Pylori Gastritis Patients Research Articles

Immune evasion by proteolytic shedding of natural killer group 2, member D ligands in Helicobacter pylori infection.

Helicobacter pylori (H. pylori) uses various strategies that attenuate mucosal immunity to ensure its persistence in the stomach. We recently found evidence that H. pylori might modulate the natural killer group 2, member 2 (NKG2D) system. The NKG2D receptor and its ligands are a major activation system of natural killer and cytotoxic T cells, which are important for mucosal immunity and tumor immunosurveillance. The NKG2D system allows recognition and elimination of infected and transformed cells, however viruses and cancers often subvert its activation. Here we aimed to identify a potential evasion of the NKG2D system in H. pylori infection. We analyzed expression of NKG2D system genes in gastric tissues of H. pylori gastritis and gastric cancer patients, and performed cell-culture based infection experiments using H. pylori isogenic mutants and epithelial and NK cell lines. In biopsies of H. pylori gastritis patients, NKG2D receptor expression was reduced while NKG2D ligands accumulated in the lamina propria, suggesting NKG2D evasion. In vitro, H. pylori induced the transcription and proteolytic shedding of NKG2D ligands in stomach epithelial cells, and these effects were associated with specific H. pylori virulence factors. The H. pylori-driven release of soluble NKG2D ligands reduced the immunogenic visibility of infected cells and attenuated the cytotoxic activity of effector immune cells, specifically the anti-tumor activity of NK cells. H. pylori manipulates the NKG2D system. This so far unrecognized strategy of immune evasion by H. pylori could potentially facilitate chronic bacterial persistence and might also promote stomach cancer development by allowing transformed cells to escape immune recognition and grow unimpeded to overt malignancy.

Association between VEGF-2578 C>A Polymorphism with Gastric Premalignant Lesion in Gastritis with Helicobacter

Introduction: Gastric cancer is one of the most common causes of cancer-related deaths worldwide. Many epidemiological studies have shown several risk factors associated with the development of gastric cancer, including gastritis. The most common cause of gastritis is H. pylori infection. In the H.pylori-infected mucosa, there was a significant increase in VEGF levels. Several SNPs are thought to be involved in the etiology of malignancy, one of which is the VEGF-2578C>A polymorphism. Methods: A cross sectional study was conducted in Medan with 59 H. Pylori gastritis patients. Endoscopic examination was performed to assess the gastric mucosa. H.pylori status was determined by examination of Urea breath Test (UBT) and Campylobacter Like Organism (CLO) test followed by histopathological studies evaluating the presence of changes to pre-malignant lesions such as chronic atrophic gastritis, intestinal metaplasia, intestinal dysplasia. Genotype analysis was carried out using Polymerase Chain Reaction (RT-PCR). Data analysis was carried out by univariate and bivariate Result: Of the 59 patients with H. pylori gastritis, 35.8% of patients showed premalignant lesions. The majority of premalignant lesions had a CC genotype (37.9%, n = 11), but there was no significant relationship between the VEGF-2578 C>A polymorphism and the incidence of gastric premalignant lesions. Conclusion: Based on this study, the VEGF -2578C>A polymorphism was not associated with gastric premalignant lesions in H. pylori gastritis patients.. Keywords: Polymorphism VEGF, VEGF -2578C>A, Premalignant lesions, H. Pylori.

HELICOBACTER PYLORI CHRONIC GASTRITIS ON PATIENTS WITH PREMALIGNANT CONDITIONS: OLGA AND OLGIM EVALUATION AND SERUM BIOMARKERS PERFORMANCE.

