Chronic Superficial Gastritis Research Articles

Evaluation of serum levels of Proinflammatory Cytokines IL-8, IL-17, and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients

Gastritis can be defined as histological inflammation of the gastric mucosa. It can be classified according to the time course of the disease as acute or chronic, histological findings, anatomic location, and pathological mechanisms. The objective of this study was to evaluation of serum levels of the proinflammatory cytokines IL-8, IL-17 and IL-22 in Helicobacter pylori infection and their association with the degree of gastritis histopathology in a sample of Iraqi patients. The case-control prospective study consists of 60 patients who attended the Gastrointestinal Tract Center at Al-Kindy Teaching Hospital during the period from December 2019 to April 2020. In addition, the control group included 60 apparently healthy individuals. Biopsies from the gastric antrum and/or body mucosa were used to assess the severity of chronic inflammation, neutrophil infiltration, atrophy, intestinal metaplasia. Serum samples were obtained to determine H. pylori infection, circulating interleukin (IL)-8, IL-17, and IL-22. Results showed that the Patients’ ages with gastritis ranged from 18-75 years. The body mass index revealed that 33.33% of the patients were obese and 35% of them were overweight. Most of the patients with active chronic gastritis and superficial chronic gastritis had positive titers for anti-H. pylori IgG antibody (167.89 ± 3.18 IU/ml) and (150.74± 1.45 IU/ml) respectively, which was significantly different from the control group (4.36 ± 0.29 IU/ml) (P=0.0001). Histopathological analysis showed that all subjects experienced chronic inflammation, while neutrophil infiltration was found 36.66% and there was significant association between serum levels of IL-8, IL-17, and IL-22 with a degree of chronic inflammation and neutrophils infiltration. In conclusion, the most common cause of gastritis was H. pylori with histopathological lesions, showing neutrophils infiltration and chronic gastric mucosal inflammation associated with increased levels of IL-8, IL-17, and IL-22 in serum.

Metabolomic profiling of plasma reveals potential biomarkers for screening and early diagnosis of gastric cancer and precancerous stages

AbstractGastric cancer (GC) faces a great challenge in clinical diagnosis, that it often is detected at advanced stages and there is a loss of optimum time for treatment. Thus, it is necessary to develop effective strategies for diagnosis of GC. In this study, 82 participants were enrolled, including 50 chronic superficial gastritis (CSG) patients, 7 early gastric cancer (EGC), and 25 advanced gastric cancer (AGC) ones. Metabolites profiling on patient plasma was performed. Furthermore, the proposed biomarkers were used to create random forest models, in which discrimination efficiency and accuracy were ascertained by receiver operating characteristic (ROC) curve analysis. l‐carnitine, l‐proline, pyruvaldehyde, phosphatidylcholines (PC) (14:0/18:0), lysophosphatidylcholine (14:0) (LysoPC 14:0), lysinoalanine were defined as the potential biomarker panel for the diagnosis among CSG and EGC patients. Compared with EGC patients, PC(O‐18:0/0:0) and LysoPC(20:4(5Z,8Z,11Z,14Z)) were found to be upregulated in AGC patients, whereasl‐proline, l‐valine, adrenic acid, and pyruvaldehyde downregulated. Pathway analysis revealed several metabolism disorders, involving amino acids and lipid metabolism. ROC analysis demonstrated a high diagnostic performance in disease diagnosis between CSG and GC. The above results indicate that the biomarker panels are sensitive to early diagnosis of GC disease, which is expected to be a promising diagnostic tool for disease stratification studies.

Analysis of the relationship between oipA, babA2, babB genotypes and helicobacter pylori-related gastric precancerous lesions.

