution and density of Helicobacter pylori and associated gastritis in the stomach were studied in order to determine which biopsy sites are likely to provide the maximum yield so as to reduce the fallacious results due to sampling error. Fifty patients with upper gastrointestinal symptoms were studied. Eleven gastric biopsies from predetermined sites were obtained and subjected to ultra-rapid urease test, imprint cytology and histology. Haematoxylin and eosin stain was used for defining gastritis and other associated histopathological details. Loeffler's methylene blue stain was used to confirm the presence of H. pylori in imprint smears and histological sections. All 50 patients had H. pylori infection and evidence of chronic gastritis at one or more of the 11 biopsy sites. Maximum and minimum percentage positivity were observed at A3 (antral lesser curvature) and B4 (corpus greater curvature), respectively. Various sites in decreasing order of percentage positivity were A3 > A2 > A1 > A4 > B3 > B1 > A5 > B6 > B5 > B2 > B4. Among the biopsies obtained from the corpus, B3 (corpus lesser curvature) was the site with maximum positivity. A3 and B4 had a statistically significant difference in percentage positivity (P < 0.0001) for H. pylori and gastritis. The maximum and minimum density scores of H. pylori and gastritis were found in A3 and the B4, respectively. A3 had a significantly higher (P < 0.0001) mean density score than any other site in the stomach. The difference in the grading of H. pylori between A3 and B3 (sites of maximum positivity in antrum and corpus) was statistically significant (P < 0.0001). A statistically significant (P < 0.001) positive correlation between increasing grades of H. pylori and gastritis was observed at the site of maximum density. Eighty per cent of the patients had antral predominant gastritis and in 82%, H. pylori was predominantly observed in antral biopsies. It is concluded that two biopsies taken from A3 are sufficient for confirmation of presence of H. pylori and associated gastritis for initiation of treatment. However, additional biopsies from B3 will help in deciding the topographic pattern of gastritis.

Quantitative result of 13C-Urea breath test does not correlate with Helicobacter pylori density in the stomach by assessing histopathology and grade of phenol red staining

'Significant difference using Mann·Whitney U. All values displayed for 1M and non-1M medians 24 hour acid clearance for the two groups was examined. Results for percentage total acid exposure time (At), total number of reflux episodes (El)' total acid clearance time (ACTl).percentage erect acid exposure time (Ae ) , erect reflux episodes (Ee) , percentage supine acid exposure time (As)and supine reflux episodes (E,) were compared for the 1M and NIM groups using the Mann-Whitney U test. The median acid exposure of the 1M group of patients was shown to be significantly higher than the non-1M group (5.2% vs 2.8%). This was most clearly displayed in the supine period where both the number of reflux episodes (2 vs I) and the acid exposure (1.4% vs 0.2%) were increased with respect to the non-1M group. Overall, the 1M group showed a significant delay in their median oesophageal acid clearance time (2.9 min vs 2.1 min). Oesophageal manometry provides important evidence of the ability of patients to effectively clear refluxate. Therefore, in addition to providing valuable pre-surgical information, manometry assist in therapeutic management. Patients with 1M should be advised to incline the upper body during rest and be provided with prolonged pharmacological acid suppression at night.

Quantitation of Helicobacter pylori in the stomach using quantitative polymerase chain reaction assays.

The density of Helicobacter pylori is thought to correlate with the degree of inflammation and thus indirectly with the outcome of the infection. Rapid quantitative assays of H. pylori in gastric or duodenal mucosa are lacking. The aim was to develop quantitative assays using the polymerase chain reaction to assess the quantity of H. pylori in the gastric mucosa. Competitive PCR was based on coamplification of a segment of the ureC sequence and an internal control using a single set of primers. PCR products were quantified colorimetrically by an enzyme-linked immunosorbent assay and compared with known quantities of the internal control standard added to the PCR reaction. The highly sensitive, noncompetitive PCR assay does not use coamplification and measures the amplified DNA sequence using a flash-type luminescent tag and a specific probe. The mouse infected model using H. pylori strain SS-1 was used to develop the assays. Quantification of H. pylori using either the competitive or noncompetitive PCR was reliable, highly sensitive and specific. The ability to rapidly quantitate H. pylori from gastric mucosa should be useful to investigate the role of H. pylori density and infection outcome, as well as to monitor the effectiveness of antibiotic treatment or vaccines against H. pylori.

Relation between clinical presentation,Helicobacter pylori density, interleukin 1β and 8 production, and cagA status

BACKGROUNDIt is not known whethercagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.AIMSTo investigate the relation between presentation, H pylori density, interleukin 1β...