scholarly journals Chronic gastritis and Helicobacter pylori in digestive form of Chagas' disease

1993 ◽  
Vol 35 (2) ◽  
pp. 117-121 ◽  
Author(s):  
A. J. A. Barbosa ◽  
D. M. M. Queiroz ◽  
A. M. M. F. Nogueira ◽  
M. J. A. Roquette Reis ◽  
E. N. Mendes ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chagas Disease ◽  
Chronic Gastritis ◽  
Antral Mucosa ◽  
Common Cause ◽  
Superficial Gastritis ◽  
H Pylori ◽  
Inflammatory Changes

Patients with the digestive form of Chagas'disease frequently present chronic gastritis. As the microorganism Helicobacter pylori is now accepted as the most common cause of human chronic gastritis, the present work was undertaken to verify a possible relationship between the presence of this bacterium and inflammatory changes of antral mucosa in chagasic patients. Seventeen chagasics, with megaesophagus and or megacolon were studied. Fragments from two different regions of antral mucosa were obtained by endoscopy, fixed in 4% neutral formaldehyde and embedded in paraffin. The sections were stained by haematoxylin and eosin for histology analysis, and by carbolfuchsin for H. pylori identification. H. pylori was found in 16 (94.1%) chagasic patients, all of them presenting chronic gastritis. Superficial gastritis was seen in 9 (52.9%) while atrophic gastritis was present in 8 (47.1%) patients. H. pylori was present on gastric mucosa of 8 (100%) patients with atrophic gastritis and of 8 (88.8%) patients with superficial gastritis. We concluded that the microorganism H. pylori should be considered a possible factor connected with the etiopathogenesis of chronic superficial and atrophic gastritis frequently observed in patients with the digestive form of Chagas' disease.

scholarly journals Statistical analysis of the сhronic gastritis in students

2020 ◽  
Vol 73 (2) ◽  
pp. 360-364
Author(s):  
Aleksandr V. Kharchenko ◽  
Nataliya V. Kharchenko ◽  
Petro M. Makarenko ◽  
Lyudmyla M. Sakharova ◽  
Pavlo V. Khomenko ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Statistical Analysis ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Mucous Membrane ◽  
Chronic Gastritis ◽  
Bacterial Contamination ◽  
The Body ◽  
Leukocyte Infiltration ◽  
Lesser Curvature

The aim: The aim of the study is a statistical analysis of the mucosa of the stomach affected by Helicobacter pylori in young people studying at the university. Materials and methods: The work contains the results of the study of chronic gastritis of type B in university volunteer students. The study was attended by students of 1-4 courses, aged 17 to 25 years, a total of 50 people. Among them were 28 men and 22 women. Results: Various forms of chronic gastritis were found in the mucosa of the topographic-anatomical sections of the stomach, 90% of which were associated with Helicobacter pylori (HP). In all departments there is a different amount of common forms of chronic gastritis. In the pyloric section only atrophic gastritis was detected – 31.0 ± 8.5. Atrophic gastritis was also dominant on the lesser curvature – 32.3 ± 7.8, but its forms were significantly (p <0.5) less pronounced than in the pyloric section. In the area of the body, the above variants of chronic gastritis were found in 34.3 ± 8.7 cases, and the majority were flat erosive gastritis 51.0 ± 9.3. There is a tendency to reduce the degree of bacterial contamination of the gastric mucosa from its pyloric section and the lesser curvature to the walls of the body. With a decrease in the degree of bacterial contamination of the gastric mucosa, the degree of leukocyte infiltration also decreases. Between the degree of contamination of the mucous membrane of Helicobacter pylori and the degree of leukocyte infiltration of the mucous membrane, the Pearson correlation coefficient is rxy – 0,935, the correlation is very strong, the coefficient of determination is D=rxy^2 – 0,874, the statistically significant dependence on the probability is 0.99. Conclusions: Atrophic or hyperplastic gastritis associated with HP is found in the gastric mucosa, respectively, 90% of cases. The degree of bacterial contamination correlates with the degree of leukocyte infiltration of the gastric mucosa. Atrophic or hyperplastic gastritis Helicobacter pylori-associated is a common disease of people in young and working age.

