scholarly journals REGULARITY OF CHANGES IN THE LEVEL OF ACIDITY, HELICOBACTER INFECTION AND CLINICAL MANIFESTATIONS IN THE FORM OF HEARTBURN IN PATIENTS WITH CHRONIC NON-ATROPHIC GASTRITIS BEFORE AND AFTER TREATMENT WITHOUT USE OF PROTON PUMP INHIBITORS

2021 ◽  
Vol 19 (4) ◽  
Author(s):  
A.A. Avramenko
Keyword(s):  
Gastric Mucosa ◽  
Atrophic Gastritis ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Clinical Manifestations ◽  
Average Level ◽  
Comparative Characteristic ◽  
Urease Test ◽  
Before And After ◽  
H Pylori

The aim of the work – to study the regularity of changes in the level of acidity, H.pylori infection and the clinical manifestation of heartburn in patients with chronic nonatrophic gastritis before and after treatment that did not include proton pump inhibitors.Material and methods. We have analyzed the results of a comprehensive examinationof 38 patients with chronic non-atrophic gastritis, suffering from heartburn, before andafter treatment that did not include proton pump inhibitors. Comprehensive examinationbefore treatment included a step-by-step pH-metry, esophagogastroduodenoscopy,double testing for Helicobacter pylori infection (urease test and microscopy of the stainedsmears-prints) using mucosal biopsy specimens from 4 topographic zones of the stomach;histological examination of the gastric mucosa, material for which was taken from thesame areas, and HELIC test. After the treatment, pH-meter control and HELIС test wereperformed.Results. When carrying out a comparative characteristic of the obtained data, ithasbeen found that the average level of acidity after the treatment increased from moderateminimal hypoacidity to pronounced absolute hyperacidity, while the average level ofcontamination of the gastric mucosa by H. pylori infection, tracked by the level of theHELIC test, decreased from 16.4 ± 0.12 mm to 2.3 ± 0.12 mm, and the "heartburn"symptom disappeared in 100% of cases.Conclusions. In the formation of the “heartburn”symptom in patients with chronicnon-atrophic gastritis, the leading factor is the level of ammonia produced by H. pyloriinfection.

scholarly journals CHARACTERISTICS OF GASTRIC MUCOSA INJURY IN PATIENTS WITH NSAID-INDUCED GASTROPATHY AND CONCOMITANT ISCHEMIC HEART DISEASE, AND WAYS TO CORRECT THIS CONDITION

2020 ◽  
Vol 20 (2) ◽  
pp. 70-75
Author(s):  
V.V. Parkhomenko ◽  
І.М. Skrypnyk ◽  
І.І. Starchenko ◽  
O.F. Gopko
Keyword(s):  
Heart Disease ◽  
Gastric Mucosa ◽  
Ischemic Heart Disease ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Morphological Changes ◽  
Ischemic Heart ◽  
Mucosal Barrier ◽  
Nsaid Gastropathy ◽  
H Pylori

The non-steroidal anti-inflammatory drugs (NSAIDs) in general clinical practice can provoke the development of NSAID-induced gastropathy, which can be complicated by bleeding. The aim of this article was to evaluate the effect of eupatilin on histological changes of the gastric mucosa in patients with NSAID-induced gastropathy and concomitant ischemic heart disease depending on the association with Helicobacter pylori. The study included 125 patients with NSAID-gastropathy and concomitant stable ischemic heart disease I-II functional class. Patients were divided into two groups: I (n=82) included individuals with NSAID-gastropathy, which was not associated with H. pylori, while II (n=43) included individuals with H. pylori-induced gastropathy. Depending on the prescribed treatment complexes, patients were subdivided as follows: I-A (n=44) included patients, who took proton pump inhibitors in standard doses and II-A group (n=23) included patients, who received antihelicobacter therapy according to Maastricht V (2016) guidelines. Patients of groups I-B (n=38) and II-B (n=20) were additionally prescribed 60 mg of eupatilin (1 tablet) 3 times a day for 28 days. The upper endoscopy with the gastric mucosa biopsy, followed by histological examination was done at the beginning of treatment and in 45±2 days. The severity of gastric mucosa erosive and ulcerative injury was assessed endoscopically using a modified Lanzascore scale; morphological changes were evaluated by a semi-quantitative method on a visual-analogue scale. H. pylori is an independent and significant factor determining the severity of endoscopic and morphological changes in NSAID-gastropathy patients with concomitant ischemic heart disease. Acid-suppressive and antihelicobacter therapy can reduce the intensity of the structural injury of the gastric mucosa, but the identified changes substantiate the feasibility of long-term proton pump inhibitors prescribed to the patients with NSAID-gastropathy. Prescribing eupatilin against the background of basic therapy can significantly reduce the severity of erosive-ulcerative gastric mucosa injury assessed by Lanzascore scale while histomorphological parameters by reducing the activity of neutrophilic inflammation, protective effect on mucosal barrier resistance and microcirculatory condition.

