Chronic Gastritis Patients Research Articles

Metabolomic Analysis of Gastric Cancer Progression within the Correa's Cascade Using Ultraperformance Liquid Chromatography-Mass Spectrometry.

Gastric cancer (GC) is among the most common cancers worldwide. Gastric carcinogenesis is a multistep and multifactorial process beginning with chronic gastritis induced by Helicobacter pylori (H. pylori) infection. This process is often described via a sequence of events known as Correas's cascade, a stepwise progression from nonactive gastritis, chronic active gastritis, precursor lesions of gastric cancer (atrophy, intestinal metaplasia, and dysplasia), and finally adenocarcinoma. Our aim was to identify a plasma metabolic pattern characteristic of GC through disease progression within the Correa's cascade. This study involved the analysis of plasma samples collected from 143 patients classified in four groups: patients with nonactive gastritis and no H. pylori infection, H. pylori infected patients with chronic active gastritis, infected or noninfected patients with precursor lesions of gastric cancer, and GC. Independent partial least-squares-discriminant binary models of UPLC-ESI(+)-TOFMS metabolic profiles, implemented in a decision-directed acyclic graph, allowed the identification of tryptophan and kynurenine as discriminant metabolites that could be attributed to indoleamine-2,3-dioxygenase upregulation in cancer patients leading to tryptophan depletion and kynurenine metabolites generation. Furthermore, phenylacetylglutamine was also classified as a discriminant metabolite. Our data suggest the use of tryptophan, kynurenine, and phenylacetylglutamine as potential GC biomarkers.

The application value in diagnosis of chronic atrophic gastritis using the magnifying endoscopy and narrow-band imaging

Objective To explore the application value in diagnosis of chronic atrophic gastritis using the magnifying endoscopy and narrow-band imaging. Methods A total of 98 cases of chronic atrophic gastritis patients was selected, and carried out the ordinary white light endoscopy, magnifying endoscopy and narrow-band imaging(ME-NBI) and pathological examination in file, followed by comparison of the results. Results The sensitivity and specificity of chronic atrophic gastritis by magnifying endoscopy and narrow-band imaging mode were 74.07% and 82.35%, respectively; which were significantly higher than that obtained by conventional endoscopy, which were 48.15% and 64.71% (P<0.05). In magnifying endoscopy and narrow-band imaging endoscopy group, 60 patients were positive, which intestinal metaplasia accounted for 35%, while in conventional endoscopy group, 39 patients were positive which was only 17.95% (P<0.05). Conclusions Magnifying endoscopy and narrow-band imaging can improve the diagnostic accuracy of chronic atrophic gastritis. Key words: Endoscopy/MT; Gastritis, atrophic/DI

Helicobacter pylori vacA Genotypes in Chronic Gastritis and Gastric Carcinoma Patients from Macau, China.

Helicobacter pylori is the major triggering factor for gastric carcinoma, but only a small proportion of infected patients develop this disease. Differences in virulence observed among H. pylori strains, namely in the vacuolating cytotoxin vacA gene, may contribute to this discrepancy. Infection with vacA s1, i1 and m1 strains increases the risk for progression of gastric premalignant lesions and for gastric carcinoma. However, in East Asian countries most of the H. pylori strains are vacA s1, regardless of the patients’ clinical status, and the significance of the vacA i1 and m1 genotypes for gastric carcinoma in this geographic area remains to be fully elucidated. The aim of the present study was to investigate this relationship in 290 patients from Macau, China. Using very sensitive and accurate genotyping methods, we detected infection with vacA i1 and with vacA m1 strains in, respectively, 85.2% and 52.6% of the patients that were infected with single genotypes. The prevalence of cagA-positive strains was 87.5%. No significant associations were observed between vacA genotypes or cagA and gastric carcinoma. It is worth noting that 37.5% of the infected patients had coexistence of H. pylori strains with different vacA genotypes. Additional studies directed to other H. pylori virulence factors should be performed to identify high risk patients in East Asia.

