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.

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 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 Gastric Polyps and Atrophic Gastritis

2021 ◽  
Vol 31 (2) ◽  
pp. 27-33
Author(s):  
I. Yu. Kolesnikova ◽  
A. S. Novikova
Keyword(s):  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Chronic Gastritis ◽  
Eradication Therapy ◽  
Chronic Atrophic Gastritis ◽  
Low Grade ◽  
Pepsinogen I ◽  
Gastric Polyps ◽  
Critical Measure ◽  
H Pylori

Aim. A study of atrophic gastritis severity and rate in patients with gastric polyps (GP).Materials and methods. The study enrolled 61 patients with hyperplastic (HGP) and 41 — with adenomatous GP (AGP). All patients had 24-h gastric pH-metry, control of the pepsinogen I, II and gastrin-17 levels, in addition to a general clinical, endoscopic, histological examination and testing for Helicobacter pylori.Results. GP patients had benign manifestations prevailed with epigastric heaviness and overflow, and a scarce history of H. pylori testing at no control of rendered eradication therapy. A symptomatic proton pump inhibitor treatment in GP was either prescribed or voluntary. Focal atrophic gastritis in endoscopy was revealed in 12 (19.7 %) HGP and 16 (39.0 %) AGP patients, diffused atrophic gastritis — in 49 (80.3 %) HGP and 25 (60.9 %) AGP patients. Low-grade chronic gastritis in histology prevailed in HGP, moderate — in AGP, and severe — in 21.9 % cases. Moderate (27.9 %) to severe (65.6 %) atrophy of gastric mucosa was registered in HGP, with 53.7 and 39.0 % respective AGP cases. Polyp dysplasia was detected in 20 % HGP and 75.6 % AGP cases. Pepsinogen I <25 µg/L at a pepsinogen I/II ratio ><3 was observed in 38 (62.3 %) HGP and 18 (43.9 %) AGP patients. Hypo- and anacidic were 65.6 % HGP and 31.7 % AGP patients. >H. pylori-positive were 52.5 % HGP and 70.7 % AGP cases.Conclusion. A largely similar aetiopathogenesis of gastric polyps and chronic atrophic gastritis warrants the H. pylori diagnosis and a more detailed patient control for chronic gastritis grading and staging, functional insufficiency of gastric mucosa and the severity of hyperplastic and dysplastic change. The H. pylori eradication, in contrast to anti-secretory therapy, allows the containment of chronic gastritis and is a critical measure in gastric cancer prevention.

scholarly journals Impact of alcohol on gastric mucosa in a population with high prevalence of Helicobacter pylori

2021 ◽  
Vol 8 (6) ◽  
pp. 764
Author(s):  
Sultan Nawahir ◽  
George Kurian ◽  
Thomas Alexander ◽  
Susy Kurian
Keyword(s):  
Gastric Mucosa ◽  
Alcohol Abuse ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Premalignant Lesions ◽  
Control Group ◽  
Chronic Alcohol ◽  
Chronic Alcohol Abuse ◽  
High Prevalence ◽  
H Pylori

Background: The purpose of the study was to see whether chronic alcohol abuse had any effect on the gastric mucosa in a population already affected by a high prevalence of Helicobacter pylori.Methods: 35 males with a history of chronic alcohol abuse were compared with 35 males who were abstinent or social drinkers. All subjects had complaints of dyspepsia. All subjects underwent endoscopy and targeted biopsies were taken from three specific sites in the stomach, namely body, antrum and incisura. Biopsies were studied to look for changes of atrophic gastritis and intestinal metaplasia. The presence or absences of H. pylori on the tissue biopsy were also recorded.Results: Atrophic gastritis were only assessable in 24 alcoholic patients and 21 non-alcoholic patients due to the inadequacy of the depth of the biopsy. AG were found to be equally distributed in both the groups. 23 (64.9%) patients in the alcoholic group and 19(54.5%) in the control group had AG (OR-1.54, p=0.47). Intestinal metaplasia was seen in 10 (28.5%) alcoholic group and 12 (34.2) in the control group (OR-0.65, p=0.45). Of the 42 subjects detected to have AG, 16 (38.1%) had IM. However, IM were always associated with AG. In addition, H. pylori were not seen to be different in the two groups. H. pylori were positive in 18 (51.4%) alcoholic and14 (40%) non-alcoholic patients (p=0.33).Conclusions: Chronic alcohol abuse doesn’t appear to have any major impact on the gastric mucosa in terms of producing premalignant lesions such as atrophic gastritis or intestinal metaplasia or enhancing the prevalence of H. pylori.

scholarly journals Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship

2021 ◽  
Vol 12 ◽  
Author(s):  
Mariagrazia Piscione ◽  
Mariangela Mazzone ◽  
Maria Carmela Di Marcantonio ◽  
Raffaella Muraro ◽  
Gabriella Mincione
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Precancerous Lesions ◽  
Eradication Therapy ◽  
Developed Countries ◽  
Gastric Carcinogenesis ◽  
Gastric Disease ◽  
Type I ◽  
H Pylori

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.