scholarly journals DIAGNOSTIC ACCURACY OF GASTROPANEL® FOR ATROPHIC GASTRITIS IN BRAZILIAN SUBJECTS AND THE EFFECT OF PROTON PUMP INHIBITORS

2020 ◽  
Vol 57 (2) ◽  
pp. 154-160
Author(s):  
Rejane MATTAR ◽  
Sergio Barbosa MARQUES ◽  
Igor Braga RIBEIRO ◽  
Thiago Arantes de Carvalho VISCONTI ◽  
Mateus FUNARI ◽  
...  
Keyword(s):  
Diagnostic Accuracy ◽  
Atrophic Gastritis ◽  
Likelihood Ratio ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Positive Likelihood Ratio ◽  
Negative Likelihood Ratio ◽  
High Sensitivity ◽  
H Pylori ◽  
Ig G

ABSTRACT BACKGROUND: It has been proposed that the combination of gastrin-17 (G-17), pepsinogens I and II (PGI and PGII), and anti-Helicobacter pylori (H. pylori) antibodies (GastroPanel®, BIOHIT HealthCare, Helsinki, Finland) could serve as biomarkers of atrophic gastritis. OBJECTIVE: This study aimed to ensure the diagnostic accuracy of GastroPanel® and evaluate the effect of proton pump inhibitors (PPIs) on these biomarkers. METHODS: Dyspeptic patients who underwent gastrointestinal endoscopy were enrolled in the present study. Histological findings, which were the gold standard to stratify groups, were as follows: no atrophy (controls); antrum atrophy; corpus atrophy; multifocal atrophy; and neoplasia. G-17, PGI, PGII, and anti-H. pylori immunoglobulin (Ig)G antibodies were assayed using commercially available kits. The ratio of PGI/PGII was calculated. RESULTS: Among 308 patients, 159 (51.6%) were PPI users. The overall prevalence of atrophy was 43.8% (n=135). Ninety-two (29.9%) patients were H. pylori positive according to anti-H. pylori IgG levels. G-17 levels were not low in those with antrum atrophy but were high in those with corpus and multifocal atrophies. PGI levels were significantly lower in those with corpus and multifocal atrophies. The sensitivity of PGI <30 µg/L to detect corpus atrophy was 50% (95% CI 27.8-72.1%), with a specificity of 93.2% (95% CI 84.3-97.5%), a positive likelihood ratio of 7.4 (95% CI 2.9-19.2), and a negative likelihood ratio of 0.5 (95% CI 0.3-0.8). A small number of subjects (n=6) exhibited moderate to intense atrophy (4%), among whom 66.7% exhibited decreased PGI levels. PPI significantly increased the levels of G-17 and PGI, except in those with corpus and multifocal atrophies, in whom PGI levels were not increased by PPIs. CONCLUSION: GastroPanel® (Gastrin-17, PGI, and PGI/PGII ratio) did not demonstrate high sensitivity for detecting gastric atrophy.