scholarly journals Association of Helicobacter pylori infection with nodular antritis and follicular gastritis

2006 ◽  
Vol 63 (3) ◽  
pp. 313-315 ◽  
Author(s):  
Ratko Tomasevic ◽  
Gradimir Golubovic ◽  
Miroslav Kiurski ◽  
Dragana Stankovic ◽  
Radoje Doder ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Case Report ◽  
Chronic Gastritis ◽  
Upper Gastrointestinal Endoscopy ◽  
Antral Mucosa ◽  
Urease Test ◽  
Sydney System ◽  
H Pylori ◽  
The Relationship ◽  
Upper Gastrointestinal

Introduction. Helicobacter pylori (H. pylori) infection is known to be the must common cause of chronic gastritis having some endoscopic and pathologic characteristies as determinated by the Sydney System for Gastritis Classification. The aim of our case report was to point out the relationship between an endoscopic finding of nodular antritis and the presence of H. pylori infection and active chronic gastritis. Case report. Our patient underwent upper gastrointestinal endoscopy for dyspeptic complaints and was diagnosed as having nodular antritis, but also underwent urease test and hystopathologic examination of antral mucosa, to determine the presence and density of H. pylori infection and the presence and severity of gastritis. After a course of anti H. pylori treatment, dyspepsia improved and new biopsy specimens obtained two months and six months afterwards revealed no pathological findings. Conclusion. The case report supported the association of H. pylori infection of lymphoid follicles with nodular gastric mucosis.

scholarly journals Tissue transglutaminase activity in human gastric mucosa according to Helicobacter pylori infection

2018 ◽  
Vol 243 (15-16) ◽  
pp. 1161-1164
Author(s):  
Maria Pina Dore ◽  
Giovanni Mario Pes ◽  
Alessandra Errigo ◽  
Alessandra Manca ◽  
Giuseppe Realdi
Keyword(s):  
Helicobacter Pylori ◽  
Animal Models ◽  
Gastric Mucosa ◽  
Natural History ◽  
Tissue Transglutaminase ◽  
Helicobacter Pylori Infection ◽  
Human Gastric Mucosa ◽  
Antral Mucosa ◽  
History Of ◽  
H Pylori

Tissue transglutaminase (t-TG) is a multifunctional protein involved in the healing of gastric erosions and ulcers in animal models. The aim of this study was to measure gastric t-TG activity in patients with dyspepsia according to Helicobacter pylori infection and cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) subtype status. Patients undergoing upper endoscopy not taking any medications were enrolled. Tissue-TG activity was determined in homogenates of antral specimens using a radiometric assay and was expressed in pmol/mg. The cagA and vacA genotypes were determined by PCR amplification using gene-specific oligoprimers. Data from 46 patients were available (17 of them were positive for H. pylori). Antral t-TG activity was significantly increased in H. pylori positive patients compared to H. pylori negative patients (6437 ± 3691 vs. 3773 ± 1530 pmol/mg; P = 0.001) according to Mann–Whitney U test. Patients with H. pylori negative gastritis had higher t-TG activity than patients with normal gastric mucosa. The specimens infected with cagA positive strains (72%) displayed greater t-TG activity than cagA negative samples (7358 ± 4318 vs. 4895 ± 1062 pmol/mg; P = 0.237). Similarly, t-TG activity was higher in H. pylori vacA s1/m1 strains vs. vacA s1/m2 (7429 vs. 5045 pmol/mg; P = 0.744), and vacA s1/m1 vs. s2/m2 (7429 vs. 4489 pmol/mg; P = 0.651) but the results were not significant. No differences were found between histology, endoscopy features and t-TG activity. These results show that t-TG activity is significantly greater in gastritis associated with H. pylori infection, suggesting that this enzyme is induced by inflammation and may have an important role in the natural history of human gastritis. Impact statement Tissue transglutaminase (t-TG) is unique among TG enzymes because of its additional role in several physiological and pathological activities, including inflammation, fibrosis, and wound healing. The presence of t-TG has previously been described in the intestine of human and animal models, yet studies on t-TG activity in human gastric mucosa are missing. Helicobacter pylori infection is the major cause of gastritis and peptic ulcers. For the first time, our results show that t-TG activity was significantly higher in antral specimens of patients with chronic active gastritis associated with H. pylori infection compared to H. pylori negative chronic gastritis and normal antral mucosa. These findings suggest that t-TG has a role in the natural history of human gastritis, which requires further investigation but may be an avenue for new therapeutic options.

