Pylori Density Research Articles

Impact of Helicobacter pylori on the development of vitamin B12 deficiency in the absence of gastric atrophy.

Cobalamin (vitamin B12) deficiency is associated with Helicobacter pylori infection. This study examined how serum vitamin B12 levels relate to gastric mucosa H. pylori density and histology, and to hematological findings in patients with minimal or no gastric atrophy. A second aim was to confirm that H. pylori eradication therapy increases serum B12. Biopsies of the gastric mucosa from a population of dyspeptic patients were graded for level of chronic inflammation, neutrophil activity, atrophy, and H. pylori density. A total of 145 H. pylori-infected patients with minimal or no atrophy were included in the study. Serum cobalamin level, hemoglobin level, and mean corpuscular volume were measured in the 145 patients before eradication therapy, and in 65 of the subjects after treatment. The hematologic findings before and after eradication therapy and correlations between serum vitamin B12 level and histologic parameters, hematologic findings, and patient age were statistically analyzed. There was no significant correlation between serum cobalamin level and patient age. Before treatment all the histopathological scores were inversely correlated with serum vitamin B12 level (p <.01) on univariate analysis. Only H. pylori density was significantly associated with B12 level on multivariate analysis. Serum hemoglobin and cobalamin levels were significantly increased after treatment, regardless of H. pylori eradication status (p <.001). The findings provide strong evidence that H. pylori infection is associated with cobalamin deficiency, and show that this is true even in patients with non-ulcer dyspepsia and minimal or no gastric atrophy.

Polaprezinc Attenuates Helicobacter pylori‐Associated Gastritis in Mongolian Gerbils

The ammonia-monochloramine system plays an important role in Helicobacter pylori-associated gastric mucosal injury. Polaprezinc, a new antiulcer agent, has a scavenging action against monochloramine. The aim of the experiment was to investigate the inhibitory effects of polaprezinc on the H. pylori-induced gastritis in Mongolian gerbils. Mongolian gerbils fasting for 24 hours were orally given culture broth containing 2-4 x 10(8) colony-forming units of H. pylori ATCC 43054 per milliliter. From 4 hours after inoculation until the end of the experiment, gerbils were given chow pellets with or without 0.02% polaprezinc. All gerbils were killed 12 weeks later. The grades of H. pylori density and histologic features of gastritis were evaluated in accordance with the Updated Sydney System. The scavenging effect of polaprezinc on monochloramine was investigated spectrophotometrically. Polaprezinc had little or no influence on the H. pylori density in both pyloric and fundic mucosae. However, it significantly attenuated the development of polymorphonuclear neutrophil activity, mononuclear infiltration, and surface epithelial erosion in both pyloric and fundic mucosae compared with those of the control group. H. pylori inoculation significantly increased the heights of both pyloric and fundic mucosae (mainly due to the increased height of foveolar hyperplasia), but polaprezinc inhibited the increase of mucosal thickness in both pyloric and fundic mucasae. No intestinal metaplasia was detected in this study. Spectrophotometric examination revealed that polaprezinc scavenged monochloramine. Polaprezinc inhibited the development of H. pylori-induced gastritis through its scavenging action against monochloramine.

Importance of Helicobacter pylori oipA in clinical presentation, gastric inflammation, and mucosal interleukin 8 production

Background & Aims: Disease-associated virulence factors of Helicobacter pylori may not be independent of one another. The aim was to determine which H. pylori virulence factor(s) was the most important predictor of severity of gastric inflammation or clinical outcome. Methods:cag Pathogenicity island (PAI), vacA babA2, and iceA status were determined by polymerase chain reaction (PCR). oipA functionality was based on switch status determined by PCR-based sequencing. A backward stepwise multiple regression analysis was performed to determine which factor(s) was the most discriminating for clinical outcome as well as the relationship to mucosal histology (H. pylori density, neutrophil infiltration, intestinal metaplasia, and gastric atrophy) and mucosal interleukin 8 (IL-8) production. Results:H. pylori were obtained from 247 patients (86 with gastritis, 86 with duodenal ulcer, and 75 with gastric carcinoma). Although oipA status was closely linked to specific cag PAI, vacA, and babA2 genotypes, only oipA status remained in the final model to discriminate duodenal ulcer from gastritis (adjusted odds ratio [OR] = 5 and 95% confidence interval [CI] = 2.1–11.9). Among the factors, only a functional oipA was significantly associated with high H. pylori density, severe neutrophil infiltration, and high mucosal IL-8 levels (P < 0.001). oipA status had no relationship to gastric atrophic changes. Conclusions:oipA functional status was related to clinical presentation, H. pylori density, and gastric inflammation. cag PAI, babA2, or vacA status appear important only as surrogate markers for a functional oipA gene.GASTROENTEROLOGY 2002;123:414-424

In situ correlation of cytokine secretion and apoptosis in Helicobacter pylori-associated gastritis.

Tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) are important for the pathogenesis of Helicobacter pylori-associated gastritis and peptic ulcer disease. Gastric biopsies from H. pylori-positive and -negative patients were used to examine the in situ correlation of TNF-alpha and IFN-gamma with epithelial cell apoptosis, bacterial load, and histological parameters of gastritis. From the same patients, we isolated H. pylori-specific T cell lines and clones and examined their ex vivo release of proinflammatory cytokines. We found a highly significant correlation of TNF-alpha and IFN-gamma production with activity and grade of gastritis (P < 0.01), H. pylori density (P = 0.01), epithelial cell apoptosis (P < 0.001), and Fas/Fas-ligand expression (P < 0.001). T cell lines and clones were all TCR-alphabeta(+) and showed T helper 1 functional phenotype. With the use of serial histological sections, this study showed for the first time the in situ correlation of TNF-alpha and IFN-gamma with epithelial cell apoptosis, bacterial load, and histological severity of disease and emphasizes the role of these cytokines in the pathophysiology of H. pylori-associated disease.

Prolonged use of proton pump inhibitors, CagA status, and the outcome of Helicobacter pylori gastritis.

To assess whether prolonged use of proton pump inhibitors (PPIs) in patients infected with Helicobacter pylori has adverse effects on gastritis. We studied 34 H. pylori-positive individuals with reflux esophagitis, Barrett esophagus, or nonulcer dyspepsia. Half of them were on maintenance treatment with PPIs (mean, 8 years) and half were not.H. pylori and CagA status were tested serologically. Gastric biopsies were classified histopathologically by the updated Sydney classification. Proton pump inhibitors in H. pylori gastritis are associated with significantly less antral inflammation and lower H. pylori density, regardless of CagA status. There was a tendency toward more antral atrophy in patients with the CagA strain who were undergoing maintenance treatment with PPIs (p = 0.08), but there was an opposite tendency in CagA-negative individuals (p = 0.08). Intestinal metaplasia was seen more frequently in CagA-positive, treated individuals (p = 0.028). These findings support the hypothesis that CagA status is important in the progression to atrophy and that maintenance treatment with PPIs accelerate this progression, while reducing inflammatory infiltration.

Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with Helicobacter pylori infection.

The aim of this study was to assess whether the endoscopic finding of antral nodularity and serum IgG antibodies to CagA are associated with higher grades of gastric inflammation. The comprehensive data of two previously published trials were reanalysed. One hundred and fifty-three children (median age 9.5 years) who underwent gastroscopy were included. Biopsy specimens from the antrum and corpus were taken to assess Helicobacter pylori status, gastritis score and lymphoid follicles. During endoscopy, antral nodularity was noted. Serum samples were assayed for IgG antibodies to CagA. The presence of antral nodularity (nod+) and positive CagA serology (CagA+) were each found in 32 of the 77 (41.5%) children who had evidence of H. pylori infection. Cross tabulation showed that 20 children (26%) were nod+/CagA+, 12 (15.5%) nod+/CagA-, 12 (15.5%) nod-/CagA+ and 33 (43%) nod-/CagA-. Gastritis score was significantly lower in nod-/CagA- children than in nod+/CagA- (p =.004), nod-/CagA+ (p =.002) and nod+/CagA+ (p <.001), both in the antrum and corpus. Completely normal gastric histology was only found in the nod-/CagA- subgroup of H. pylori-infected children (eight of 33, 24%). Regression analysis showed that antral nodularity and positive CagA serology were related to severe gastric inflammation independently of each other and age. Separate analysis showed that inflammation (p <.001), activity (p <.001) and H. pylori density (p =.002) scores were significantly lower in nod-/CagA- children compared with nod+/CagA+ children. The number of lymphoid follicles in the gastric mucosa was related to antral nodularity (p =.003) and positive CagA serology (p =.043), independently of each other. Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with H. pylori infection. The lack of both findings in the same child reflects low-grade or no gastritis.

NSAID gastric ulceration: predictive value of gastric pH, mucosal density of polymorphonuclear leukocytes, or levels of IL-8 or nitrite.

