Chronic Superficial Gastritis Group Research Articles

The metabolites mainly composed of lipids in tongue coating are non-invasive potential biomarkers for chronic gastritis

The changes in tongue coating metabolites in patients with chronic gastritis (CG) under different gastroscopy indicators were analyzed, and these metabolites were screened for potential non-invasive biomarkers to assist in the diagnosis of chronic gastritis. The technology of gas chromatography and liquid chromatography combined with mass spectrometry has been used to more comprehensively detect tongue coating metabolites of 350 CG patients. Spearman correlation analysis and random forest algorithm were used to screen metabolites that can serve as potential biomarkers. Compared with healthy individuals, CG group showed significant changes in the content of 101 metabolites, with an increase in the content of 54 metabolites and a decrease in the content of 47 metabolites. These differential metabolites are mainly composed of 47 lipids and lipid like substances. 1 metabolite was associated with bile reflux, 1 metabolite was associated with gastric mucosal erosion, 10 metabolites were associated with atrophy, 10 metabolites were associated with intestinal metaplasia, and 3 metabolites were associated with Helicobacter pylori infection. The ROC model composed of 5 metabolites can distinguish between CG group and healthy individuals, with an accuracy of 95.4%. The ROC model composed of 5,6-Dihydroxyindole can distinguish between chronic superficial gastritis group and chronic atrophic gastritis group, with an accuracy of 75.3%. The lipids and lipid like metabolites were the main abnormal metabolites in patients with chronic gastritis. It was worth noting that the content of Sphinganine 1-phase, 4-Ipomenol, and Nervonic acid in tongue coating increased, and the content of 1-Methyladenosine and 3-Hydroxycapric acid decreased, which helped to identify CG patients. The decrease in the content of 5,6-dihydroxyindole reminded patients that the development trend of CG was shifting from superficial to atrophic or even intestinal metaplasia. The detection of these metabolic markers of tongue coating was expected to be developed as a non-invasive and convenient technology in the future to assist us in monitoring and diagnosing the occurrence and development of CG.

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.

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.

Expression of Wnt3, β-catenin and MMP-7 in gastric cancer and precancerous lesions and their correlations with Helicobacter pylori infection.

To compare the expression of the Wnt signaling-associated proteins (Wnt3, β-catenin, MMP-7) in gastric cancer and precancerous lesions with positive and negative Helicobacter pylori (H.pylori, Hp) infection, and to further explore the mechanisms underlying the Wnt signaling pathway involving in the formation of gastric cancer and its relationship with Hp infection. The complete paraffin samples with pathologically confirmed diagnosis, who came from the First Hospital of Changsha from January 2018 to April 2020, were collected. All samples were randomly divided into a gastric cancer group (n=57), a precancerous lesion group (n=84), and a chronic superficial gastritis group (n=25). Improved Giemsa staining was used to detect Hp infection, and according the results of Hp infection the above groups were divided into a Hp positive subgroup and a negative subgroup. The expressions of Wnt3, β-catenin and MMP-7 were examined with immunohistochemistry. The Wnt3, β-catenin, and MMP-7 were highly expressed in the gastric cancer group and the gastric precancerous lesion group. The Wnt3 and MMP-7 were highly expressed in cytoplasm, and β-catenin showed a tendency of cell membrane transferring to cytoplasm and nucleus, which was characterized by "nuclear translocation". The positive rates of the Wnt3, β-catenin, and MMP-7 expressions in the gastric cancer group were higher than those in the precancerous lesion group and the chronic superficial gastritis group (all P<0.05), which showed a gradually increasing trend with the deterioration of differentiation degree. In addition, the expressions of Wnt3, β-catenin, and MMP-7 in the Hp positive subgroup in the gastric cancer group and the precancerous lesion group were higher than those in the Hp negative subgroup (all P<0.05). Aberrant activation of Wnt signaling pathway is involved in the occurrence and development of precancerous lesions and gastric cancer, and which is related with Hp infection. Meanwhile, the Wnt3, β-catenin and MMP-7 may be used as molecular markers for early diagnosis of gastric cancer and indicators to judge the degree of differentiation and malignancy of gastric cancer.

Protein expression trends of DNMT1 in gastrointestinal diseases: From benign to precancerous lesions to cancer.