H. pylori chronic atrophic gastritis is a premalignant lesion, and its staging, according to OLGA and OLGIM systems aims to identify patients at increased risk of developing gastric cancer and optimize their follow-up. GastroPanel®, serum biomarkers panel including pepsinogen I (PGI), pepsinogen II (PGII), Gastrin 17 (G17) and anti- H. pylori antibodies is a noninvasive test for adenocarcinoma risk assessment in chronic H. pylori gastritis patients. Prospective study to evaluate the concordance between OLGA and OLGIM grading systems, as well as to evaluate GastroPanel´s performance in patients with premalignant lesions secondary to H. pylori chronic gastritis in Brazil. Patients with H. pylori chronic gastritis with premalignant lesions confirmed by histology were recruited from the gastrointestinal clinic of a University Hospital. All participants underwent endoscopic examination with biopsies which were reported according to updated Sydney system and premalignant lesions grading systems (OLGA and OLGIM). Blood samples were collected for biomarkers serological analysis (GastroPanel®, Biohit, Helsinki, Finland). The cut off values used to define high risk patients were those recommended by the manufacturer: PGI ≤30 µm/L and PGI/PGII ≤3. 41 patients were recruited: 28 women, 13 men, mean age 67.3 (47-89, SD: 9.6) years. By OLGA system, were obtained: OLGA 0 (n=1), OLGA I (n=7), OLGA II (n=17), OLGA III (n=9), and OLGA IV (n=7). By OLGIM system, were obtained: OLGIM 0 (n=14), OLGIM I (n=5), OLGIM II (n=10), OLGIM III (n=10), and OLGIM IV (n=2). Regarding histological staging among patients staged as low risk (OLGA/OLGIM 0, I and II) and high risk (OLGA/OLGIM III and IV) for gastric cancer development, the concordance rate found between both classifications was 85.4%. Considering high risk patients, those patients thus included in at least one of the systems the final distribution of our sample considered 24 low-risk and 17 high-risk patients for the development of gastric cancer. To determine by GastroPanel® whether the patient would be at low or high risk of developing gastric cancer, PGI showed a sensitivity, specificity and accuracy of 0.47 (95%CI: 0.26-0.69), 0.67 (95%CI: 0.47-0.82), and 0.58 (95%CI: 0.43-0.72), respectively, while PGI/PGII showed sensitivity, specificity and accuracy of 0.06 (95%CI: 0.01-0.27), 0.83 (95%CI: 0.64-0.93) and 0.51 (95%CI: 0.36-0.66), respectively. The histological classifications OLGA and OLGIM presented a substantial concordance rate among themselves. Simultaneous use of both histological classification systems increased the identification's rate of high-risk patients. Biomarker analysis was not effective to distinguish low to high risk patients in the studied population. Further studies are needed to validate its use in clinical practice in Brazil.

The Differences Level of Resistin between Positive and Negative Helicobacter pylori Gastritis and its Correlation with Nutritional Status

Background: H. pylori gastritis can be related to people with obesity and metabolic syndrome. The mechanism underlying the relationship between them is suspected to be caused by adipocytokine called resistin. Objective: to analyze the difference level of resistin between positive and negative H. pylori gastritis patients and their relationship with nutritional status.Method: This cross sectional study was done in the Gastroenterology department of General Hospital Adam Malik, Medan, from May to October 2019. Patients with gastritis diagnosed by endoscopy underwent rapid urease test (RUT), resistin, albumin, hemoglobin tests, also body mass index (BMI) and waist circumference (WC) were measured.Results: Sixty gastritis patients found by endoscopic examination, 29 (48.33%) was H. pylori positive and 31 (51.67%) was negative. No significant differences were found between BMI, WC, and albumin against H. pylori gastritis with p values 0.099, 0.055, and 0.528, respectively. Hemoglobin was found significant with a p 0.009. The mean resistin in the positive H. pylori group was 7.62 ng/ml while the negative was 3.23 ng/ml, and statistically significant (p 0.001). There was a strong positive correlation between resistin levels with BMI and WC (BMI p 0.01, r 0.577; WC p 0.001, r 0.592).Conclusion: Resistin levels in gastritis with H. pylori positive are higher than H. pylori negative, body mass index and waist circumference have a strong relationship with resistin levels in patients with positive H. pylori gastritis, hemoglobin is lower in H. pylori positive than negative gastritis.