NSAID use and Helicobacter pylori both cause damage to the gastric mucosa and can cause peptic ulcers. Our aim was to test the relationship between gastric mucosal polymorphonuclear leukocyte (PMN) infiltration and the severity of NSAID-induced gastric injury. H. pylori density, mucosal interleukin-8 (IL-8), and nitrite levels were assessed after receiving placebo and again after receiving 1000 mg of naproxen daily for three days. Histology was graded using a visual analog scale (0-5). IL-8 levels were assayed by ELISA and nitrite levels by Griess reaction. Eleven healthy volunteers with H. pylori infection entered. All had normal-appearing gastric mucosa after placebo. Postnaproxen gastric damage included three with none, one with mild, three with moderate, two with severe, and three were very severe mucosal injury (including one with an ulcer >5 mm). There was an inverse correlation between endoscopic score and the pH of the gastric juice post-therapy (R = -0.77, P = 0.004). There was no significant change in histologic or biochemical parameters from pretreatment levels. And none of the parameters (eg, PMN density) predicted endoscopic outcome. In conclusion, there was no relation between mucosal PMN density and endoscopic mucosa injury. PMN infiltration, while not predictive, may be a surrogate for an H. pylori infection-related increased risk of NSAID ulcers.

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.

Colonisation density and topographic localisation of Helicobacter pylori do not depend on the cagA status.

To explore the correlation between the cagA status of Helicobacter pylori and the density and topographic localisation of H pylori. Gastric antral biopsy specimens were taken from 716 consecutive patients, including 293 H pylori positive patients (124 men, 169 women; mean age, 52.6 years; range, 12-87). A serum sample was taken for determination of IgG anti-CagA antibodies (sensitivity of 94.4% and specificity of 92.5%). The density of H pylori was assessed semiquantitatively (grades I-IV) in biopsy specimens stained with the modified Giemsa stain. Topographic localisation was classified as follows: score A, H pylori closely attached to the mucosa; score B, H pylori attached to the mucosa and in the mucus; and score C, H pylori solely in the mucus. CagA antibodies were present in 154 (52.5%) of the patients. There was no significant difference in colonisation density and cagA status: grade I, 23 (14%); grade II, 78 (50.6%); grade III, 42 (27.5%); and grade IV, 11 (7.2%) in the cagA(+) strains and 29 (21.2%), 57 (40.8%), 38 (27%), and 15 (11%), respectively, in the cagA(-) strains. There was no difference in topographic localisation between cagA(+) and cagA(-)H pylori. Mean anti-CagA titres were 0.84, 0.84, 0.89, and 0.73 in patients with grades I-IV bacterial density, respectively. Antibody titres do not correlate with H pylori density and there is no difference in density between cagA(+) and cagA(-)H pylori strains. In addition there is no difference in topographic localisation between cagA(+) and cagA(-) H pylori strains.

Correlation between Helicobacter pylori infection, gastric inflammation and serum homocysteine concentration.

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. 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. 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 micromol/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. The postulated link between H. pylori infection and ischemic heart disease, if it actually exists, is unlikely to be mediated through hyperhomocysteinemia.

Study Of The Relation Between Helicobacter Pylori Infection And Gastric Interleukin (8) In Patients With Chronic Liver Disease

Helicobacter pylori (H pylori) is a gram negative spirally shaped bacterium. It is known to be the most common important cause of gastritis, peptic ulcer, non ulcer dyspepsia and gastric carcinoma. The frequency and importance of gastric mucosal lesion in patients with chronic liver disease (CLD) have been increasingly recognized in recent years. IL-8 a potent leukocyte chemo–attractant cytokine produced by H pylori. It promotes polymorphnuclear leucocytes (PMNs) and mononuclear cells (MNCs) accumulation in gastric mucosa.This work aimed to clarify the relation between H pylori and IL-8 production in various chronic liver disease (CLD) lesions. Eighty patients were included in this study, 50 with CLD and 30 dyspeptic patients without CLD. Gastric mucosal biopsies were examined histopathologically for H pylori, cellular infiltration and associated pathology, together with culture of H pylori and assessment of IL-8 level in gastric tissue supernatant. 30/50 (60%) CLD patients,10/15 (66.6%) patients with non gastric dyspepsia, and 14/15 (93.3%) patients with gastric dyspepsia were positive for H pylori. There was no relationship between the prevalence of H pylori and the aetiology of CLD. No significant difference was observed in CLD patients’ group as regard to H pylori and Child grading, degree of varices, gastric or liver histopathology. Statistical difference in H pylori prevalence between patients with CLD and those with gastric dyspepsia was significant. IL-8 showed significant increase in H pylori positive vs H pylori negative patients. Positive correlation was found between H pylori density and tissue IL-8 and cellular infiltration. In conclusion the liver status does not play a role in the prevalence of H pylori infection, further studies to investigate the relation between virulent H pylori and IL-8 are needed.