CHRONIC HELICOBACTER PYLORI GASTRITIS: THE ERADICATION EFFICACY&amp;NBSP;OF THE&amp;NBSP;BISMUTH-CONTAINING QUADRUPLE REGIMEN (EBMT)

Background: there has not been yet any research on the effectiveness of H. pylori eradication of bismuth-containing quadruple regimen on chronic gastritis patients in our country. Objective: to evaluate H. pylori eradication rate of bismuth-containing quadruple regimen according to intention to treat (ITT), per protocol (PP) analysis, the rate of side effects and medication compliance. Subjects and Methods: from March 2014 to January 2016 we used bismuth-containing quadruple regimen (EBMT) 10 days for H. pylori eradication therapy for 166 chronic gastritis patients diagnosed based on clinical, endoscopic, rapid urease test, histology and culture. Patients were evaluated side effects and medication compliance at the end of treatment (day 11-14). To assess the eradication, repeating endoscopy with both rapid urease test and histological examination were performed at 4 to 8 weeks after stopping treatment course. Results: H. pylori eradication rates on ITT and PP analysis overall, for naïve patients, after one and more two eradication failures were respectively: 80.72-89.33%, 79.51-90.65%, 91.67-91.67% and 75.00-78.95%. Medication adherence rate was 96.99%. The rates of patients experiencing moderate, severe and very severe side effects were: 19.88%, 0.60% and 1.81%. Conclusion: the EBMT 10-day regimen attained high eradication rates in chronic gastritis patients with rare serious side effects and the high compliance rate. We should apply bismuth-containing quadruple regimen in H. pylori eradication therapy for naïve patients or after one eradication failure. Key words: bismuth-containing quadruple regimen, EBMT, eradication, chronic Helicobacter pylori gastritis

An Observational Study on Aberrant Methylation of Runx3 With the Prognosis in Chronic Atrophic Gastritis Patients.

The aim of this study is to discuss whether the methylation levels of Runx3 could be used as the early biomarker for predicting the prognosis in chronic atrophic gastritis (CAG) patients. A total of 200 subjects including 60 controls without CAG (Group 1), 70 patients with mild CAG (Group 2), and 70 patients with moderate and severe CAG (Group 3) were recruited for this cross-sectional investigation in the Department of Gastroenterology in Daqing Oilfield General Hospital from July 2013 to May 2014. The MlALDI-TOF-MS was used to measure the methylation levels of Runx3 in all of the subjects. Real-time quantitative reverse transcription polymerase chain reaction and western blotting were chosen to determine the expression levels of Runx3. The correlations between methylation levels of Runx3 among these CAG patients and their prognosis were shown by logistic regression models. The results demonstrated that the methylation levels of CpG13, CpG14, and CpG15 in Runx3 were higher in Group 3 than those in Groups 1 and 2 (P <0.05), whereas the mRNA and protein expression levels of Runx3 were lower in Group 3 than those in Groups 1 and 2 (P <0.05). There were significantly negative correlations between the methylation levels of Runx3 with its expression and the healing prognosis of CAG patients. In brief, this study proved that the hypermethylation modifications of CpG13, CpG14, and CpG15 in the promoter region of Runx3 could result in the down regulation of Runx3 expression to affect the prognosis of CAG. So the methylation levels of these CpG sites in Runx3 in the peripheral blood can be used as the biomarker for predicting the healing prognosis of CAG patients.