To investigate the distribution of helicobacter pylori-related genotypes of oipA, babA2, and babB in patients with gastrointestinal diseases. The retrospective study was conducted at the Jiamusi College, Heilongjiang University of Traditional Chinese Medicine, Harbin, China, and comprised data from February 2017 to May 2020 of patients of either gender 20-80 years who underwent gastroscopy. An instrument based on polymerase chain reaction was used to amplify oipA, babA2 and babB genes, and their distribution in terms of gender, age and pathological types was analysed. Among the 116 patients, 52(44.8%) had oipA genotype, 48(41.2%) babA2, and 72 (62.1%) babB, respectively, and the size of amplified products of 486bp, 219bp and 362bp, respectively. The infection rate of oipA and babB genotypes was highest [26(50.0%) and 31(43.1%)]in those aged 61-80 years, and lowest [9(17.3%) and 15(20.8%)]in those aged 20-40 years. The infection rate of babA2 genotype was highest [23(47.9%)] in those aged 41-60 years, and lowest [12(25.0%)] in those aged 61-80 years. Male patients were under a higher [28(53.9%) and 26(54.2%)] rate of infection with oipA and babA2, and female patients has a higher [40(55.6%)] rate of infection with babB. Among Hp-infected patients with digestive diseases, babB genotype was mainly found in patients with chronic superficial gastritis[17(58.6%)], duodenal ulcer[17(85.0%)], chronic atrophic gastritis[19(59.4%)] and gastric ulcer[16(72.7%)], while oipA genotype was mainly found in patients with gastric cancer[8(61.5%)]. Chronic superficial gastritis, duodenal ulcer, chronic atrophic gastritis, and gastric ulcer may have a close bearing on babB genotype infection, while oipA genotype infection may be associated with gastric cancer.

Clinical and gastroscopic features of children with cyclic vomiting syndrome: an analysis of 63 cases

To study the clinical and gastroscopic features of children with cyclic vomiting syndrome. A retrospective analysis was performed on the medical data of 63 children with cyclic vomiting syndrome who were hospitalized and followed up in Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University from August 2019 to March 2022. Among the 63 children, there were 30 boys and 33 girls, with a mean age of 6.11 years, a mean course of disease of 2.57 years, and a mean vomiting period of 4.04 days. The most common accompanying symptom was listlessness or somnolence (55/63, 87%), followed by anorexia (45/63, 71%), abdominal pain or abdominal discomfort (40/63, 63%), constipation (19/63, 30%), salivation (12/63, 19%), nausea (11/63, 17%), headache (11/63, 17%), fever (6/63, 10%), and rash (1/63, 2%). All 63 children underwent gastroscopy, among whom 3 had no marked abnormalities, 22 (35%) had chronic superficial gastritis or chronic non-atrophic gastritis alone, and 38 (60%) had other abnormal changes aside from chronic gastritis (16 children with reflux esophagitis, 12 with bile reflux gastritis, 13 with duodenitis, 10 with erosive gastritis, and 5 with gastric or duodenal ulcer). Among the 63 children, 42 underwent pathological examinations of gastric mucosa, among whom 5 had no marked abnormalities, 34 had mild chronic gastritis, 2 had moderate chronic gastritis, and 1 had severe chronic gastritis. Among the 63 children, 15 received 24-hour dynamic esophageal pH monitoring during the interictal period, among whom 9 children were found to have pathological acid reflux. In addition to recurrent vomiting, most children with cyclic vomiting syndrome also have the symptoms such as somnolence or listlessness, anorexia, and abdominal pain. The main manifestation on gastroscopy is chronic gastritis, and most children may also have reflux esophagitis, bile reflux gastritis, and erosive gastritis. Mild chronic gastritis is the main pathological change of gastric mucosa.

Differences in gastric microbiota and mucosal function between patients with chronic superficial gastritis and intestinal metaplasia.

Chronic superficial gastritis (CSG) and intestinal metaplasia (IM) can further develop into gastric cancer, which seriously endangers the health of people all over the world. In this study, the differences in gastric microbiota between CSG patients and IM patients were detected by 16S rRNA gene sequencing. As the expression levels of mucin and CDX2 are closely related to IM, the expression differences of mucin (MUC2 and MUC5AC) and CDX2 in the gastric mucosa of CSG patients and IM patients were detected by Western blot and qRT-PCR. The results showed that both Faith_pd and Observed_species indexes of microbiota in the gastric juice of CSG patients were significantly higher than those of IM patients. At the genus level, Thermus and Anoxybacillus were dominant in the gastric juice of IM patients, and Helicobacter was dominant in the gastric juice of CSG patients. Non-metric multidimensional scaling (NMDS) demonstrated that the dispersion of samples in the CSG group is greater than that in the IM group, and some samples in the CSG group are clustered with samples in the IM group. The KEGG metabolic pathway difference analysis of gastric juice microbiota in CSG and IM patients revealed that the gastric juice microbiota in the CSG and IM patients were significantly enriched in the amino acid metabolism, carbohydrate metabolism, and metabolism of cofactors and vitamins, and the functional differences between the two groups were mainly concentrated in the bacterial secretion system (VirB1, VirB2, VirB3, VirD2, and VirD4). In conclusion, there are significant differences in gastric microbiota and mucosal function between the CSG and IM patients. Moreover, the results of this study may provide a new means for the detection of CSG and IM and a new direction for the prevention and treatment of CSG and IM.