BACKGROUNDIn recent years, the incidence of gastrointestinal (GI) cancer in China has increased annually. Early detection and appropriate therapy are considered to be the key to treat GI cancer. DNMT1 takes an active part in the advancement of GI cancer, which will change as the disease progresses. But its expression characteristics in the dynamic variations of GI carcinogenesis are still unclear.AIMTo investigate the expression characteristics of DNMT1 in different GI diseases.METHODSWe detected the expression of DNMT1 in 650 cases of different GI diseases by immunohistochemistry, including 90 cases of chronic superficial gastritis (CSG), 72 cases of atrophic gastritis with intestinal metaplasia (AG/GIM), 54 cases of low-grade intraepithelial neoplasia (GLIN), 66 cases of high-grade intraepithelial neoplasia (GHIN), 71 cases of early gastric cancer (EGC), 90 cases of normal intestinal mucosa (NIM), 54 cases of intestinal low-grade intraepithelial neoplasia (ILIN), 71 cases of intestinal high-grade intraepithelial neoplasia (IHIN), and 82 cases of early colorectal cancer (ECRC).RESULTSIn the CSG group, all cases showed weakly positive or negative expression of DNMT1. However, in other four groups (AG/GIM, GLIN, GHIN, and EGC), the positive expression rate gradually increased with the severity of the diseases; the negative or weakly positive cases accounted for 55.56% (40/72), 38.89% (21/54), 1.52% (1/66), and 1.41% (1/71), respectively. Besides, the moderately positive cases were 44.44% (32/72), 57.41% (31/54), 80.30% (53/66), and 43.66% (31/71), respectively. The strongly positive cases only existed in the GLIN (3.70%, 2/54), GHIN (18.18%, 12/66), and EGC (54.93%, 39/71) groups. The differences between any two groups were statistically significant (P < 0.05). Similarly, in the NIM group, cases with weakly positive expression of DNMT1 were predominant (91.11%, 82/90), and the rest were moderately positive cases (8.89%, 8/90). In the ILIN, IHIN, and ECRC groups, the rates of cases with weak or negative expression of DNMT1 were 46.30% (25/54), 12.68% (9/71), and 4.88% (4/82), respectively; with moderately positive expression were 53.70% (29/54), 71.83% (51/71), and 34.15% (28/82), respectively; and with strongly positive expression were 0.00% (0/54), 15.49% (11/71), and 60.98% (50/82), respectively. The differences between any two groups were also statistically significant (P < 0.05).CONCLUSIONThe overexpression of DNMT1 protein could effectively predict early GI cancers and severe precancerous lesions, which may have potential clinical application value.

Helicobacter pylori infection in Lhasa People's Hospital from 2009 to 2013

Objective To investigate the infection status of Helicobacter pylori (Hp) in a Lhasa hospital. Methods A retrospective survey of Hp infection from 2009 to 2013 was conducted in Lhasa People's Hospital. The data of 14C-urea breath test and gastroscopy were analyzed. Results A total of 2 908 patients were enrolled, 1 518 (52.20%) were Hp positive, including 1 061 males (1 061/1 939, 54.72%) and 457 females (457/969, 47.16%). The Hp infection rate in males was higher than that in females (χ2=14.788, P= 0.000). The Hp infection rate by years from 2009 to 2013 was 55.97%(267/477), 49.79%(239/480), 54.66%(375/686), 52.06%(291/559) and 49.15%(347/706), respectively. The infection rate in 2013 was significantly lower than that in 2009 and 2011 (P=0.021, 0.040). There were no significant differences in Hp infection rates among Tibetan, Han and Hui ethnic groups. In 2020 cases who underwent endoscopic examination, 1 098 had Hp positive (54.36%). The Hp infection rate in chronic superficial gastritis group(39.91%) was significantly lower than that in erosive gastritis (χ2=30.143, P=0.000), gastric ulcer (χ2=22.434, P=0.000), gastric polyps (χ2=9.627, P=0.002), gastric cancer (χ2=9.506, P=0.002), duodenal ulcer (χ2=54.158, P=0.000), duodenitis (χ2=14.966, P=0.000) and compound ulcer groups (χ2=8.582, P=0.003). The Hp infection rate in duodenal ulcer group(68.42%) was significantly higher than that in chronic superficial gastritis (χ2=54.158, P=0.000), erosive gastritis (χ2=6.733, P=0.009), atrophic gastritis (χ2=21.496, P=0.000) and gastric ulcer groups (χ2=8.940, P=0.003). Conclusion Hp infection rate appears a decreasing trend in Lhasa area in last 5 years; among various gastro-duodenal diseases patients with duodenal ulcer have a highest Hp infection rate. Key words: Helicobacter pylori; Gastrointestinal diseases; Retrospective studies