scholarly journals Influence of duodenogastric reflux in the gastric mucosa histological changes of rats infected with Helicobacter pylori

2016 ◽  
Vol 43 (4) ◽  
pp. 235-242 ◽  
Author(s):  
JOSÉ CARLOS RIBEIRO DE ARAUJO ◽  
JORGE JOSÉ DE CARVALHO ◽  
HUMBERTO OLIVEIRA SERRA
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Partial Gastrectomy ◽  
Duodenogastric Reflux ◽  
Histological Changes ◽  
Positive Correlation ◽  
Male Wistar Rats ◽  
H Pylori ◽  
The One

ABSTRACT Objective: to evaluate the influence of Duodenal reflux in histological changes of the gastric mucosa of rats infected with Helicobacter pylori submitted to pyloroplasty. Methods: after two weeks of acclimation, we infected 30 male Wistar rats with Helicobacter pylori. We randomly divided them into three groups: one submitted to pyloroplasty, another to partial gastrectomy and the third, only infected, was not operated. After six months of surgery, euthanasia was carried out. Gastric fragments were studied by light microscopy to count the number of H. pylori, and to observe the histological changes (gastritis, metaplasia, dysplasia and neoplasia). We confirmed these changes by immunohistochemistry using the molecular markers PCNA and TGF-beta. Results: the animals submitted to pyloroplasty had higher percentage of colonization by H. pylori (median=58.5; gastrectomy=16.5; control=14.5). There was a positive correlation between the amount of H. pylori and the occurrence of chronic gastritis present in the antral fragments. Neoplasia occurred in 40% of rats from the group submitted to pyloroplasty. The staining with PCNA and TGF-ß confirmed the histopathological changes visualized by optical microscopy. Conclusions: the antral region was the one with the highest concentration of H. pylori, regardless of the group. There was a positive correlation between the appearance of benign disorders (chronic gastritis, metaplasia, dysplasia) and cancer in mice infected with H. pylori submitted to pyloroplasty.

scholarly journals Systemic and local immune responses againstHelicobacter pylori urease in patients with chronic gastritis: distinct IgA and IgG productive sites

Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 168-175 ◽  
Author(s):  
S Futagami ◽  
H Takahashi ◽  
Y Norose ◽  
M Kobayashi
Keyword(s):  
B Cells ◽  
Gastric Mucosa ◽  
Immune Responses ◽  
Atrophic Gastritis ◽  
Gastric Juice ◽  
Chronic Gastritis ◽  
Specific Antibody ◽  
Histopathological Analysis ◽  
Grade Ii ◽  
H Pylori

Background—Helicobacter pylori urease is a major target for immune responses among various bacterial components in H pyloriinfected patients.Aims—To analyse the relation between systemic and local humoral immune responses toH pylori urease and grades of chronic gastritis.Patients—Seventy five patients with chronic gastritis associated with H pyloriinfection were classified into three groups (grade I, superficial gastritis; II, atrophic gastritis, quiescent; or III, atrophic gastritis, active).Methods—Anti-H pylori urease specific antibodies in the serum, gastric juice, and biopsy specimens were determined by ELISA or western blotting analysis. The sites for H pylori urease and its specific antibody producing B lymphocytes were confirmed by immunohistochemical analysis.Results—In the sera of patients with grade I gastritis, weak IgG but relatively strong IgA responses toH pylori urease were observed; dominant strong IgG responses were detected in grade II gastritis. In grade III gastritis, significant IgG and IgA responses were obtained. A similar pattern of IgA and IgG responses was detected in gastric juice and tissue. H pylori urease specific, antibody producing B cells were not found in the gastric mucosa of patients with grade I gastritis despite the presence of such B cells in the duodenal bulb. Specific B cells were observed in the gastric mucosa of patients with grade II and III gastritis with atrophy.Conclusions—PurifiedH pylori urease, together with localisation of its specific antibody producing B cells, are useful for serological testing and histopathological analysis for determining the stage of chronic gastritis and studying the pathogenesis ofH pylori infection.