EFFICACY OF RACM REGIMEN ON HELICOBACTER PYLORI ERADICATION IN PATIENTS OF CHRONIC GASTRITIS

Background: H. pylori eradication still remains a challenge to clinicians, especially with the increasing antibiotic-resistant H. pylori. Concomitant therapy showed effective, even in some multiresistant population, but data in Vietnam is still very limited. The study ''Study of Helicobacter pylori eradication with RACM regimen in chronic gastritis patients at Da Nang Hospital from 1/4/2014 to 30/6/2015, is aimed at: (1) Evaluating the results of Helicobacter pylori eradication of Amoxicillin-Clarithromycin-Rabeprazole-Metronidazole therapy for 14 days.(2) Assessing some side effects of this regimen.Method: prospective, consisting of 83 patients examined and treated in Danang hospital from1/ 4/2014 to 30/6/2015, H.pylori was tested by rapid Urease test; H.pylori positive patients received RACM for 14 days. Results: H.pylori eradication rate was 83.1%. H. pylori eradication rates in different locations: antrum 63.8%, higher than corpus (17.4%), antrum and corpus (18.8%), with statistical significance at p&lt;0.05. Common side effects was nausea (27.7%), diarrhea (19.3%). Abdominal pain, lightheadedness, dizziness, insomnia, headache account for low percentage: 8%; 6%; 3,6% and 2.4% respectively. Conclusion: The effect of 14 day RACM regimen for H. pylori eradication was 83.1%, common side effects are nausea (27.7%), diarrhea (19.3%). Key words: chronic gastritis;H. pylori; eradication of H. pylori(ITT); RACM regimen.

Combined Secretomics and Transcriptomics Revealed Cancer-Derived GDF15 is Involved in Diffuse-Type Gastric Cancer Progression and Fibroblast Activation.

Gastric cancer is classified into two subtypes, diffuse and intestinal. The diffuse-type gastric cancer (DGC) has poorer prognosis, and the molecular pathology is not yet fully understood. The purpose of this study was to identify functional secreted molecules involved in DGC progression. We integrated the secretomics of six gastric cancer cell lines and gene expression analysis of gastric cancer tissues with publicly available microarray data. Hierarchical clustering revealed characteristic gene expression differences between diffuse- and intestinal-types. GDF15 was selected as a functional secreted molecule owing to high expression only in fetal tissues. Protein expression of GDF15 was higher in DGC cell lines and tissues. Serum levels of GDF15 were significant higher in DGC patients as compared with healthy individuals and chronic gastritis patients, and positively correlated with wall invasion and lymph node metastasis. In addition, the stimulation of GDF15 on NIH3T3 fibroblast enhanced proliferation and up-regulated expression of extracellular matrix genes, which were similar to TGF-β stimulation. These results indicate that GDF15 contributes to fibroblast activation. In conclusion, this study revealed that GDF15 may be a novel functional secreted molecule for DGC progression, possibly having important roles for cancer progression via the affecting fibroblast function, as well as TGF-β.

Helicobacter pylori Infection Increases Frequency of PDCA-1+ (CD317+) B-cell Subsets

As a newly discovered B-cell subset, PDCA-1(+) Bcells have been shown to participate in the immune clearance of invading pathogens. The prominence of PDCA-1(+) Bcell immunity in the pathogenesis of Helicobacter pylori infection prompted us to explore the potential role of this subset in gastric H. pylori infection. H. pylori infection was determined by (14)C-urea breath test and Western blot. The frequency of the different sub-compartments of PDCA-1(+) Bcells and their relation to serum cytokines was determined in 33 H. pylori-infected and 14 uninfected patients and in 12 healthy controls (HC). In comparison to uninfected individuals, there was a significantly increased frequency of PDCA-1(+) Bcells, PDCA-1(+)IgM(+) Bcells, CD93(+)PDCA-1(+) Bcells, CD93(+)PDCA-1(+)IgM(+) Bcells, CD137(+)PDCA-1(+) Bcells and CD137(+)PDCA-1(+)IgM(+) Bcells were detected in patients with H. pylori infection, corresponding to increased levels of serum IFN-α and IgM in this group. Compared with H. pylori-positive (HP(+)) chronic non-atrophic gastritis patients, a larger proportion of PDCA-1(+) Bcells, CD93(+)PDCA-1(+) Bcells and CD137(+)PDCA-1(+) Bcells were observed in HP(+) patients suffering from atrophic gastritis or HP(+) peptic ulcers. The frequency of the PDCA-1(+) Bcell compartment is increased during H. pylori infection. Our data support the potential role of this B-cell subset in the pathogenesis of H. pylori-dependent gastritis.

