scholarly journals Gastric juice analysis during endoscopy detects atrophic gastritis and H. pylori

2008 ◽  
Vol 5 (2) ◽  
pp. 67-67
Gut ◽  
1998 ◽  
Vol 43 (2) ◽  
pp. 168-175 ◽  
Author(s):  
S Futagami ◽  
H Takahashi ◽  
Y Norose ◽  
M Kobayashi

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.


Author(s):  
Anastasiya O. Sablina ◽  
Oleg A. Sablin ◽  
Julia V. Andreeva ◽  
Gennadii G. Rodionov ◽  
I. I. Shantyr ◽  
...  

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.


2018 ◽  
Vol 01 (1) ◽  
Author(s):  
Takalkar U Vidyadhar

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.


2018 ◽  
Vol 27 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Gintare Dargiene ◽  
Greta Streleckiene ◽  
Jurgita Skieceviciene ◽  
Marcis Leja ◽  
Alexander Link ◽  
...  

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum.Results: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26–2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26–2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed.Conclusions: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.


2021 ◽  
Author(s):  
Ombretta Repetto ◽  
Valli De Re ◽  
Paolo Giuffrida ◽  
Marco Vincenzo Lenti ◽  
Raffaella Magris ◽  
...  

Abstract Background Autoimmune atrophic gastritis (AAG) is a chronic disease that can progress to gastric cancer (GC). To better understand AAG pathology, this proteomics study investigated gastric proteins whose expression levels are altered in this disease and also in GC. Methods Using two-dimensional difference gel electrophoresis (2D-DIGE), we compared protein maps of gastric corpus biopsies from AAG patients and controls. Differentially abundant spots (|fold change|≥ 1.5, P < 0.01) were selected and identified by LC–MS/MS. The spots were further assessed in gastric antrum biopsies from AAG patients (without and with Helicobacter pylori infection) and from GC patients and unaffected first-degree relatives of GC patients. Results 2D-DIGE identified 67 differentially abundant spots, with 28 more and 39 less abundant in AAG-corpus than controls. LC–MS/MS identified these as 53 distinct proteins. The most significant (adjusted P < 0.01) biological process associated with the less abundant proteins was “tricarboxylic acid cycle”. Of the 67 spots, 57 were similarly differentially abundant in AAG-antrum biopsies irrespective of H. pylori infection status. The differential abundance was also observed in GC biopsies for 14 of 28 more abundant and 35 of 39 less abundant spots, and in normal gastric biopsies of relatives of GC patients for 6 and 25 spots, respectively. Immunoblotting confirmed the different expression levels of two more abundant proteins (PDIA3, GSTP gene products) and four less abundant proteins (ATP5F1A, PGA3, SDHB, PGC). Conclusion This study identified a proteomics signature of AAG. Many differential proteins were shared by GC and may be involved in the progression of AAG to GC.


1998 ◽  
Vol 114 ◽  
pp. A183 ◽  
Author(s):  
A. Kokkola ◽  
P. Puolakkainen ◽  
H. Rautelin ◽  
P. Sipponen ◽  
M. Färkkilä ◽  
...  

2020 ◽  
Author(s):  
Shihua Wu ◽  
Chunmei Bao ◽  
Ruilin Wang ◽  
Xiaomei Zhang ◽  
Sijia Gao ◽  
...  

Abstract Background: Zuojin Pill (ZJP), a famous Chinese medicinal formula, widely accepted for treatment of chronic atrophic gastritis (CAG) in China. This study aimed to explore the therapeutic effects and mechanisms of ZJP in Helicobacter pylori (H. pylori) - induced chronic atrophic gastritis (CAG) in vivo and in vitro. Methods: CAG rat model was induced by H. pylori. ZJP (0.63, 1.26, and 2.52 g/kg, respectively) was administered orally for four weeks. Therapeutic effects of ZJP were identified by H&E staining and serum indices. In addition, cell viability, morphology and proliferation were detected by cell counting kit-8 (CCK8) and high-content screening assay (HCS), respectively. Moreover, relative mRNA expression and protein expression related to JMJD2B/COX-2/VEGF axis was detected to investigate the potential mechanisms of ZJP in CAG. Results: Results showed the symptoms (weight loss and gastric mucosa damage) of CAG were alleviated, and the contents of TNF-α in serum was markedly decreased after treating with ZJP. Moreover, cell viability, proliferation and morphology changes of GES-1 cells were ameliorated by ZJP intervention. In addition, proinflammatory genes and JMJD2B/COX-2/VEGF axis related genes were suppressed by ZJP administration in vitro and in vivo. Meanwhile, immunohistochemistry (IHC) and western blot confirmed down-regulation of these genes by ZJP intervention. Conclusion: ZJP treatment can alleviate gastric mucosal damage induced by H. pylori via JMJD2B/COX-2/VEGF axis.


2018 ◽  
Vol 06 (07) ◽  
pp. E830-E837 ◽  
Author(s):  
Kazumi Togo ◽  
Tetsuya Ueo ◽  
Kenshi Yao ◽  
Kurato Wada ◽  
Hideho Honda ◽  
...  

Abstract Background and study aims The presence of white opaque substance (WOS) is an endoscopic marker of intestinal metaplasia. Considering that the nature of WOS is absorbed lipid droplets, lipase plays an important role in the lipid absorption process and is inactivated at strong acidity. WOS may only be present in a hypochlorhydria state following Helicobacter pylori infection, and, thus, may not be highly sensitive marker, especially in H. pylori-eradicated patients. We investigated the relationship between WOS and gastric acid conditions. Patients and methods A total of 501 patients were retrospectively evaluated for the presence of WOS at 2 regions of interest using magnifying narrow-band imaging. The pH level of collected gastric juice was also measured. Study end points were (1) prevalence of WOS and its relationship with gastric juice pH in 3 groups: H. pylori-uninfected, H. pylori-infected, and H. pylori-eradicated; (2) the relationship between prevalence of WOS and gastric juice pH before and after proton pump inhibitor (PPI) administration in 29 H. pylori-eradicated cases. Results Prevalence of WOS was 0 % (0 /206), 28.4 % (31/109), and 3.2 % (6/186) in the H. pylori-uninfected, H. pylori-infected, and H. pylori-eradicated groups, respectively. Mean gastric juice pH was significantly higher in WOS-positive cases than in WOS-negative cases in the H. pylori-infected and H. pylori-eradicated groups (P < 0.0001). Mean gastric juice pH increased from 1.1 to 6.9 after PPI administration and WOS prevalence increased from 0 % (0/29) to 45 % (13/29) of cases. Conclusion The prevalence of WOS is closely associated with the neutralization of intragastric pH.


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