Association Between C1019T Polymorphism in the Connexin 37 Gene and Helicobacter Pylori Infection in Patients with Gastric Cancer

To investigate the association between the connexin 37 C1019T polymorphism and Helicobacter pylori infection in patients with gastric cancer. 388 patients with gastric cancer (GC), 204 with chronic superficial gastritis (CSG) were studied. H. pylori was detected by gastric mucosal biopsies biopsy dyeing method. Connexin 37 gene polymorphism 1019 site genotypes were determined by gene sequencing technology. Genotypes and alleles frequencies were compared. (1) Connexin37 gene 1019 site distribution frequency (CC type, TC type, TT type) in the CSG group was 18.1%, 45.1% and 36.8%; in the stomach cancer group it was 35.1%, 45.9% and 19.%, conforming to the Hardy-Weinberg euilibrium. (2) In comparison with CSG group, the frequency of Connexin37 C allele was higher in the gastric cancer group (58.0% vs 40.7%, OR=2.01, 95%CI=1.58-2.57, P<0.01). The prevalence of gastric cancer risk was significantly increased in the carriers of C allele (CC+TC) than in TT homozygote (OR=2.47, 5%CI=1.68-3.610. (3) Gastric cancer patients complicated with Hp infection 211 cases, gastric cancer group of the male patients with HP positive patients with 187 cases, 40 cases of female patients with negative patients, 24 cases were HP positive, negative in 137 cases, control group male patients, 28 cases were Hp positive, negative in 95 patients, female patients with Hp positive 6 cases, 75 cases were negative. On hierarchical analysis, the male group OR value was 15.9 (95%CI to 9.22-27.3), and the female OR was 2.19 (95%CI 0.88-5.59), indicating a greater contribution in males (P<0.01). After elimination of gender effects, positive HP and gastric cancer were closely related (OR 8.82, 95% CI: 5.45-14.3). (4) The distribution frequency of C allele in patients with Hp infection was much higher than that in Hp negative cases in the GC group (64.5% vs 47.0%, OR=2.05, 95%CI=1.54-2.74, P<0.01). Compared with TT homozygotes, (CC+TC) genotype prevalence of gastric cancer risk increased significantly (OR=2.96, 5%CI=1.76-2.99). The T allele in the connexin37 gene might not only be associated with gastric cancer but also with H. pylori infection.

Association of the human leukocyte antigen class II alleles with chronic atrophic gastritis and gastric carcinoma in Koreans

Gastric carcinogenesis is a multi-step process and is influenced by several etiological agents, including the host's genetic factors. Since whether a patient remains with chronic superficial gastritis (CSG) or progresses to either chronic atrophic gastritis (CAG) or gastric carcinoma (GC) could be a genetic predisposition unique in each population, we hypothesized that host human leukocyte antigen (HLA) alleles could be discriminative in predicting the risk of CSG progression to precancerous CAG and GC in Koreans. A total of 165 patients with gastric disorders (CSG, 62; CAG, 69 and GC, 34), were selected to investigate the association of HLA class II alleles with the progression of CSG to CAG or GC. HLA genotypes were obtained by the polymerase chain reaction-sequence based typing method. The phenotypic frequencies of DRB1*1101 and DQA1*0505 were significantly higher in the CAG group compared to those in the CSG group. In the subjects with Helicobacter pylori (H. pypori) (+), the frequencies of DRB1*1501 and DQB1*0602 were significantly lower in the CAG compared to those in the CSG. Further analysis showed that sex (P < 0.05, OR = 0.41-0.42) and age (P < 0.05, OR = 1.05) also affected the risk of progression from CSG to CAG in H. pylori (+) patients carrying the DRB1*1501 or DQB1*0602 allele. Additionally, the frequency of DRB1*0404 in the GC group was significantly higher than that in the gastritis group. Our findings strongly imply an association between HLA class II alleles and the risk of CAG development and GC progression in Koreans.

Distribution of H.pylori antigens in gastric mucosa and its significance.

