Severe Gastritis Research Articles

Association of eating habits and clinical symptoms in atrophic gastritis patients

Atrophic gastritis is one of the most common gastric diseases, and many risk factors may increase the risk. This study aimed to assess the relationship between dietary factors and clinical symptoms of patients with atrophic gastritis. A cross-sectional study was conducted from October 2018 to October 2020 in the Center of Gastroenterology and Hepatology of Bach Mai Hospital with a total of 3508 atrophic gastritis patients aged ≥40 years (female/male ratio was 1.68). All patients were interviewed based on a designed questionnaire and underwent a gastroscopy procedure. The most common symptoms were epigastric pain (73.9%), belching/heartburn (42.4%), the feeling of fullness (41%), reflux symptom (15.4%). A majority of patients had mild atrophic gastritis (C1, C2) (80.4%), followed by moderate atrophic gastritis (C3, O1) (17%), and severe atrophic gastritis (O2, O3) (2.6%). A diet with much deep-fried or grilled food increased the risk of epigastric pain (OR 1.343; 95%CI 1.002-1.801); diets with much meat or nuts increased the risk of the feeling of fullness (meat: OR 1.296; 95%CI 1.100-1.526 and nuts: OR 1.316; 95%CI 1.033-1.676), and belching/heartburn (meat: OR 1.243; 95%CI 1.058-1.461 and nuts: OR 1.376; 95%CI 1.082-1.751). Diets with much salt or nuts increased the risk of reflux symptoms (salt: OR 1.359; 95%CI 1.055-1.752 and nuts: OR 1.532; 95%CI 1.023-2.293). A diet with many vegetables was a protective factor that can help to decrease the risk of moderate and severe atrophic gastritis (OR 0.616; 95%CI 0.403-0.941). In conclusion, diets and food types are factors that affect the risk of clinical symptoms among patients with atrophic gastritis, so the action of adjusting diets and daily food also play an important role in atrophic gastritis.

Interleukin-1β and Interleukin-1 receptor antagonist gene polymorphism in pediatric patients with Helicobacter pylori-associated chronic gastritis.

The severity of Helicobacter pylori infection is determined by the interplay between bacterial virulence, host genetic and environmental factors. This study aimed to identify interleukin-1 beta (IL-1β) and interleukin receptor antagonist (IL-1RN) gene polymorphisms and their associations with H. pylori infection, and severity of chronic gastritis in Egyptian children. A case control study was conducted on 100 children (50 H. pylori positive and 50 controls). Genotyping of IL-1β-31 gene was done by PCR-CTPP (confronting two-pair primers), of IL-1β-511 was performed using allele specific PCR, and investigation of the variable number tandem repeat polymorphism of the IL-1RN gene was done by PCR. The genotype C/T of IL1β-511 was the predominant genotype (36/50; 72%) among H. pylori positive cases (p ≤ 0.001). The presence of C/T genotype at position 511 of IL1β was associated with increased risk of infection with H. pylori (p ≤ 0.001, odds ratio = 6.612) and with more severe disease (p = 0.004, odds ratio = 8.333). No association of IL-1β-31 or IL-1RN gene polymorphisms with H. pylori infection or with risk of severe gastric diseases was found. Children who carry two polymorphisms are almost four times at risk for development of H. pylori infection (p = 0.026, odds ratio = 3.937). Polymorphism at position -511 of IL1β gene is associated with increased risk of H. pylori infection as well as of severe corpus gastric disease in Egyptian children. This population should be considered a high-risk group, which needs regular gastric endoscopic surveillance, and should be target for H. pylori eradication. Lay summaryThe genotype C/T of IL1β-511 gene was the predominant genotype (36/50; 72%) among H. pylori positive children. Polymorphism at position -511 of IL1β gene is associated with increased risk of Helicobacter pylori infection as well as of severe corpus gastric disease in Egyptian children. No association of IL-1β-31 or IL-1RN gene polymorphisms with H. pylori infection or with risk of severe gastric diseases in Egyptian children.