scholarly journals Gastrin: From physiology to gastrointestinal malignancies

Function ◽  
2021 ◽  
Author(s):  
Suzann Duan ◽  
Karen Rico ◽  
Juanita L Merchant
Keyword(s):  
Gene Regulation ◽  
Gastric Mucosa ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Peptide Hormone ◽  
Cell Types ◽  
Neuroendocrine Neoplasms ◽  
Gastrointestinal Malignancies ◽  
Distinct Cell ◽  
H Pylori

Abstract Abetted by widespread usage of acid-suppressing proton pump inhibitors, the mitogenic actions of the peptide hormone gastrin are being revisited as a recurring theme in various gastrointestinal malignancies. While pathological gastrin levels are intricately linked to hyperplasia of enterochromaffin-like cells leading to carcinoid development, the signaling effects exerted by gastrin on distinct cell types of the gastric mucosa are more nuanced. Indeed, mounting evidence suggests dichotomous roles for gastrin in both promoting and suppressing tumorigenesis. Here we review the major upstream mediators of gastrin gene regulation, including inflammation secondary to H. pylori infection and the use of proton pump inhibitors. We further explore the molecular biology of gastrin in gastrointestinal malignancies, with particular emphasis on the regulation of gastrin in neuroendocrine neoplasms. Finally, we highlight tissue-specific transcriptional targets as an avenue for targetable therapeutics.

scholarly journals Different dose of new generation proton pump inhibitors for the treatment of Helicobacter pylori infection: A meta-analysis

2021 ◽  
Vol 35 ◽  
pp. 205873842110303
Author(s):  
Wenwen Gao ◽  
Xiang Zhang ◽  
Yanhui Yin ◽  
Shuwen Yu ◽  
Lu Wang
Keyword(s):  
Helicobacter Pylori ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Eradication Rate ◽  
Standard Dose ◽  
Statistical Significance ◽  
High Dose ◽  
Clarithromycin Resistance ◽  
H Pylori ◽  
New Generation

The evidence on whether high-dose new generation proton pump inhibitors (PPIs) including rabeprazole and esomeprazole achieve a higher eradication rate of Helicobacter pylori has not been assessed. The primary comparison was eradication and adverse events (AEs) rate of standard (esomeprazole 20 mg bid, rabeprazole 10 mg bid) versus high-dose (esomeprazole 40 mg bid, rabeprazole 20 mg bid) PPIs. Sub-analyses were performed to evaluate the eradication rate between Asians and Caucasians, clarithromycin-resistance (CAM-R) strains, and clarithromycin-sensitivity (CAM-S) strains of different dose PPIs. We conducted a literature search for randomized controlled trials comparing high-with standard-dose esomeprazole and rabeprazole for H. pylori eradication and AEs. A total of 12 trials with 2237 patients were included. The eradication rate of high-dose PPIs was not significantly superior to standard-dose PPIs regimens: 85.3% versus 84.2%, OR 1.09 (0.86–1.37), P = 0.47. The high dose induced more AEs than those of the standard dose, but didn’t reach statistical significance (OR 1.25, 95% CI: 0.99–1.56, P = 0.06). Subgroup analysis showed that the difference in eradication rate of PPIs between high- and standard-dose groups were not statistically significant both in Asians (OR 0.99, 95% CI 0.75–1.32, P = 0.97) and Caucasians (OR 1.27, 95% CI 0.84–1.92, P = 0.26). Furthermore, there were similar eradication rates in CAM-S (OR 1.2; 95% CI 0.58–2.5; P = 0.63) and CAM-R strains (OR 1.08; 95% CI 0.45–2.56; P = 0.87) between the standard-and high-dose groups. High and standard dosages of new generation of the PPIs showed similar H. pylori eradication rates and AEs as well as between Asian versus Caucasian populations, with or without clarithromycin-resistance. However, further studies are needed to confirm.

scholarly journals Duodenal Dysbiosis and Relation to the Efficacy of Proton Pump Inhibitors in Functional Dyspepsia