Plasma-Methylated SEPT9 for the Noninvasive Diagnosis of Gastric Cancer.

Gastric cancer (GC) is one of the most prevalent cancers globally. This study was designed to evaluate the potential performance of plasma SEPT9 methylation (mSEPT9) as a noninvasive biomarker for the diagnosis of GC. A total of 182 participants, i.e., 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), 30 with gastric ulcer (GU), and 26 with gastric polys (GP), were recruited. The mSEPT9 level was measured using real-time polymerase chain reaction. As a diagnostic target, mSEPT9 (1/3 algorithm) had a sensitivity of 48.33 (95% confidence interval (CI): 35.40-61.48%) and a specificity of 86.89% (95% CI: 79.28-92.09%), and mSEPT9 (2/3 algorithm) had a sensitivity of 33.33 (95% CI: 22.02-46.79%) and a specificity of 98.36% (95% CI: 93.61-99.72%). The area under the receiver operating characteristic curve (ROC) curve of mSEPT9 was 0.698 (95% CI: 0.609-0.787) for the differentiation of GC from benign gastric diseases. The effectiveness of mSEPT9 (1/3 algorithm) was superior to that of CEA, CA19-9, and CA72-4. mSEPT9 was positively correlated with T, N, M, and the clinical stage of GC. Plasma mSEPT9 might serve as a useful and noninvasive biomarker for the diagnosis of GC.

The emerging double-edged sword role of Sirtuins in the gastric inflammation-carcinoma sequence revealed by bulk and single-cell transcriptomes.

Histone modification and the inflammation-carcinoma sequence (ICS) have been acknowledgedly implicated in gastric carcinogenesis. However, the extremum expression of some histone modification genes (HMGs) in intestinal metaplasia (IM) rather than GC obscures the roles of HMGs in ICS. In this study, we assumed an explanation that the roles of HMGs in ICS were stage specific. Bulk RNA-seq on endoscopy biopsy samples from a total of 50 patients was accompanied by reanalysis of a set of published single-cell transcriptomes, which cross-sectionally profiled the transcriptomic features of chronic superficial gastritis (SG), atrophy gastritis (AG), IM, and early gastric cancer (GC). Differential analysis observed significantly peaked expression of SIRT6 and SIRT7 at IM. Weighted correlation network analysis on bulk transcriptome recognized significant correlations between SIRT1/6 and IM. The single-cell atlas identified one subgroup of B cells expressing high level of TFF1 (TFF1 hi naive B cell) that theoretically played important roles in defending microbial infection, while SIRT6 displayed a positive correlation with TFF1 low naive B cells. Moreover, gene set enrichment analysis at different lesions (SG-AG, AG-IM, and IM-GC) highlighted that gene sets contributing to IM, e.g., Brush Border, were largely enriched from co-expressing genes of Sirtuins (SIRTs) in AG-IM. Surveys of the genes negatively correlated with SIRT6 in public databases considered SIRT6 as tumor suppressors, which was confirmed by the cell proliferation and migration assays after transient transfection of SIRT6 overexpression vector into AGS cells. All the above observations were then confirmed by serial section-based immunohistochemistry against Ki-67, MUC2, MUC5AC, p53, and SIRT6 on the endoscopic submucosal dissection tissue. By contrast, the expression of the other HMGs varied even opposite within same family. Taken together, this study preliminarily demonstrated the two-edged sword role of SIRTs in ICS and, by extension, showed that the roles of HMGs in ICS were probably stage specific. Our study may provide new insights into and attract attention on gastric prevention and therapy targeting HMGs.