Quadruple regimens using domestically manufactured drugs in gastritis and duodenal ulcer patients for Helicobacter pylori eradication: a perspective, multicenter, randomized controlled trial

To observe the effects and safety of quadruple regimens including domestically manufactured rabeprazole used as first line/initial therapy for Helicobacter pylori(H.pylori) eradication in gastritis and duodenal ulcer patients, and to investigate the effects of extended use of bismuth after the quadruple therapy on eradication of H. pylori. From January to August 2013, 430 patients with chronic gastritis or duodenal ulcer who were confirmed as H. pylori positive in gastroscopy for upper gastrointestinal symptoms were enrolled from 12 centers in China for initial treatment using quadruple regimens for H. pylori eradication. The study was a prospective, multicenter, randomized double-blinded double-dummy parallel-controlled clinical trial. The 310 chronic gastritis patients were divided into 2 groups: group A1 was given quadruple regime (rabeprazole+ amoxicillin+ clarithromycin+ bismuth potassium citrate) for 10 days followed by bismuth-placebo for 21 days; group A2 was given the quadruple regimen for 10 days and then bismuth potassium citrate for 21 days. The duodenal ulcer patients were given the quadruple for 10 days, then rabeprazole for 14 days. All the patients took (13)C urea breath test to detect H. pylori 28 days after medicine withdrawal. Altogether 428 cases were enrolled and 404 completed the trial. The total eradication rate in the chronic gastritis patients was 85.1% (262/308, intention-to-treat (ITT)analysis), which was 81.7% (125/153, ITT) in the A1 group and 88.4% (137/155, ITT) in the A2 group; the eradication rate in the duodenal ulcer patients was 85.8% (103/120, ITT). No severe adverse effects were reported. The symptoms (pain, burning sensation, reflux, belching, nausea, and vomiting) improvement status was similar among A1 and A2 groups. The quadruple regimen using rabeprazole manufactured in China and administered for 10 days as first line/initial therapy in chronic gastritis and duodenal ulcer patients could achieve good H. pylori eradication rate. The extended use of bismuth after 10-day quadruple regimen might further improve the eradication rate. The regimens containing proton-pump inhibitor and bismuth may be well tolerated and safe in clinical application.

Association between serum levels of high sensitive C-reactive protein and inflammation activity in chronic gastritis patients

ABSTRACTBackground Gastritis is an important premalignant lesion and recent studies suggested a production of inflammatory cytokine-like C-reactive protein during gastritis. This study aimed to determine any relationship between high sensitive C-reactive protein (hs-CRP) and inflammation activity among patients with gastritis. Methods Demographic and clinical variables of participants were collected by a validated questionnaire. Using histology of the gastric mucosa, Helicobacter pylori status was investigated and serum concentrations of hs-CRP were measured among dyspeptic patients. Correlation between hs-CRP serum levels and inflammation activities was evaluated by logistic regression analysis. The relation between active inflammation and other variables was evaluated by logic link function model. Results Totally 239 patients (56.6% female) were analysed. The prevalence of mild, moderate and severe inflammation activities was 66.5%, 23.8% and 9.6% respectively. Mean ± SD of hs-CRP among men and women were 2.85 ± 2.84 mg/dl and 2.80 ± 4.80 mg/dl (p = 0.047) respectively. Mean ± SD of hs-CRP among patients with H. pylori infection, gland atrophy, metaplasia and dysplasia were 2.83 ± 3.80 mg/dl, 3.52 ± 5.1 mg/dl, 2.22 ± 2.3 mg/dl and 5.3 ± 5.04 mg/dl respectively. Relationship between hs-CRP and inflammation activities (p < 0.01) was significant. A significant relationship between dysplasia and hs-CRP (p < 0.04) was revealed. A significant relationship between age and hs-CRP was detected (p < 0.05). Conclusion Although serum hs-CRP is not a specific biomarker for gastritis, elevated hs-CRP levels may be considered as a predictive marker of changes in gastric mucosa and a promising therapeutic target for patients with gastritis.