The Comparison of Tnf α (Tumor Necrosis Factor α) Serum Levels Between Cytotoxin - Associated Gene A (Caga) Positive and Negative in Patients with Gastritis Helicobacter pylori

Background: Helicobacter pylori (H. pylori) infection is the common cause of chronic gastritis in the world that is around 80% in addition to other causes such as autoimmune diseases, drugs, idiopathic and others. The pathogenesis of H. pylori associated with virulence factors consisting of cytotoxin - associated gene A (CagA) and vacuolating cytotoxin A (Vaca). In the case of gastritis occurred acute and chronic inflammatory responses and activation cytokines that cause inflammation of mucous which TNF-α levels increased in patients gatritis H. pylori. Levels of serum TNF-α was found higher in patients infected with H. pylori with CagA positive. The purpose of this study is to investigate the comparison between TNF-α serum level in H. pylori gastritis patients with Cag A (+) and CagA (-).Method: The study was conducted with a cross-sectional design in 30 patients with dyspepsia, using PADYQ score. We performed gastroscopy, biopsy, and CLO test to prove the existence of H. pylori. Furthermore, we used PCR to assess CagA (+) and CagA (-), and ELISA method to measure TNF-α serum level.Results: From 30 subjects, 18 men (60%), 12 women (40%), and the mean age was 53.5 years, the majority of the ethnic was Bataknese (53.3%), patients with H. pylori gastritis with CagA (+) were 21 (70%) and patients with H. pylori gastritis with CagA (-) were 9 (30%). We found the mean serum levels of TNF-α was higher (3.48) in H. pylori gastritis with CagA (+) than the CagA (-) (1.29) with p value was 0.001.Conclusion: We found increased serum levels of TNF-α in patients with CagA (+) compared to Cag A (-) H. pylori gastritis.

The Characteristics of Severe Iron Deficiency Anemia in Children and Adolescents

Results: The rate of severe IDA among IDA patients was higher in female than male. Patients from age 1 to 6 and adolescents over the age of 13 outnumbered others, and the majority of adolescent patients were female. Among weight groups, low weight-for-ages (less than 3 rd percentile) was prevail (20%). There were no statistical differences between laboratory results of symptomatic patients and those of asymptomatic ones (25.4%). The common causes of severe IDA were; long-term exclusive breast feeding (13.0%), menorrhagia (10.0%), H. pylori gastritis (9.2%), upper GI bleeding (9.2%) and malnutrition (8.5%). All were treated with oral or intravenous iron replacement therapy and after 3 months, laboratory results were significantly improved. In cases of H. pylori gastritis, iron replacement therapy in conjunction with H. pylori eradication showed better efficacy in treatment. Conclusion: The importance of severe IDA should not be underestimated. Especially with female adolescents, H. pylori gastritis patients, and athletes, it is still more important

Hypovitaminosis D as Predisposing Factor for Atrophic Type A Gastritis: a Case–Control Study and Review of the Literature on the Interaction of Vitamin D with the Immune System

1,25-Dihydroxyvitamin D displays immunoregulatory and anti-inflammatory properties, and the cells involved in innate and adaptive immune response express the vitamin D receptor and can both produce and respond to this hormone. This article aims at describing the complex immune regulatory role of vitamin D and depicting whether a correlation exists between atrophic type A gastritis and hypovitaminosis. We studied 62 autoimmune gastritis (AIG) patients and compared them to 54 lymphocytic gastritis patients, 21 Helicobacter pylori gastritis patients and 212 healthy subjects. We also statistically analyzed vitamin D concentration in 36,384 outpatients referred to our clinical laboratories. 25-Hydroxyvitamin D levels, the measurable metabolite used to determine vitamin D status in plasma, were measured by a chemiluminescent method. Average level of 25-OHD in AIG subjects was 9.8 ± 5.6 ng/mL (95% confidence interval (CI) 8.4-11.2), 11.1 ± 8.4 (CI 7.5-14.7) in H. pylori gastritis patients, 22.2 ± 13.5 (CI 18.6-25.8) in nonspecific lymphocytic gastritis patients, 21.3 ± 12.2 (CI 19.7-22.9) in healthy subjects, and 21.8 ± 13.1 (CI 21.7-21.9) in the 36,384 outpatients. Vitamin D levels in AIG patients were significantly lower than in patients with nonspecific gastritis or in the general population, supporting the hypothesis that hypovitaminosis D might be a risk factor for the development of autoimmune diseases. The low vitamin D concentration in H. pylori gastritis patients might act as predisposing factor for a more severe Th1-type aggression to the stomach epithelium.