Differential Expression of α-Enolase in Clinical Gastric Tissues and Cultured Normal/Cancer Cells in Response to Helicobacter pylori Infection and cagA Transfection.

Background and Objectives: The role of α-enolase (ENO1) in Helicobacter pylori-related gastric lesions might be a critical factor in the pathogenesis, but remains undefined. Materials and Methods: This study investigated the differential expression of α-enolase in clinical gastric specimens and cultured normal/cancer cells in response to H. pylori (cagA+) infection and cagA transfection using qPCR, Western blots and histochemical methods. Results: A total of 172 gastric specimens were collected from 142 patients, the former comprising chronic superficial gastritis (CSG), precancerous diseases (PCDs, including atrophic gastritis, intestinal metaplasia and dysplasia) and gastric cancer (GC) cases. Among the CSG and PCD cases, the H. pylori-infected group had significantly elevated ENO1 mRNA levels compared with the uninfected group. In the GC cases, differential ENO1 expressions were detected between the cancer tissues and the paracancerous tissues. Notably, significant difference was first detected between the GC cell (AGS) and the normal cell (GES-1) as a response of ENO1 to H. pylori infection and cagA transfection. Conclusions: This report reveals that ENO1 expression is associated with H. pylori infection, cagA transfection, co-culture duration, multiplicity of infection, gastric normal/cancerous cell lines and cellular differentiation. The findings may be crucial bases for further ascertaining H. pylori pathogenic mechanism and formulating novel therapeutic and diagnostic strategies.

Plasma Methylated RNF180 for Noninvasive Diagnosis of Gastric Cancer.

Background RNF180 is a tumor suppressor gene involved in cell development, proliferation, and apoptosis. Methylation of RNF180 (mRNF180) leads to low expression of RNF180, which is closely related to the occurrence and development of gastric cancer (GC). This study was designed to evaluate the potential performance of plasma mRNF180 as noninvasive biomarker for the diagnosis of GC. Methods A total of 156 participants, including 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), and 30 with gastric ulcer (GU) were recruited for this study. Plasma mRNF180 level was measured using real-time polymerase chain reaction. Results As a diagnostic target, mRNF180 had a sensitivity of 71.67% (95% CI: 58.36%–82.18%) and specificity of 59.38% (95% CI: 48.85%–69.14%). The area under the ROC curve value of mRNF180 was 0.731 (95% CI: 0.648%–0.813%) for differentiation of GC from benign gastric diseases (BGD). The effectiveness of mRNF180 was superior to that of CEA, CA199, and CA724. mRNF180 was positively correlated with age, tumor size, T stage, N stage, M stage, and clinical stage of patients with GC. Conclusions Plasma mRNF180 might serve as a useful and noninvasive biomarker for the diagnosis of GC and can be used to evaluate its prognosis.

Metabolic alterations of short-chain fatty acids and TCA cycle intermediates in human plasma from patients with gastric cancer

AimsShort-chain fatty acids (SCFAs) are produced by gut microbiota from dietary fiber. Since absorbed SCFAs could be introduced into the tricarboxylic acid (TCA) cycle in host cells, the relationships between SCFAs and TCA cycle intermediates might influence to energy metabolism in the human body. For this reason, information on profile changes between SCFAs and TCA cycle intermediates could help unveil pathological mechanisms of gastric cancer. Main methodsA gas chromatography-tandem mass spectrometry (GC–MS/MS) method was developed to simultaneously determine SCFAs and TCA cycle intermediates in human plasma from patients with chronic superficial gastritis (CSG), intestinal metaplasia (IM), and gastric cancer. We applied a tetra-alkyl ammonium pairing method to prevent loss of volatile SCFAs and base decarboxylation of TCA cycle intermediates during sample preparation. To assess gastric diseases, metabolic alterations of SCFAs and TCA cycle intermediates in human plasma with gastric disorders were analyzed by their plasma levels. Key findingsSignificantly different metabolic alterations based on the plasma levels of SCFAs and TCA cycle intermediates were investigated in cancer metabolic pathways. Not only propionate and butyrate, mainly produced by gut microbiota, were significantly decreased, but also cis-aconitate, α-ketoglutarate, and fumarate were significantly increased in plasma with IM or gastric cancer, compared to CSG. Further, based on ratios of product to precursor, three metabolic pathways (succinate/propionate, succinate/α-ketoglutarate, and cis-aconitate/citrate) were supposed to be distorted between gastric diseases. SignificanceIn conclusion, propionate, cis-aconitate, α-ketoglutarate, and fumarate could be used to assess the progression of gastric cancer.