To investigate the distribution of H.pylori antigens in the gastric mucosa in patients with H.pylori infection, and the relationship between the distribution and gastric cancer. Of 112 patients confirmed by pathological study to have chronic superficial gastritis, precancerous changes (chronic atrophic gastritis, intestinal metaplasia or atypical hyperplasia) and gastric cancer, 28 were H.pylori negative and 84 were H.pylori positive. H.pylori antigens in the gastric mucosa were detected by immunohistochemistry. The H.pylori positive group, comprised 12 of 22 (50.0%) in the chronic superficial gastritis group, 22 of 25 (88.0%) in the precancerous changes group and 13 of 35 (37.1%) in the gastric cancer group. The positive rates of H.pylori antigens in the cytoplasm progressively increased, respectively at 0.0% (0/12), 63.6% (14/22) and 84.6% (11/13) for the same groups (chi(2)=19.76, P=0.000); H.pylori antigens were located in the mucus layer and above the neck of the mucosal gland in 9 of 12 (75.0%) cases with chronic superficial gastritis, at the neck of the mucosal gland and the isthmus in 12 of 22 (54.5%) cases with precancerous changes, below the isthmus in 9 of 13 (69.2%) cases with gastric cancer (chi(2)=25.30, P=0.000). In the H.pylori negative group, no H.pylori antigen was observed. With the progression of chronic superficial gastritis-->precancerous changes-->gastric cancer, H.pylori antigens progressively migrated from the outer part to the inner part of the cell, and from the superficial to the deep gastric mucosa.

Inactivation of PTEN is associated with increased angiogenesis and VEGF overexpression in gastric cancer.

To investigate the expression of PTEN/MMAC(1)/TEP(1) and vascular endothelial growth factor (VEGF), their roles in biologic behavior and angiogenesis and their association in gastric cancer. Immunohistochemical staining was used to evaluate the expression of PTEN, VEGF and microvascular density (MVD) on paraffin-embedded sections in 70 patients with primary gastric cancer and 24 patients with chronic superficial gastritis (CSG). Expression of PTEN, VEGF and MVD were compared with clinicopathological features of gastric cancer. The relationship between expression of PTEN, VEGF and MVD as well as the relationship between PTEN and VEGF expression in cancer cells were investigated. PTEN expression significantly decreased (t = 3.98, P<0.01) whereas both VEGF expression and MVD significant increased (t = 4.29 and 4.41, respectively, both P<0.01) in gastric cancer group compared with CSG group. PTEN expression was significantly down-regulated (t = 1.95,P<0.05) whereas VEGF expression (t = 2.37, P<0.05) and MVD (t = 3.28, P<0.01) was significantly up-regulated in advanced gastric cancer compared with early-stage gastric cancer. PTEN expression in gastric cancer showed a negative association with lymph node metastasis (t = 3.91, P<0.01), invasion depth (t = 1.95, P<0.05) and age (t = 4.69, P<0.01). MVD in PTEN-negative gastric cancer was significantly higher than that in PTEN-positive gastric cancer (t = 3.69, P<0.01), and there was a negative correlation between PTEN expression and MVD (gamma= -0.363, P<0.05). VEGF expression was positively associated with invasion depth (especially with serosa invasion, t = 4.69, P<0.01), lymph node metastasis (t = 2.31, P<0.05) and TNM stage (t = 3.04, P<0.01). MVD in VEGF-positive gastric cancer was significantly higher than that in VEGF-negative gastric cancer (t = 4.62, P<0.01), and there was a positive correlation between VEGF expression of and MVD (gamma= 0.512, P<0.05). VEGF expression in PTEN-negative gastric cancer was significantly stronger than that in PTEN-positive gastric cancer (t = 2.61, P<0.05), and there was a significantly negative correlation between the expression of VEGF and PTEN (gamma= -0.403, P<0.05). Our results imply that inactivation of PTEN gene and over-expression of VEGF contribute to the neovascularization and progression of gastric cancer. PTEN-related angiogenesis might be attributed to its up-regulation of VEGF expression. PTEN and VEGF could be used as the markers reflecting the biologic behaviors of tumor and viable targets in therapeutic approaches to inhibit angiogenesis of gastric cancers.

The expression of hTERT mRNA and cellular immunity in gastric cancer and precancerosis.