Systematic review: Heliocobacter pylori infection and impaired drug absorption

Impaired acid secretion may affect drug absorption and may be consequent to corporal Helicobacter pylori-gastritis, which may affect the absorption of orally administered drugs. To focus on the evidence of impaired drug absorption associated with H. pylori infection. Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980-April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. In all, five studies investigated impaired absorption of l-dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21-54% increase in l-dopa in Parkinson's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori-gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori-gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH.

Chronic Gastritis and Bone Mineral Density in Women

We conducted a cross-sectional study of bone mineral density in women with Helicobacter pylori gastritis or autoimmune gastritis. Eighty-five patients were enrolled: 24 patients (mean age 55.2 +/- 13.5 years) with autoimmune gastritis, 34 patients (mean age 63.7 +/- 7.3 years) with H. pylori gastritis, and 27 H. pylori-negative patients with normal gastric mucosa (mean age 62.5 +/- 7.0 years). Gastric mucosa was evaluated by histology and immunohistochemistry. Bone mineral density was measured by dual-energy X-ray absorptiometry. Autoimmune gastritis patients presented severe gastric body mucosa atrophy, based on the absence of parietal cells in 15 (62.5%) patients and the presence of only scattered parietal cells in the remaining nine (37.5%) patients. Among the H. pylori gastritis patients, 21 (62%) presented with different degrees of gastric mucosa atrophy. Bone mineral densities (mean +/- SD, g/mm(2)) were not different among patients with autoimmune gastritis and H. pylori gastritis and the controls. Our results suggest that H. pylori-associated gastritis and autoimmune gastritis would not to be risk factors for decreased bone mineral density in women.

Upregulation of CCL20 and Recruitment of CCR6+Gastric Infiltrating Lymphocytes inHelicobacter pyloriGastritis

Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, leading to chronic gastritis, peptic ulcers, and gastric cancer. There is increased T-cell infiltration at the site of infection with H. pylori. CCR6, a specific beta-chemokine receptor for CCL20 (MIP-3alpha/LARC/exodus), has recently been reported to mediate lymphocyte homeostasis and immune responses in mucosal tissue, and it may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation. In this study, we investigated the role of CCR6 and its ligand, CCL20, in inducing an inflammatory response in the gastric mucosa during H. pylori infection. Gastric infiltrating T lymphocytes were isolated from endoscopic biopsy specimens of H. pylori gastritis patients and analyzed for the expression of the CCR6 chemokine receptor. Our results demonstrated that there was significantly increased CCR6 expression in CD3(+) T cells infiltrating the gastric mucosa, and the CCR6 ligand, the CCL20 chemokine, was selectively expressed in inflamed gastric tissues. The production of CCL20 was upregulated in response to H. pylori in gastric epithelial cells when there was stimulation by the proinflammatory cytokines interleukin-1beta and tumor necrosis factor alpha. Furthermore, recombinant CCL20 induced lymphocyte chemotaxis migration in fresh gastric T cells ex vivo, indicating that the gastric T cells could migrate toward inflammatory sites via CCR6/CCL20 interaction. Our results suggest that the interaction between CCL20 and CCR6 may play a role in chemokine-mediated lymphocyte trafficking during gastric inflammation in Helicobacter infection.