Feasibility of olfactomedin 4 as a molecular biomarker for early diagnosis of gastric neoplasia after intestinal metaplasia

Objectives This study discusses whether olfactomedin 4 (OLFM4) could be used as a sensitive and specific biomarker in the early diagnosis of gastric cancer (GC) after gastric intestinal metaplasia (GIM). Methods An integrative analysis combining data derived from the Gene Expression Omnibus (GEO) and cBioPortal databases was performed to investigate the potential molecular biomarker. Immunohistochemistry and quantitative real-time polymerase chain reactions were used to measure the expression of messenger ribonucleic acid (mRNA) and protein by OLFM4. In combination with the gastroscopic findings and the OLFM4 expression in GIM-GC, a predictive model was established. The receiver operator characteristic curve (ROC) was applied to assess the diagnostic value of the model for GIM-GC. Results According to the GEO and cBioPortal databases, OLFM4 was identified as a key gene in the diagnosis of GIM-GC. Higher protein expression of OLFM4 was found in GIM and GIM-GC compared with chronic superficial gastritis (GS) (p < 0.05). The positive expression rate of OLFM4 in paracancerous tissue (GCP) was higher than in GIM (p > 0.05). There was no significant difference between GIM-GC and GCP (p > 0.05). The mRNA expression of OLFM4 was similar to the protein expression, and the positive expression rate was higher in early GIM-GC than in GIM (p < 0.05). Conclusion Olfactomedin 4 could be used as a biomarker for the early diagnosis of GIM-GC, and the logistic predictive model could be an effective tool for increasing the early diagnostic rate.

Clinicopathological Significance and Molecular Mechanism of AKT/GSK3β Pathway-based Fibrillin-1 Expression in Gastric Cancer Progression.

This research was developed to explore the significance of fibrillin-1 (FBN1) in the progression of gastric cancer and its relationship with the activation of the AKT/glycogen synthase kinase-3beta (GSK3β) pathway. For this aim, immunohistochemical assays were adopted to detect FBN1 expression in chronic superficial gastritis, chronic atrophic gastritis, gastric cancer, and normal mucosa. The expression of FBN1 in gastric cancer and adjacent tissue samples was detected by reverse transcription-quantitative (RT-q) PCR and Western blot, and the relationship between FBN1 and the clinicopathological features of gastric cancer patients was analyzed. Lentivirus was utilized to construct SGC-7901 gastric cancer cell lines stably overexpressing and silencing FBN1, and the effects on cell proliferation, colony formation, and apoptosis were analyzed. AKT, GSK3β, and their phosphorylated proteins were detected by Western blot. Results showed that the positive expression rate of FBN1 increased successively in chronic superficial gastritis, chronic atrophic gastritis, and gastric cancer. FBN1 was up-regulated in gastric cancer tissues and correlated with the depth of tumor invasion. Overexpression of FBN1 promoted the proliferation and colony formation of gastric cancer cells, inhibited apoptosis, and promoted the phosphorylation of AKT and GSK3β. Silencing FBN1 expression inhibited the proliferation and clonal formation of gastric cancer cells, promoted apoptosis, and inhibited the phosphorylation of AKT and GSK3β. In conclusion, FBN1 was up-regulated in gastric cancer tissues and correlated with the depth of gastric tumor invasion. FBN1 silencing inhibited the progression of gastric cancer through the AKT/GSK3β pathway.