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non—Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.

Do some patients with Helicobacter pylori infection benefit from an extension to 2 weeks of a proton pump inhibitor–based triple eradication therapy?

OBJECTIVES: Seven-day proton pump inhibitor (PPI)–based triple therapies are the first-line anti- Helicobacter pylori regimens; to date, however, there is still no agreement concerning all the predictors of H. pylori cure under these regimens. The aim of this prospective study was to evaluate whether patients with certain pretreatment characteristics may benefit from an extension from 1 to 2 wk of treatment with lansoprazole, amoxycillin, and clarithromycin. METHODS: A total of 142 patients with H. pylori infection ascertained by means of gastric histopathology and 13C urea breath test (UBT) participated in this study. In all patients H. pylori density was determined at histology both on antral and corpus biopsies, and H. pylori culture with antibiotic susceptibility testing; IgG anti– H. pylori titers were also determined before therapy. Patients were randomized to receive 1-wk versus 2-wk of treatment with lansoprazole (30 mg b.i.d.), clarithromycin (500 mg b.i.d.), and amoxycillin (1 g b.i.d.). The association between eradication and potential predictors was analyzed by means of unconditional logistic regression models and stratified according to the duration of treatment. A stepwise regression analysis was performed to identify variables discriminated between subjects, using eradication status as the dependent variable. RESULTS: The overall eradication rates for 1- and 2-wk treatments were 74.6% and 85.9% (intention-to-treat analysis) and 81.5% and 89.1% (per-protocol analysis), respectively ( p = NS). Multivariate discriminant analysis selected as the variables independently related to eradication cigarette smoking (OR = 3.98), δ of 13C-UBT higher than 35 (OR = 9.21) and IgG anti- H. pylori titer ≥93 (OR = 0.24) for the whole series of subjects. Stratified analysis according to the duration of therapy selected H. pylori density as the only predictor of eradication in the group treated for 1 wk (OR = 8.11). In contrast, no significant predictors were found in the group treated for 2 wk. CONCLUSIONS: Patients with a high intragastric bacterial load, as detected by histology (grade 3) or 13C-UBT (δ > 35) may benefit from an extension to 2 wk of triple therapy with lansoprazole, amoxycillin, and clarithromycin.

Helicobacter pylori Genotypes May Determine Gastric Histopathology

The outcome of Helicobacter pylori infection has been associated with specific virulence-associated bacterial genotypes. The present study aimed to investigate the gastric histopathology in Portuguese and Colombian patients infected with H. pylori and to assess its relationship with bacterial virulence-associated vacA, cagA, and iceA genotypes. A total of 370 patients from Portugal (n = 192) and Colombia (n = 178) were studied. Corpus and antrum biopsy specimens were collected from each individual. Histopathological features were recorded and graded according to the updated Sydney system. H. pylori vacA, cagA, and iceA genes were directly genotyped in the gastric biopsy specimens by polymerase chain reaction and reverse hybridization. Despite the significant differences between the Portuguese and Colombian patient groups, highly similar results were observed with respect to the relation between H. pylori genotypes and histopathology. H. pylori vacA s1, vacA m1, cagA+ genotypes were significantly associated with a higher H. pylori density, higher degrees of lymphocytic and neutrophilic infiltrates, atrophy, the type of intestinal metaplasia, and presence of epithelial damage. The iceA1 genotype was only associated with epithelial damage in Portuguese patients. These findings show that distinct H. pylori genotypes are strongly associated with histopathological findings in the stomach, confirming their relevance for the development of H. pylori-associated gastric pathology.

The Prevalence of Helicobacter pylori Infection and the Pattern of Gastritis in Barrett’s Esophagus

Background/Aim: Acid output is related to the gastritis pattern in Helicobacter pylori infection. The hypothesis to be tested is that gastritis in patients with Barrett’s esophagus, defined as columnar epithelia lined lower esophagus (CELLO) with intestinal metaplasia (IM), is antrum predominant. Patients and Methods: Patients undergoing esophagogastroduodenoscopy were investigated for CELLO. The gastritis parameters H. pylori density, activity, and chronicity were graded in biopsy specimens of antrum and corpus. IM was assessed in biopsies from CELLO patients. In a prospective part, 19 patients with CELLO with IM were compared with 38 age-matched control patient with dyspepsia. Results: Of 200 patients with CELLO, 85% had a short segment (<3 cm), 15% a segment of ≧3 cm. IM was present in 36% of cases with a short CELLO and in 84% of patients with a long segment. The H. pylori prevalence was 50%, independent of the length of CELLO or the presence of IM. The gastritis phenotype was minimally antrum predominant. The antrum/corpus distribution was not related to the length of CELLO or the presence of IM and not different from controls. The activity in corpus and antrum was lower in patients with CELLO with IM as compared with patients with CELLO without IM or controls. Conclusions: A high proportion of patients with CELLO are H. pylori infected. The pattern of H. pylori gastritis is characterized by a pangastritis with low activity which is not likely to predispose to an increase in acid output after eradication.