2021 ◽  
Vol 22 (24) ◽  
pp. 13609
Author(s):  
Lucas Wauters ◽  
Raúl Y. Tito ◽  
Matthias Ceulemans ◽  
Maarten Lambaerts ◽  
Alison Accarie ◽  
...  
Keyword(s):  
Functional Dyspepsia ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Potential Role ◽  
Short Term ◽  
Beneficial Effects ◽  
Rrna Sequencing ◽  
Before And After

Proton pump inhibitors (PPI) may improve symptoms in functional dyspepsia (FD) through duodenal eosinophil-reducing effects. However, the contribution of the microbiome to FD symptoms and its interaction with PPI remains elusive. Aseptic duodenal brushings and biopsies were performed before and after PPI intake (4 weeks Pantoprazole 40 mg daily, FD-starters and controls) or withdrawal (2 months, FD-stoppers) for 16S-rRNA sequencing. Between- and within-group changes in genera or diversity and associations with symptoms or duodenal factors were analyzed. In total, 30 controls, 28 FD-starters and 19 FD-stoppers were followed. Mucus-associated Porphyromonas was lower in FD-starters vs. controls and correlated with symptoms in FD and duodenal eosinophils in both groups, while Streptococcus correlated with eosinophils in controls. Although clinical and eosinophil-reducing effects of PPI therapy were unrelated to microbiota changes in FD-starters, increased Streptococcus was associated with duodenal PPI effects in controls and remained higher despite withdrawal of long-term PPI therapy in FD-stoppers. Thus, duodenal microbiome analysis demonstrated differential mucus-associated genera, with a potential role of Porphyromonas in FD pathophysiology. While beneficial effects of short-term PPI therapy were not associated with microbial changes in FD-starters, increased Streptococcus and its association with PPIeffects in controls suggest a role for duodenal dysbiosis after long-term PPI therapy.

scholarly journals Factors affecting Helicobacter pylori eradication using a seven-day triple therapy with a proton pump inhibitor, tinidazole and clarithromycin, in brazilian patients with peptic ulcer

2001 ◽  
Vol 56 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Fernando Marcuz Silva ◽  
Schlioma Zaterka ◽  
Jaime Natan Eisig ◽  
Ethel Zimberg Chehter ◽  
Décio Chinzon ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Proton Pump Inhibitor ◽  
Triple Therapy ◽  
Proton Pump ◽  
Eradication Rate ◽  
Response To Therapy ◽  
Urease Test ◽  
Previously Treated Patients ◽  
Previously Treated ◽  
H Pylori

Triple therapy is accepted as the treatment of choice for H. pylori eradication. In industrialized countries, a proton pump inhibitor plus clarithromycin and amoxicillin or nitroimidazole have shown the best results. Our aims were: 1. To study the eradication rate of the association of a proton pump inhibitor plus tinidazole and clarithromycin on H. pylori infection in our population. 2. To determine if previous treatments, gender, age, tobacco, alcohol use, and non-steroidal anti-inflammatory drugs (NSAIDs) change the response to therapy. METHODS: Two hundred patients with peptic ulcer (upper endoscopy) and H. pylori infection (histology and rapid urease test - RUT) were included. A proton pump inhibitor (lansoprazole 30 mg or omeprazole 20 mg), tinidazole 500 mg, and clarithromycin 250 mg were dispensed twice a day for a seven-day period. Eradication was assessed after 10 to 12 weeks of treatment through histology and RUT. RESULTS: The eradication rate of H. pylori per protocol was 65% (128/196 patients). This rate was 53% for previously treated patients, rising to 76% for not previously treated patients, with a statistical difference p<0.01. No significant difference was observed regarding sex, tobacco use, alcohol consumption, and NSAID use, but for elderly patients the difference was p = 0.05. Adherence to treatment was good, and side effects were mild. CONCLUSIONS: A proton pump inhibitor, tinidazole, and clarithromycin bid for seven days resulted in H. pylori eradication in 65% of the patients. Previous treatments were the main cause of treatment failure.