Analysis of Gastric Diseases and Their Symptoms Based on Indexes of Pepsinogen I (PGI) and Pepsinogen II (PGII): Take 1106 Patients as Samples

In this study, preoperative analysis of 1106 gastropathy patients with abdominal pain, vomiting, dyspepsia, and other symptoms was conducted. Independent sample t -test and correlation analysis and other ways were used for data cleansing and analysis. Findings were as follows: (1) Samples of different genders showed significance in PGI and PGII. The PGI and PGII values of women were significantly lower than those of men. (2) Age showed a significant positive correlation with PGI and PGII, which indicates that as the age increases, the PGI and PGII values become higher. (3) There was a significant negative correlation between age and abdominal pain. This signified that the younger the patient is, the more likely they will suffer abdominal pain. (4) PGI displayed a positive correlation with abdominal pain in the digestive tract (dyspepsia, gastrointestinal ulcers, gastrointestinal bleeding, etc.). It indicated that the higher the PGI value is, the more likely the patients will suffer abdominal pain and gastrointestinal diseases (dyspepsia, gastrointestinal ulcer, gastrointestinal hemorrhage, etc.). (5) PGII displayed a significant positive correlation with gastrointestinal diseases (dyspepsia, gastrointestinal ulcer, gastrointestinal hemorrhage, etc.) and a negative correlation with gastropathy (acute gastritis, chronic superficial gastritis, gastric ulcer, etc.). It indicated that the higher the value of PGII is, the more likely the patients will suffer symptoms of gastrointestinal diseases (dyspepsia, gastrointestinal ulcer, gastrointestinal hemorrhage, etc.), while less likely the patients will suffer gastropathy (acute gastritis, chronic superficial gastritis, gastric ulcer, etc.).

Inflammatory map of the gastroduodenal mucosa in patients with upper gastrointestinal symptoms. The role of H. pylori infection

Introduction and aimThe gastric mucosa has been studied since the pre-Helicobacter pylori (H. pylori) era, but the complete descriptions of the stomach and duodenum have been anecdotal, and those of the distal duodenum, exceptional. Our aim was to evaluate the different epidemiologic characteristics and the gastroduodenal inflammatory status in patients with upper gastrointestinal symptoms. Materials and methodsWe studied 138 patients divided into: the non-ulcer group (functional dyspepsia [n = 77] and GERD [n = 27]) and the ulcer group (peptic ulcer [n = 13] and duodenal ulcer [n = 21]). Ten biopsy samples (2 from the corpus, 3 from the antrum, 3 from the proximal duodenum, and 2 from the distal duodenum) were taken in each patient for histologic and/or microbiologic study. ResultsThe prevalence of dyspepsia, functional dyspepsia, and H. pylori was 80.4%, 69.4%, and 82.6%, respectively. The frequency of superficial chronic gastritis in the corpus was significantly higher in the ulcer group vs. the non-ulcer group, whereas there was more chronic atrophic gastritis in the antrum in the ulcer group (P < 0.05). Duodenitis was significantly more frequent in the ulcer group vs. the non-ulcer group, in both the proximal and distal duodenum. Pangastroduodenitis was a significant finding in the ulcer group. In both groups, chronic gastritis (corpus and antrum) and duodenitis (proximal and distal) were significantly related to the presence of H. pylori. Proximal duodenitis is not an uncommon finding in functional dyspepsia (37.7%) and is twice as frequent as distal duodenitis (16.9%). ConclusionsThe ulcer group presented with a gastroduodenal inflammatory map different from that of the non-ulcer group and was characterized by a higher frequency of superficial chronic gastritis in the corpus, chronic atrophic gastritis in the antrum, and a very high frequency of proximal duodenitis.

Mapa inflamatorio de la mucosa gastroduodenal en pacientes con síntomas gastrointestinales altos. Protagonismo de la infección por H. pylori