INTERACTION BETWEEN H. PYLORI AND NSAIDS: PREDICTIVE VALUE OF DENSITY OF POLYMORPHONUCLEAR LEUKOCYTES, MUCOSAL AND GASTRIC JUICE NUTRITE LEVELS

BackgroundAlthough nonsteroidal anti‐inflammatory drugs (NSAIDs) use and H. pylori are the most common causes of peptic ulcers, it remains unclear whether there is an interaction between them.AimTo test whether there was a relationship between polymorphonuclear leukocyte (PMN) infiltration of the gastric mucosa and severity of NSAID‐induced gastric mucosal injury.MethodsH. pylori density, mucosal interleukin‐8 (IL‐8) levels as well as gastric mucosal and juice nitrite levels were assessed in normal volunteers before and after receiving 600 mg of naproxen (twice a day for 3 days). Histology was graded using a visual analogue scale from 0 (absent/normal) to 5 (maximal intensity). IL‐8 levels were assayed by ELISA and nitrite levels by Griess reaction. Endoscopic damage was graded from none to severe (large erosions or ulcers).ResultsEleven healthy volunteers with active H. pylori infection and normal appearing gastric mucosa were entered. The post‐NSAID endoscopic scores were 0 = 3, mild = 1 moderate = 4, and severe = 3. None of the pretreatment histologic or biochemical parameters (e.g., PMN density, mucosal Il‐8 or nitrite levels) predicted endoscopic outcome nor was there a significant changes from pretreatment levels. There was an inverse correlation between endoscopic score and the pH of the gastric juice post‐therapy (R‐0.669, p=0.02).ConclusionsThe hypothesis that the intensity of PMN infiltration in the mucosa correlated with risk of ulcer development was not confirmed. PMN infiltration is likely a surrogate for an H. pylori infection‐related increased risk of NSAID ulcers.

Argyrophilic nucleolar organizer regions in Helicobacter pylori -associated gastric lesionsNote

Three hundred and fifty biopsies from patients undergoing upper gastrointestinal endoscopy were studied for histopathological changes, H. pylori infection and argyrophilic nucleolar organizer region (AgNOR) counts. Histopathological examination revealed normal gastric mucosa in 10 (2.85%), gastritis in 254 (72.56%), intestinal metaplasia in 12 (4.0%), dysplasia in 13 (3.7%) and adenocarcinoma in 61 (17.4%). The mean (SD) AgNOR count was 1.66 (0.20) in normal, 2.43 (0.64) in gastritis, 3.09 (0.52) in intestinal metaplasia, 4.17 (0.31) in dysplasia, and 6.57 (0.98) in carcinoma. A statistically significant difference was observed between the AgNOR count of normal gastric mucosa and gastritis (p<0.001), gastritis and dysplasia (p<0.001), and dysplasia and adenocarcinoma (p<0.001). A statistically significant increase in mean AgNOR count was found with increase in H. pylori density in gastric biopsies (p<0.001) with gastritis. No significant difference was observed between mean AgNOR count of intestinal and diffuse type carcinomas. The AgNOR count in gastric biopsies with adenocarcinoma and H. pylori infection was 7.03 (0.85) as compared to 6.89 (0.73) in gastric biopsies with evidence of adenocarcinoma but without H. pylori infection. The difference was not statistically significant. The findings support the role of H. pylori as a promoting agent in gastric carcinogenesis by stimulating gastric epithelial cell proliferation at the stage of chronic inflammation, thereby making the cells more susceptible to endogenous or exogenous carcinogenic agents.

Effect of antibiotic therapy on acid secretion H. pylori density, inflammation and mucosal interleukin-I (IL-1B) levels in corpus gastritis

Effect of antibiotic therapy on acid secretion H. pylori density, inflammation and mucosal interleukin-I (IL-1B) levels in corpus gastritis

H. pylori density and gastritis activity are higher in patients with duodenal ulcerated lesions and lower for patients with gastric ulcerated lesions in comparison with patients with non-ulcer dyspepsia

H. pylori density and gastritis activity are higher in patients with duodenal ulcerated lesions and lower for patients with gastric ulcerated lesions in comparison with patients with non-ulcer dyspepsia

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.