scholarly journals State of lipid peroxidation and antioxidant defense in chronic gastritis associated with Helicobacter pylori-infection in middle-aged males

2020 ◽  
Vol 10 (4) ◽  
pp. 741-746
Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov ◽  
N. M. Titova
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Chronic Gastritis ◽  
Antioxidant Defense ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Metabolism Enzymes ◽  
H Pylori

Helicobacter pylori is the most widespread human pathogen, with prevalence reaching up to 20—40% and 80— 90% of adult infection in developed and developing countries, respectively. Many authors consider this infection as a major factor in the development of gastric cancer. In case of H. pylori infection, free homogeneous oxidation is augmented, that elevates the blood amount of POL products. Hyperproduction of reactive oxygen species stimulates free radical POL, accompanied by membrane destruction, damage to proteins, lipids, and DNA. Thus, the destruction of the intracellular and cell outer membranes occurs resulting in cell death. In diseases associated with H. pylori infection, there is a dysregulation of the lipid peroxidation system — antioxidant defense contributing to inconsistency in the regeneration phases triggering disease progression. The aim of our work was to study indicators of POL (diene conjugates, malonic dialdehyde) and antioxidant protection (AOP) (superoxide dismutase enzymes, catalase) in chronic gastritis and chronic atrophic gastritis associated with H. pylori infection. In patients with CG associated with H. pylori as well as CAG and CAG associated with H. pylori they were featured with increased amount of primary (↑DC) and end TBA-active products of lipid peroxidation (↑MDA), whereas activity of superoxide dismutase was decreased, additionally highlighted with reduced catalase activity (↑CAT) in CAG and CAG associated with H. pylori. H. pylori just triggers the mechanisms of ROS generation in host cells. The energy of redox reactions is used by the microorganism to carry out its physiological functions and serves as a factor in its own pathogenicity, the ROS generated in such reactions can have a damaging effect on the structure of gastric mucosa. In addition, examining H. pylori genome has shown that it bears the genes encoding oxidative metabolism enzymes, such as SOD, catalase, nitroreductase, flavodoxin oxidoreductase. Long-term persistence of H. pylori in the gastric mucosa paralleled with its increased biomass accounts for it being the main source of ROS production able to augment lipid peroxidation and cause damage to the membrane structures and DNA of gastric epithelium cells.

scholarly journals Review of Research on Routes of Helicobacter pylori Infection

2015 ◽  
Vol 4 (2) ◽  
pp. 45-49
Author(s):  
Hang Li
Keyword(s):  
Helicobacter Pylori ◽  
Drinking Water ◽  
Peptic Ulcer ◽  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Gastric Adenocarcinoma ◽  
Precancerous Lesions ◽  
Natural Environments ◽  
H Pylori

AbstractIn recent years, many scholars conducted in-depth research onHelicobacter pyloriand identified it as an important pathogen of chronic gastritis and peptic ulcer.H. pylorialso causes also and contributes to precancerous lesions (atrophic gastritis and intestinal metaplasia) and is closely related to occurrence and development of gastric adenocarcinoma and gastric mucosa-associated lymphoma. This study summarizes biological characteristics, epidemic status, and infection route ofH. pyloriand reviews research on roles of natural environments, especially drinking water, during infection.

scholarly journals Association of Helicobacter pylori vacA polymorphisms with the risk of gastric precancerous lesions in a Moroccan population

2021 ◽  
Vol 15 (08) ◽  
pp. 1124-1132
Author(s):  
Mohamed Reda Jouimyi ◽  
Ghizlane Bounder ◽  
Imane Essaidi ◽  
Hasna Boura ◽  
Wafaa Badre ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
High Risk ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Precancerous Lesions ◽  
Gastric Lesions ◽  
D Region ◽  
Reliable Marker ◽  
H Pylori