Introduction and aimThe gastric mucosa has been studied since the pre-Helicobacter pylori (H. pylori) era, but the complete descriptions of the stomach and duodenum have been anecdotal, and those of the distal duodenum, exceptional. Our aim was to evaluate the different epidemiologic characteristics and the gastroduodenal inflammatory status in patients with upper gastrointestinal symptoms. Materials and methodsWe studied 138 patients divided into: the non-ulcer group (functional dyspepsia [n=77] and GERD [n=27]) and the ulcer group (peptic ulcer [n=13] and duodenal ulcer [n=21]). Ten biopsy samples (2 from the corpus, 3 from the antrum, 3 from the proximal duodenum, and 2 from the distal duodenum) were taken in each patient for histologic and/or microbiologic study. ResultsThe prevalence of dyspepsia, functional dyspepsia, and H. pylori was 80.4%, 69.4%, and 82.6%, respectively. The frequency of superficial chronic gastritis in the corpus was significantly higher in the ulcer group vs. the non-ulcer group, whereas there was more chronic atrophic gastritis in the antrum in the ulcer group (P<0.05). Duodenitis was significantly more frequent in the ulcer group vs. the non-ulcer group, in both the proximal and distal duodenum. Pangastroduodenitis was a significant finding in the ulcer group. In both groups, chronic gastritis (corpus and antrum) and duodenitis (proximal and distal) were significantly related to the presence of H. pylori. Proximal duodenitis is not an uncommon finding in functional dyspepsia (37.7%) and is twice as frequent as distal duodenitis (16.9%). ConclusionsThe ulcer group presented with a gastroduodenal inflammatory map different from that of the non-ulcer group and was characterized by a higher frequency of superficial chronic gastritis in the corpus, chronic atrophic gastritis in the antrum, and a very high frequency of proximal duodenitis.

Observation on the Effect of Modified Chaihu Xiangsu Decoction on Chronic Superficial Gastritis and Analysis on the Influence of HAMA and HAMD Scores

Observation on the Effect of Modified Chaihu Xiangsu Decoction on Chronic Superficial Gastritis and Analysis on the Influence of HAMA and HAMD Scores

Evaluation of the Gastric Microbiome in Patients with Chronic Superficial Gastritis and Intestinal Metaplasia

ObjectiveTo evaluate the gastric microbiome in patients with chronic superficial gastritis (CSG) and intestinal metaplasia (IM) and investigate the influence of Helicobacter pylori (H. pylori) on the gastric microbiome. MethodsGastric mucosa tissue samples were collected from 54 patients with CSG and IM, and the patients were classified into the following four groups based on the state of H. pylori infection and histology: H. pylori-negative CSG (n=24), H. pylori-positive CSG (n=14), H. pylori-negative IM (n=11), and H. pylori-positive IM (n=5). The gastric microbiome was analyzed by 16S rRNA gene sequencing. ResultsH. pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM. In H. pylori-positive subjects, the bacterial abundance and diversity were significantly lower than in H. pylori-negative subjects. The H. pylori-negative groups had similar bacterial composition and bacterial abundance. The H. pylori-positive groups also had similar bacterial composition but different bacterial relative abundance. The relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella were richer in the I-HP group than in G-HP group, especially Neisseria (t=175.1, P<0.001). ConclusionsThe gastric microbial abundance and diversity are lower in H. pylori- infected patients regardless of CSG and IM. Compared to H. pylori-positive CSG group and H. pylori-positive IM, the relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella is higher in H. pylori-positive patients with IM than in H. pylori-positive patients with CSG, especially Neisseria.

Study of the correlation between the expression of nuclear factor kappa B and proliferation regulatory proteins and chronic superficial gastritis

Background/Aim. Cell proliferation and the regulation of protein expression play an important role in gastritis, but in chronic superficial gastritis (CSG), they are rarely reported. The aim of this study was to determine the relationship between the expression of nuclear factor kappa B (NF-?B) and regulatory proteins and the rat CSG. Methods. The CSG rat model was established artificially, by chemical agents and irregular diet. The expression of epidermal growth factor receptor (EGFR) and proliferating cell nuclear antigen (PCNA) in the gastric mucosa of CSG rats was measured by immunohistochemistry, while mRNA expression levels of NF-?B p65 were detected by in situ hybridization. Results. There was more obvious infiltration of inflammatory cells in the gastric mucosa of CSG rats than in that of control rats, and the inflammation score was significantly increased. The expression levels of PCNA, EGFR, and NF-?B p65 mRNA in the gastric mucosal cells of CSG model rats increased significantly. Correlation analysis showed that the inflammation score was positively correlated with the expression levels of NF-?B p65 mRNA and EGFR, while it presented no significant correlation with the expression level of PCNA. In addition, there was a significant positive correlation between NF-?B p65 mRNA and EGFR levels. Conclusion. High expression of NF-?B and EGFR plays an important role in the occurrence and progression of CSG, and it is significantly positively correlated with the degree of inflammation in the gastric mucosa. Therefore, changes in NF-?B and EGFR expression may be used as important indicators for the assessment of CSG; changes in their expression levels are helpful to assess the degree of gastric mucosal lesions and progression of CSG.