A new understanding of the H. pylori eradication mechanism

2019 ◽  
Author(s):  
Shanshan Su ◽  
Guo-qi Zheng ◽  
Ying-ying Liu ◽  
Yu-fei Liang ◽  
Hui Song ◽  
...  
Keyword(s):  
Gastric Juice ◽  
Intervention Group ◽  
Control Group ◽  
Rapid Urease Test ◽  
Mucus Layer ◽  
Culture Methods ◽  
Detection Rates ◽  
Urease Test ◽  
Gastric Lumen ◽  
H Pylori

Abstract Background: Helicobacter pylori (H. pylori) cannot usually be detected in the gastric juice and it is thought that H. pylori may be implanted under the mucus layer for long term. The mechanisms of action of proton pump inhibitor (PPI), antibiotics, and bismuth for H. pylori eradication are not entirely clear. Our study aimed to determine the role of PPI on the movement of H. pylori across the mucus layer to the gastric lumen and the mechanism of PPI, antibiotics, and bismuth on H. pylori eradication. Methods: Patients with H. pylori infection were intravenous injected with PPI (intervention group, n=31) or without PPI (control group, n=37). The presence of H. pylori in the gastric juice was evaluated by the rapid urease test (RUT), polymerase chain reaction (PCR), and culture methods. Results: The H. pylori positive detection rates were all significantly higher among patients in the intervention group than among patients in the control group by the RUT (P < 0.0001), PCR (P < 0.0001), and culturing (P = 0.0386). Conclusion: H. pylori can penetrate across the mucus layer to the gastric lumen following PPI intervention. The direct antimicrobial activity of PPI might because of diminished numbers of H. pylori due to probiotics in the gastric lumen. Antibiotics and bismuth might play a local sterilization role in the gastric lumen when H. pylori penetrate across the mucus layer.

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 The Presence of Periodontal Pathogens in Gastric Cancer

2020 ◽  
Author(s):  
Marcel A. de Leeuw ◽  
Manuel X. Duval
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Eradication Therapy ◽  
Downstream Processing ◽  
Data Sets ◽  
Periodontal Pathogens ◽  
Public Data ◽  
H Pylori ◽  
Pathogen Spectrum

BackgroundThe microbiome is thought to play a role in the development of gastric cancer (GC). Several studies have put forward putatively carcinogenic species in addition to Helicobacter pylori, but are not in perfect alignment, possibly due to variable parameters in the experiments, including downstream processing. Meta-analyses have not been published so far, so there is lack in clinical guidance beyond H. pylori eradication therapy.MethodsHere, we analysed gastric mucosa samples from nine public data sets, including GC samples. Using both unsupervised and supervised learning, we defined fine grain bacterial networks of gastric mucosa and identified species associated with tumor status of samples.ResultsWe found anatomic locations and cohort regions among the possible factors leading to the observation of study specific gastric microbiomes. Despite this variability, the periodontal species Fusobacterium nucleatum, Parvimonas micra and Peptostreptococcus stomatis were found in association with tumor status in several datasets. The three species were predicted to be in interaction by ecological network analysis and also formed the intersection of tumor associated species between four GC data sets and five colorectal cancer (CRC) data sets we reanalyzed. We formulated a probiotic composition putatively competing with the GC pathogen spectrum, from correlation analysis in a large superset of gut samples (n=17,800) from clinical- and crowd-sourced studies.ImplicationsThe overlapping bacterial pathogen spectrum between two gastrointestinal tumor types, GC and CRC, has implications for etiology, treatment and prevention. In vitro testing results reported in literature suggest H. pylori eradication treatment should be efficient against the GC pathogen spectrum, yet the existence of an upstream periodontal reservoir is of concern. To address this, we propose longer term use of the formulated probiotics composition.

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