Complete Genome Sequence of Helicobacter pylori Strain 7C Isolated from a Mexican Patient with Chronic Gastritis.

Helicobacter pylori-induced gastritis is a risk factor for developing gastric pathologies. Here, we report the complete genome sequence of a multidrug-resistant H. pylori strain isolated from a chronic gastritis patient in Mexico City, Mexico. Nonvirulent VacA and cag-pathogenicity island (PAI) genotypes were found, but the presence of a potential mobilizable plasmid carrying an IS605 element is of outstanding interest.

Eradication of Helicobacter pylori Infection Restores ki67, p53, and Cyclin D1 Immunoreactivity in the Human Gastric Epithelium.

INTRODUCTIONWe evaluated the effect of Helicobacter pylori (HP) eradication on p53, cyclin D1 expression, and cell proliferation in gastric mucosa.MATERIALS AND METHODSWe assessed p53, cyclin D1, and ki67 immunoexpression in gastric mucosa from 31 HP chronic gastritis patients and 12 controls. Reassessment was performed 6 months after successful HP eradication.RESULTSSuccessful eradication resulted in significant decrease of p53 (1.53 ± 0.16 vs 0.83 ± 0.19, P = 0.01) and ki67 (9.84 ± 0.96 vs 4.77 ± 0.27, P < 0.001) staining in the antrum. Similarly, p53 immunoreactivity significantly decreased in the corpus (1.27 ± 0.20 vs 0.46 ± 0.15, P = 0.02), while there was a trend for decreased corpus cyclin D1 and ki67 expression (0.17 ± 0.07 vs 0.0, P = 0.08 and 8.71 ± 1.24 vs 5.85 ± 0.54, P = 0.09, respectively). Importantly, after successful HP eradication, the immunoreactivity of the studied parameters was similar to that of controls.CONCLUSIONSuccessful HP infection eradication restores p53, cyclin D1, and ki67 immunoreactivity in the gastric mucosa to the level of controls.

TCF7L2 rs7903146 polymorphism is associated with gastric cancer: A case-control study in the Venezuelan population.

To explore the association between TCF7L2 rs12255372 and rs7903146 single nucleotide polymorphisms (SNPs) and gastric cancer risk in Venezuelan patients. We performed a case-control study including 122 paraffin-embedded archived intestinal-type gastric cancer samples and 129 biopsies obtained by superior endoscopy from chronic gastritis patients. Gastric cancer samples were classified according the degree of carcinoma differentiation. Genomic DNA was extracted from tissues, and the two SNPs of TCF7L2 gene (rs12255372 and rs7903146) were genotyped by polymerase chain reaction-restriction fragment length polymorphism reactions. Multiple regression analysis with adjustments for age and gender were performed and best-fitting models of inheritance were determined. Statistic powers were post-hoc calculated. After adjusting for age and sex the TCF7L2 rs7903146 TT genotype was associated with gastric cancer risk under the recessive genetic model (OR = 3.11, 95%CI: 1.22-7.92, P = 0.017). We further investigated the distribution of rs12255372 and rs7903146 genotypes according gastric cancer stratified by degree of differentiation, and we observed that carriers of rs7903146 T allele (CT + TT vs CC) had a significantly increased risk of moderate/well differentiated gastric cancer (dominant model, OR = 2.55, 95%CI: 1.35-4.80, P = 0.004), whereas the rs7903146 TT genotype was associated with poorly differentiated gastric cancer in the recessive model (OR = 3.65, 95%CI: 1.25-10.62, P = 0.018). We did not find association between rs12255372 SNP and the susceptibility of developing gastric cancer. TCF7L2 rs7903146 polymorphism is associated with gastric cancer risk in the Venezuelan population, and could be related to determine the degree of differentiation of tumor cells.

Factors affecting occurrence of gastric varioliform lesions: A case-control study.