Are physicians ready to comply with the guidelines for diagnosis and management of Helicobacter pylori-associated diseases: the survey results 2020–2021

Objective: To assess compliance of physicians with diagnostic and management guidelines for H. pylori-associated diseases with a question-naire-based survey.Materials and methods: We conducted an anonymous voluntary online survey of 775 physicians of the following specialties: internal medicine 459 (59.2%), gastroenterology 279 (36%), and endoscopy 34 (4.4%). The respondents expressed their level of agreement with the questionnaire items as follows: 0 – I do not know, 1 – disagree, 2 – partially agree, and 3 – fully agree.Results: 613 (79.4%) of the physicians fully agreed to diagnose and treat H. pylori in patients with chronic atrophic gastritis, 602 (78.0%) in the 1 st degree relatives of gastric cancer patients, 525 (68.0%) in patients with chronic superficial gastritis, 423 (54.8%) in peptic ulcer at remission, and 336 (43.4%) in those with dyspepsia syndrome. The physicians were equally compliant with eradication therapy in the patients, for whom long term use of proton pump inhibitors (PPI) or non-steroid anti-inflammatory drugs (NSAID) is being planned (386 (50.0%) and 397 (51.4%), respectively). Internists were less compliant with diagnosis and management of H. pylori in patients taking both PPI (χ2 = 66.525, p = 0.004) and NSAID (χ2 = 103.354, p = 0.003). Among the primary diagnostic tools for H. pylori the physicians preferred 13/14С-urease breath test (545 physicians, or 70.6%) and gastric bioptate morphology (574, or 74.4%), and among the control diagnostic methods they chose fаeces analyses (enzyme-linked immunosorbent assay and polymerase chain reaction). The respondents considered bismuth-enhanced standard triple therapy with clarithromycin to be the most effective regimen for the 1 st line eradication therapy (606, 78.5%). To increase the efficacy of eradication therapy, the physicians were more prone to administer esomeprazole or rabeprazole (70.6%), bismuth-based agents (79.4%), than to use rebamipid (35%), probiotics (44.9%) and/or to double PPI doses (44.2%). The respondents expressed their concerns with low patient compliance to treatment (59.4%) and limited diagnostic capabilities (49.4%).Conclusion: Physician's compliance with the guidelines on diagnosis and management of H. pylori-associated diseases is adequate and might depend on both their awareness and availability of the proposed diagnostic and therapeutic methods.

Histopathological Diagnosis System for Gastritis Using Deep Learning Algorithm

Objective To develope a deep learning algorithm for pathological classification of chronic gastritis and assess its performance using whole-slide images (WSIs). Methods We retrospectively collected 1,250 gastric biopsy specimens (1,128 gastritis, 122 normal mucosa) from PLA General Hospital. The deep learning algorithm based on DeepLab v3 (ResNet-50) architecture was trained and validated using 1,008 WSIs and 100 WSIs, respectively. The diagnostic performance of the algorithm was tested on an independent test set of 142 WSIs, with the pathologists' consensus diagnosis as the gold standard. Results The receiver operating characteristic (ROC) curves were generated for chronic superficial gastritis (CSuG), chronic active gastritis (CAcG), and chronic atrophic gastritis (CAtG) in the test set, respectively. The areas under the ROC curves (AUCs) of the algorithm for CSuG, CAcG, and CAtG were 0.882, 0.90S and 0.910, respectively. The sensitivity and specificity of the deep learning algorithm for the classification of CSuG, CAcG, and CAtG were 0.790 and 1.000 (accuracy 0.880), 0.985 and 0.829 (accuracy 0.901), 0.952 and 0.992 (accuracy 0.986), respectively. The overall predicted accuracy for three different types of gastritis was 0.867. By flagging the suspicious regions identified by the algorithm in WSI, a more transparent and interpretable diagnosis can be generated. Conclusion The deep learning algorithm achieved high accuracy for chronic gastritis classification using WSIs. By pre-highlighting the different gastritis regions, it might be used as an auxiliary diagnostic tool to improve the work efficiency of pathologists.