Gastric Mucosa Epithelial Cell Kinetics Are Differentiated by Anatomic Site and Helicobacter Pylori Infection

Changes in epithelial cell turnover related to Helicobacter pylori infection may contribute to gastric cancer development. The response of different anatomic sites of the gastric mucosa to H. pylori is not known. We studied apoptosis and cell proliferation at the grater and lesser curvature of the antrum and corpus, the fundus, and the cardia from 9 H. pylori gastritis patients and 11 H. pylori-negative controls with normal histology. Proliferation was highest at the major curve of the antrum and lowest at the fundus, and apoptosis was highest at the cardia and lowest at the major curve of the antrum in both H. pylori gastritis and normal mucosa. Proliferation was significantly higher at all anatomic sites, while apoptosis was significantly lower only at the major and lesser curve of the corpus in H. pylori gastritis compared with normal controls. Our data suggest that gastric mucosa epithelial cell kinetics is differentiated by the anatomic site and H. pylori infection.

Serum and plasma concentration of oxidant and antioxidants in patients of Helicobacter pylori gastritis and its correlation with gastric cancer

Serum superoxide dismutase, plasma ascorbic acid and lipid peroxidation in H. pylori gastritis and gastric cancer patients were compared with values for age matched healthy subjects. Serum superoxide dismutase and serum malondialdehyde were analyzed spectrophotometrically whereas plasma ascorbic acid was determined by colorimetric method. Significant increase in serum superoxide dismutase and serum malondialdehyde and significant decrease in plasma ascorbic acid were observed in H. pylori gastritis and gastric cancer patients compared to control subjects. The concentration of serum superoxide dismutase and serum malondialdehyde was significantly higher and plasma ascorbic acid was significantly lower in gastric cancer as compared to H. pylori gastritis patients. Our results demonstrate that a correlation existed between the concentration of serum superoxide dismutase, plasma ascorbic acid and lipid peroxidation in H. pylori gastritis and gastric cancer patients.

Study of p53 immunostaining in the gastric epithelium of cagA-positive and cagA-negative Helicobacter pylori gastritis.

p53 mutations are an early event in the multistep progression of gastric carcinoma. These mutations are often present in dysplastic and intestinal metaplastic gastric epithelium. However, the presence of immunohistochemically detectable p53 protein and p53 mutations in nondysplastic/nonmetaplastic gastric mucosa is more controversial. Recent reports have suggested that immunohistochemically detectable p53 protein may be present in the gastric epithelium of Helicobacter pylori gastritis. Furthermore, because cagA-positive H. pylori is associated with greater mucosal injury but decreased apoptosis, it would be interesting to determine if this phenotype is associated with greater immunostaining of p53, as the wild-type p53 gene helps to initiate apoptosis. One hundred thirty-five patients with H. pylori-associated gastritis were immunohistochemically stained for p53 and quantified for the extent and intensity of the staining using a semiquantitative method (0, nil staining; 6, extensive and strong staining). The cagA status of the organism was determined by Western blot. Thirty-one patients (23%) showed strong p53 staining (> or = 4 of 6) in inflamed but otherwise normal gastric epithelium. In the 123 cagA-positive H. pylori gastritis patients, the average p53 staining score was 2.5 of 6. This is significantly higher than the corresponding score of 1.7 of 6 observed in the 12 patients with cagA-negative H. pylori gastritis (P = 0.04). Our results indicate that p53 protein is immunohistochemically detectable even before gastric metaplastic/dysplastic change occurs. The results also suggest that cagA-positive H. pylori might be associated with greater p53 immunohistochemical staining. This would indicate that p53 immunohistochemical staining does not reliably differentiate between gastric dysplasia and reactive inflammatory atypia. If the p53 protein detected is a consequence of mutation, this would help to explain why cagA-positive H. pylori gastritis is associated with decreased apoptosis.