To investigate the factors influencing the occurrence of gastric varioliform lesions (GVLs) and their possible link with gastric cancer. A 1:1 matched case-control study was performed to retrospectively analyze data from 1638 chronic gastritis patients who had undergone gastroscopy at one of two Chinese hospitals between 2009 and 2014. Patients with GVLs (cases) were compared to those without such lesions (controls). Endoscopic and pathological findings were recorded, along with interview information on Helicobacter pylori (H. pylori) infection, medical, drug and family histories, lifestyle and eating habits. The association between each factor and the occurrence of GVLs was estimated, and then multivariate conditional logistic regression was used to evaluate the independent factors. The frequency and severity of glandular atrophy, intestinal metaplasia (IM) and low-grade intraepithelial neoplasia were significantly increased in the GVL group (P < 0.01). Overall analysis showed that H. pylori infection [3.051 (2.157, 4.317), P <0.001], allergic respiratory diseases [3.636 (2.183, 6.055), P < 0.001], work-related stress [2.019 (1.568, 2.600), P < 0.001], irregular meals [2.300 (1.462, 3.619), P < 0.001], high intake of spicy food [1.754 (1.227, 2.507), P = 0.002] and high intake of fresh fruit [0.231 (0.101, 0.529), P = 0.001] were significantly correlated with the occurrence of GVLs (positively, except for the latter). Stratified analyses indicated that pickled food consumption in patients over 50 years old [7.224 (2.360, 22.115), P = 0.001] and excessive smoking in men [2.013 (1.282, 3.163), P = 0.002] were also positively correlated, and that, for antral GVLs, vegetable consumption [0.491 (0.311, 0.776), P = 0.002] was negatively correlated. Seven risk factors and two protective factors are determined for GVLs, which were found to be associated with premalignant abnormalities.

Expression and clinical significance of cyclooxygenase-2 and interleukin-32 in primary gastric B-cell lymphoma.

Cyclooxygenase-2 (COX-2) and interleukin-32 (IL-32) expression has been examined in various carcinomas and inflammations, and has been suggested to be significant in tumor progression and prognosis. The present study was conducted to investigate the expression of COX-2 and IL-32 in primary gastric B-cell lymphoma in order to define their clinical significance and their association with Helicobacter pylori (Hp) infection. COX-2 and IL-32 protein expression was detected in 31 primary gastric B-cell lymphoma patients and 19 chronic gastritis patients with immunohistochemistry. COX-2 and IL-32 expression was significantly higher in primary gastric lymphoma (PGL) tissues compared with gastritis tissues (51.6 vs. 21.1% for COX-2, P=0.032; and 58.1 vs. 26.3% for IL-32, P=0.029) and was significantly higher in Hp+ lymphoma tissues compared with Hp- lymphoma tissues (66.7 vs. 20% for COX-2, P=0.015; and 71.4 vs. 30% for IL-32, P=0.029). In the PGL tissues, the expression level of COX-2 was positively correlated with the expression level of IL-32, and the two were each positively correlated with Hp infection (P=0.004 for COX-2 and IL-32; P=0.01 for COX-2 and Hp infection; and P=0.003 for IL-32 and Hp infection). COX-2 expression was found to be significantly associated (P<0.05) with an aggressive tumor type, higher expression of Ki-67, frequent lymph node metastasis and advanced stage. IL-32 expression was found to be significantly correlated (P<0.05) with frequent lymph node metastasis and an advanced stage. The survival time was longer in the COX-2- and IL-32- lymphoma patients compared with the COX-2+ and IL-32+ lymphoma patients, but these differences were not statistically significant. These results suggested that Hp infection and the expression of COX-2 and IL-32 were closely linked with each other, and that the overexpression of COX-2 and IL-32 was correlated with tumor progression in primary gastric B-cell lymphoma, thus indicating potential novel therapeutic target.