scholarly journals Long-term use of proton-pump inhibitors and risk of gastric cancer: a review of the current evidence

2019 ◽  
Vol 12 ◽  
pp. 175628481983451 ◽  
Author(s):  
Ka Shing Cheung ◽  
Wai K. Leung
Keyword(s):  
Gastric Cancer ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Randomized Clinical Trials ◽  
Bacterial Overgrowth ◽  
Current Evidence ◽  
Neoplastic Progression ◽  
Increased Risk ◽  
H Pylori

Gastric cancer remains one of the leading cancers in the world with a high mortality, particularly in East Asia. Helicobacter pylori infection accounts for the majority of the noncardia gastric cancers by triggering gastric inflammation and subsequent neoplastic progression. Eradication of H. pylori can reduce, but not totally eliminate, subsequent risk of developing gastric cancer. Proton-pump inhibitors (PPIs) are one of the most widely prescribed medications worldwide. With their profound gastric-acid suppression, there are concerns about a possible carcinogenic role in gastric cancer, due to induced hypergastrinemia, gastric atrophy and bacterial overgrowth in the stomach. While randomized clinical trials to establish causality between long-term PPI use and gastric cancer are lacking, current evidence based on observational studies suggests PPIs are associated with an increased gastric cancer risk. However, opinions on causality remain divergent due to unmeasured and possible residual confounding in various studies. Our recent study has showed that even after H. pylori eradication, long-term PPI use is still associated with an increased risk of gastric cancer by more than twofold. Hence, long-term PPIs should be used judiciously after considering individual’s risk–benefit profile, particularly among those with history of H. pylori infection. Further well-designed prospective studies are warranted to confirm the potential role of PPIs in gastric cancer according to baseline gastric histology and its interaction with other chemopreventive agents like aspirin, statins and metformin.

scholarly journals In vitro antibacterial activity of omeprazole and its selectivity for Helicobacter spp. are dependent on incubation conditions.

1996 ◽  
Vol 40 (3) ◽  
pp. 621-626 ◽  
Author(s):  
J E Sjöström ◽  
J Fryklund ◽  
T Kühler ◽  
H Larsson
Keyword(s):  
Antibacterial Activity ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Bactericidal Activity ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Antibacterial Activities ◽  
In Vitro Antibacterial Activity ◽  
H Pylori

Factors affecting the in vitro antibacterial activity of omeprazole were studied. Our data show that 3H-labeled omeprazole covalently bound to Helicobacter pylori and to other gram-negative and gram-positive bacteria. The compound was found to bind to a broad range of proteins in H. pylori, and at pH 5, binding was enhanced 15-fold compared with binding at pH 7. The bactericidal activity correlated to the degree of binding, and at pH 5, a pH at which omeprazole readily converts to the active sulfenamide form, beta-mercaptoethanol, a known scavenger of sulfenamide, and fetal calf serum, to which noncovalent protein binding of omeprazole is known to occur, reduced the level of binding and almost entirely abolished the bactericidal activity. At pH 7 the killing activities of omeprazole and structural analogs (e.g., proton pump inhibitors) were dependent on the time-dependent conversion (half-life) to the corresponding sulfenamide. The bactericidal activity exerted by the sulfenamide form at pH 5 was not specific for the genus Helicobacter. However, in brucella broth at pH 7 with 10% fetal calf serum, only Helicobacter spp. were susceptible to omeprazole, with MBCs in the range of 32 to 64 micrograms/ml, and MBCs for more stable proton pump inhibitors were higher. Wild-type H. pylori and its isogenic urease-deficient mutant were equally susceptible to omeprazole. Thus, the urease is not a lethal target for omeprazole action in H. pylori. In conclusion, the antibacterial activities of omeprazole and analogs are dependent on pH and the composition of the medium used. Thus, at a low pH in buffer, these compounds have a nonselective action, whereas in broth at neutral pH, the mechanism of action is selective for Helicobacter spp.

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