Introduction: Helicobacter pylori infection is the major risk factor of atrophic gastritis and intestinal metaplasia. The vacA gene is one of the most virulence factors of H. pylori and genetic diversity in its s, m, i, and d regions is associated with gastric lesions severity. This study aimed to investigate the association of vacA s, m, i, and d regions with the risk of atrophic gastritis and intestinal metaplasia in a Casablanca population. Methodology: A total of 210 patients suffering from gastric lesions (chronic gastritis, atrophic gastritis, and intestinal metaplasia) were enrolled. The type of lesion was diagnosed by histological examination. Detection of H. pylori infection and genotyping of vacA regions were carried out by PCR. Results: The prevalence of H. pylori was 95%. The most common vacA genotypes were s2 (51.5%), m2 (77%), i2 (60.5%), and d2 (58.5%). VacA s1, m1, and i1 genotypes were associated with a high risk of intestinal metaplasia, while the vacA d1 genotype increases the risk of atrophic gastritis and intestinal metaplasia. The most common vacA combination was s2/m2/i2/d2 (52%), and it was more detected in chronic gastritis. The moderate virulent vacA combination (s1/m2/i1/d1) increases the risk of atrophic gastritis, while the most virulent vacA combination (s1/m1/i1/d1) increases the risk of intestinal metaplasia. Conclusions: Genotyping of vacA d region might be a reliable marker for the identification of vacA virulent strains that represent a high risk of developing precancerous lesions (atrophic gastritis and intestinal metaplasia).

scholarly journals H. pylori eradication therapy: impact of gastric mucosa atrophy on transport of amoxicillin to H. pylori colonization area

2021 ◽  
Vol 13 (2) ◽  
pp. 57-66
Author(s):  
Anastasiya O. Sablina ◽  
Oleg A. Sablin ◽  
Julia V. Andreeva ◽  
Gennadii G. Rodionov ◽  
I. I. Shantyr ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Gastric Juice ◽  
Eradication Therapy ◽  
Oral Drug ◽  
Antral Mucosa ◽  
Drug Infusion ◽  
Gastric Lumen ◽  
H Pylori ◽  
Systemic Transport

AIM: The aim was to assess systemic transport of amoxicillin, the most common antibiotic in H. pylori eradication regimens to the gastric in atrophic gastritis. MATERIALS AND METHODS: Systemic transport of amoxicillin to the gastric lumen of rats was evaluated in washes from the gastric mucosa in the model of atrophic gastritis after intravenous drug infusion. Transport of amoxicillin from bloodstream to the gastric lumen was also assessed in patients with atrophic and non-atrophic gastritis in aspirated via nasogastric probe gastric juice after oral drug administration. Amoxicillin concentration was measured in samples using liquid chromatography-mass spectrometry. RESULTS: In rats with induced atrophic gastritis, hyperemia and acute erosions of the gastric mucosa, as well as microscopic signs of non-active chronic body gastritis and non-active antral atrophic gastritis were found. Amoxicillin concentration in washes from the gastric mucosa was significantly (p 0.01) higher in rats of experimental group than in control group at all time points (30, 60, 120, 240 min after drug infusion). The lowest mean amoxicillin concentration in gastric juice was observed in patients with antral atrophy (p 0.01). The maximum amoxicillin concentration in gastric secretion was found at the 180th min of aspiration in patients with atrophy of gastric mucosa, while in patients of the group of comparison it was found at 30-120th min of aspiration. CONCLUSIONS: Acute gastric mucosa erosions enhance amoxicillin delivery to gastric lumen in rats. Atrophy of antral mucosa more than in the corpus is characterized by decreased amoxicillin transfer from systemic bloodstream to gastric lumen in patients after oral amoxicillin intake. The gastric mucosa atrophy should be taken into consideration while predicting the efficacy of H. pylori eradication therapy in patients with chronic gastritis.

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