DETERMINATION OF MUTATIONS IN 23S RRNA GENE OF HELICOBACTER PYLORI AND THE ASSOCIATION OF THESE GENE MUTATIONS WITH CLARITHROMYCIN-RESISTANCE IN CHRONIC GASTRITIS

Background: Resistance of Helicobacter pylori to clarithromycin is mostly due to the point mutations in the 23S rRNA. The aims of the present study were to determine mutations in domain V of 23S rRNA gene of Helicobacter pylori in chronic gastritis patients by sequencing; and to assess the association of these mutations with clarithromycin-resistant phenotype determined by E-test. Patients and methods: Gastric mucosal biopsy specimens from 170 patients with chronic gastritis were entered in the study. DNA was extracted from biopsy specimens obtained by endoscopy and prepared for sequencing domain V of gene 23S rRNA. 80 biopsy specimens were determined MIC by E-test. Results: Eight point mutations were detected. At 2142 and 2143 sites of gene, A2143G and A2142G mutations were detected in 35.3% and 3.5%, respectively. Six remaining mutations were G2172T (0.6%), T2182C (86.5%), C2195T (5.3%), A2223G (42.9%), T2244C (98.2%) và A2302G (8.8%). A2143G mutation was associated with clarithromycin-resistant phenotype, OR = 368.58 (95%CI: 34.53 – 3934.12). The rate of clarithromycin-resistance in the group with A2143G mutation was 96.7%, while in the group without A2143G mutation was 10%. Predicted probabilities for clarithromycin-resistance were calculated by logistic regression model with the accuracy rate of 96.1%. Conclusions: There was the association between A2143G mutation and clarithromycin-resistant phenotype. Genotypes determined by sequencing domain V of 23S rRNA gene could be used to predict the probabilities of clarithromycin-resistance. Key words: 23S rRNA gene, clarithromycin-resistance, Helicobacter pylori

Clinical aspects of chronic gastritis in patients with concomitant arterial hypertension

Aim: The work deals with special features of chronic gastritis clinical course with comorbid arterial hypertension.Methods: 96 patients underwent complex examination: 62 patients with combined clinical course of arterial hypertension and chronic gastritis and 34 ones with isolated chronic gastritis. All patients underwent clinical, laboratory and instrumental examination.Result: At analysis of results it was established that in the 1 group of patients took place the more heavy clinical course and the main complaints were presented as pain syndrome (of an acute, nagging character especially in epigastric zone or without strict localization that took place after ingestion), dyspeptic syndrome (with predominant meteorism, spreading feeling in epigastrium and eructation) and asthenoneurotic syndrome (with sleep disorders, general weakness and work disability) as opposed to patients of the 11 group whose pain syndrome was predominantly stable or periodic of an acute character in epigastric zone. Among complaints that are specific for dyspeptic syndrome prevailed eructation, spreading feeling in epigastrium and nausea. At the same time the chronic gastritis duration and pain syndrome intensity correlated with helicobacterial infection and comorbidity.Conclusions: Combined pathology is characterized with more intense clinical symptomatology as a direct consequence of mutual influence of diseases. The researches aimed at the study of clinical features of comorbid states allow the grounded approach to its therapy with special attention to all aspects of interaction

Randomized double-blind clinical trial of Moluodan () for the treatment of chronic atrophic gastritis with dysplasia.

To assess the efficacy and safety of Moluodan () in treating dysplasia in chronic atrophic gastritis (CAG) patients. This was a multi-centered, double-blind, randomized controlled trial. The total of 196 subjects were assigned to receive either Moluodan or folic acid in a 2:1 ratio by blocked randomization. Mucosa marking targeting biopsy (MTB) was used to insure the accuracy and consistency between baseline and after 6-month treatment. Primary outcomes were histological score, response rate of pathological lesions and dysplasia disappearance rate. Secondary endpoints included gastroscopic findings, clinical symptom and patient reported outcome (PRO) instrument. Dysplasia score decreased in Moluodan group (P =0.002), significance was found between groups (P =0.045). Dysplasia disappearance rates were 24.6% and 15.2% in Moluodan and folic acid groups respectively, no significant differences were found (P =0.127). The response rate of atrophy and intestinal metaplasia were 34.6% and 23.0% in Moluodan group, 24.3% and 13.6% in folic acid group. Moluodan could improve erythema (P =0.044), and bile reflux (P =0.059), no significance between groups. Moluodan was better than folic acid in improving epigastric pain, epigastric suffocation, belching and decreased appetite (P <0.05), with symptom disappearance rates of 37% to 83%. Moluodan improved dysplasia score in histopathology, and erythema and bile reflux score in endoscopy, and superior to folic acid in improving epigastric pain, epigastric suffocation, belching and decreased appetite. [ChiCTR-TRC-00000169].