To observe the expression of Human telomerase reverse transcriptase (hTERT) in gastric carcinomas and precancerosis lesions, to evaluate the immune state of such patients, and to then study the clinical significance of hTERT and immune state for the diagnosis, treatment and prognosis of gastric cancer. In situ hybridization was used to detect the expression of hTERT mRNA in 116 endoscopic of gastric mucosa. Analyzed tissue samples were as follows: 30 cases of chronic superficial gastritis (CSG), 44 of precancerosis lesions (including 27 of chronic atrophic gastritis, 8 of adenomatous polyp and 9 of gastric ulcer) and 42 of gastric cancer (GC). In addition, the T lymphocyte subsets (CD3(+), CD4(+), CD8(+), CD4(+)/CD8(+)) and natural killer cells (NK) in peripheral blood were determined by flow cytometric analysis (FCM) in 30 cases of CSG, 27 of precancerosis (chronic atrophic gastritis, CAG), and 42 of GC. The data were compared with those of normal control (NC). The detected positive rate of hTERT varied as follows: 86 % (36/42) in GC, 36 % (16/44) in precancerosis lesions and 0 % (0/30) in CSG. The expression of hTERT mRNA was not associated with patient gender, tumor location, macroscopic type, lymph node metastasis, or degree of differentiation. It was found that the CD3(+), CD4(+) of the CSG group were lower than that of NC (P<0.05). Meanwhile, the T lymphocyte subsets (CD3(+), CD4(+), CD4(+)/CD8(+) ratio) and NK cells of CAG were remarkably lower than that of NC and CSG groups (P<0.05-0.01). Values of T cells and NK cells of the GC group were significantly abnormal when compared with the CAG group (P<0.05-0.01). Furthermore, with tumor progression, the function of T cells was weakened gradually. The expression of telomerase may be a crucial step in gastric carcinogenesis and increased hTERT mRNA may serve as a novel marker for diagnosis of GC. The immune state of patients with GC and precancerosis was somewhat depressed, which indicates the importance of cellular immunological assays in cancer patients.

Study on clinical pathology and immunohistochemistry of chronic erosive gastritis.

To study the clinical pathology of chronic erosive gastritis (CEG) and determine the expression of epithelial tumor markers, oncoprotein p21 and carcinoembryonic antigen (CEA), and G cells by immunohistochemistry. Gastric mucosal biopsies from 40 CEG cases were examined. Histopathology and Helicobacter pylori (Hp) infection were determined by light microscopy. Thirty-one biopsies from CEG cases were immunostained with antibodies against p21, CEA, proliferation cell nuclear antigen (PCNA), and gastrin using the labeled streptavidin-biotin (LSAB) method. A total of 35/40 (87.5%) CEG lesions showed antral location; 75% of the lesions were associated with different degrees of atrophic change. Twenty percent presented with mild and moderate atypia of mucosal epithelia and 27.5% showed intestinal metaplasia. Acute inflammatory changes were observed in 25% of the cases. Hp was identified in 40.0% of the specimens. Immunohistochemistry studies showed that 67.7% of the CEG mucosal epithelial samples expressed oncoprotein p21 and 29.0% expressed CEA, rates significantly higher than those observed in control samples from a chronic superficial gastritis group. However, PCNA and gastrin expression in mucosal G cells was not significantly different between CEG samples and samples from the control group (P > 0.05). CEG is a chronic gastric mucosal proliferative lesion that expresses higher levels of p21 and CEA than control samples. Our observations suggest that antral location of the lesion and Hp infection do not participate in the pathological process of CEG.

Relationship between histology and gastric juice pH and nitrite in the stomach after operation for duodenal ulcer.

One hundred patients who had undergone operation for duodenal ulcer (68 vagotomy and gastroenterostomy; seven vagotomy and pyloroplasty; 22 gastrectomy and three gastroenterostomy) 10 or more years previously each underwent endoscopy. Biopsies were taken and gastric juice aspirated for measurement of pH and nitrite concentration. Patients were divided into five histological grades; chronic superficial gastritis (+/- minimal atrophic gastritis) (35), atrophic gastritis/intestinal metaplasia (30), mild dysplasia (21), moderate/severe dysplasia (13) and carcinoma (one). A wide spectrum of pH values was found with 35 patients having a fasting intragastric pH below 4.0 and 65 above 4.0. A strong relationship was found between histological grade and pH. Patients with chronic superficial gastritis had a fasting intragastric pH below 4.0 more frequently than those with moderate/severe dysplasia (p less than 0.001). Gastric juice nitrite concentrations were higher in the moderate/severe dysplasia group than in the chronic superficial gastritis group (p = 0.02). The strong correlation between pH and nitrite concentration, previously documented, was confirmed. The implications of these findings in the pathogenesis of carcinogenesis in the postoperative stomach are discussed.