Effect of Rebamipide on the Premalignant Progression of Chronic Gastritis: A Randomized Controlled Study.

Chronic gastritis frequently progresses into precancerous intestinal metaplasia and intraepithelial neoplasia lesions. Rebamipide is a free radical scavenger and we assessed its efficacy on clinical symptoms, gastric mucosal lesions, pathologic grade, and immunohistochemistry in chronic gastritis patients. 178 eligible patients were randomized into treatment and control groups. Both groups followed an optimized lifestyle for 26 weeks, but the treatment group was additionally medicated with rebamipide 0.1 g three times per day. Upper gastrointestinal endoscopy was performed in all patients to evaluate the severity of gastritis by the Modified Lanza Scoring (MLS) and histological changes were evaluated by the Updated Sydney System Score (USSS). Gastric mucosa immunohistochemistry in the treatment group was performed using the intestinal metaplasia markers caudal type homeobox transcription factor 2 (CDX2) and trefoil factor 3 (TFF3) detection. There were significant outcome differences between the treatment and control groups regarding the clinical symptom scores (2.62 ± 1.86 vs. 1.55 ± 1.61, P = 0.0001), gastric mucosal lesion scores (0.57 ± 1.05 vs. 0.16 ± 0.90, P = 0.002), and inflammation (P < 0.05). Only in the treated patients were the rates of intestinal metaplasia (P = 0.017 vs. P = 0.123) and low-grade intraepithelial neoplasia (P = 0.005 vs. P = 0.226) significantly reduced after 26 weeks. The percentages of CDX2 (31.5 vs. 15.7%, P = 0.021) and TFF3 (44.9 vs. 25.8%, P = 0.012) expressing gastric mucosa cells were significantly lower after rebamipide medication than pre-treatment values. Rebamipide improved the clinical symptoms, gastric mucosal lesions, and pathological grades of chronic gastritis patients and decreased the expression rates of CDX2 and TFF3 in gastric cells.

Intermittent treatment of recurrent type-1 gastric carcinoids with somatostatin analogues in patients with chronic autoimmune atrophic gastritis

BackgroundOptimal management and treatment of type-1 gastric carcinoids is under debate. AimsThis prospective study evaluates the outcome of patients with recurrent type-1 gastric carcinoids treated with somatostatin analogues. MethodsFrom 2000 to 2013, among a population of 107 chronic atrophic gastritis patients, 25 (20% males, median age 62 years) developed type-1 gastric carcinoids and underwent regular clinical and endoscopic follow-up (median 77 months, range 6–165) after the initial treatment. Those patients showing recurrent disease were treated with somatostatin analogues until carcinoid disappearance. Results12/25 patients (33% males, median age 65 years) showed recurrent gastric carcinoids and were treated with somatostatin analogues for a median duration of 12 months. Median gastrin and chromogranin A levels, which were 802pg/mL and 33U/L, respectively, decreased to 299pg/mL (p=0.002) and 15.6U/L (p=0.001) at the end of the treatment. Gastric carcinoids disappeared after a median length of treatment of 12 months. After a median time of 19.5 months from somatostatin analogues discontinuation, 4/12 patients (25% males, median age 56 years) showed a further recurrence. A new cycle of treatment was performed successfully. ConclusionsThis study confirms that type-1 gastric carcinoids are a recurring disease and somatostatin analogues, administered on 12-month cycles, represent an effective treatment.