The role of T helper 17 cells in Helicobacter pylori associated chronic gastritis

Background: T helper 17 (Th-17) cell, a proinflammatory subset of CD4 T cells, have an essential role in immunity against Helicobacter pylori (H. pylori) infection. Objectives: This study aimed to evaluate expression of selected Th-17 cells associated cytokines (IL17, IL-21, IL-22, IL-23, IL-26 and TNF-α) in H. pylori-infected patients and to recognize their responsibility in H. pylori associated chronic gastritis with different severity. Methodology: This study is a case control study. The case group included 25 H. pyloripositive patients suffering from chronic gastritis. The control group included 25 age and sex-matched healthy individuals without any dyspeptic symptoms and negative for H. pylori. Infection with H. pylori in all participants was determined by detection of H. pylori stool antigen by enzyme-linked immunosorbent assay (ELISA) kit. Certain cytokines expression (IL-17, IL-21, IL-22, IL-23, IL-26 and TNF-α) in serum samples from all participants were tested using ELISA. Results: Comparing the serum cytokines expression in cases and controls, IL-17, IL-21 IL-23 and TNF-α were significantly higher in cases while IL-22 and IL-26 were higher in cases but not statistically significant. Both serum IL-17 and TNF-α expressions were statistically significant higher in cases with moderate or severe forms of chronic gastritis than in cases with mild form of chronic gastritis. However, the levels of IL-21, IL-22, IL-23 and IL-26 showed insignificant variation regarding chronic gastritis severity. Conclusion: Th-17 cells are responsible for the pathogenesis of H. pylori infection and the severity of gastritis. So, down regulation of Th-17 cells associated cytokines offers a promising therapy to diminish H. pylori associated gastritis.

Differential E-cadherin expression in helicobacter-related gastric pathology

Background and aims E-cadherin plays an important role in the maintenance of cell–cell adhesion. Loss of E-cadherin expression is fundamental in the development of many epithelial malignancies. Helicobacter pylori (H. pylori) is an important etiological factor in the development of many gastric diseases, including gastritis, peptic ulcer disease, and gastric carcinoma. In this study, we related different histopathological findings to the absence and presence of helicobacter infection, and investigated E-cadherin expression in H. pylori-negative and H. pylori-positive gastritis. This study aimed to find the prevalence of H. pylori colonization in chronic gastritis patients and its association with different histomorphological changes of chronic gastritis. Also, we aimed to evaluate E-cadherin expression in chronic gastritis as a prestage in the development of gastric carcinoma, and its relation to H. pylori. Materials and methods In total, 40 cases of gastritis samples were obtained by endoscopy; hematoxylin and eosin staining, Giemsa stain, and E-cadherin immunostain were done; we related different histopathological findings to the absence and presence of helicobacter infection. Also, we reported the changes in E-cadherin expression in relation to histopathological findings of chronic gastritis, and investigated E-cadherin expression in H. pylori-negative and H. pylori-positive gastritis. Results H. pylori was seen in 62.5% of cases. There was a statistically significant correlation between the presence of H. pylori and increase of the severity of chronic inflammation, neutrophilic activity, and presence of glandular atrophy (P=0.05, 0.003, and 0.04), respectively. Also, there was a significant decrease in E-cadherin expression with the increase in the severity of chronic inflammation, neutrophilic activity, and presence of glandular atrophy (P=0.04, 0.05, and 0.03), respectively. A statistically significant correlation between the presence of H. pylori and decrease in E-cadherin expression was found (P=0.01). Conclusion In chronic gastritis, there is high prevalence of H. pylori infection and decrease in E-cadherin expression. Also, there is an increase in the severity of chronic gastritis with the increase in the prevalence of H. pylori and this is associated with a decrease in E-cadherin expression, which precedes gastric carcinoma.

Gastric cancer – histopathological correlations between tumor and non-tumor gastric mucosa changes

Gastric cancer is a widely geographically distributed malignancy with high prevalence, therefore being a serious health problem that needs standardized methods for early diagnosis and treatment. The aim of the study was to evaluate the correlation of some epidemiological and clinical data with the histological features. The study group was made up of 66 patients that underwent surgical removal of the gastric neoplasm, and the pathological exam showed the morphological features of the tumor, as well as the ones of the unaffected mucosal tissue. Topographically, the highest incidence of the tumor was registered in the gastric antrum, but in recent years, an increased incidence of the superior gastric pole localization was recorded. The macroscopic aspects reveal that the ulcerated type 2 Borrmann is the most frequent, and alongside type 3 Borrmann, the ulcer-infiltrative type represents most of the gastric antrum cancers. The analysis of the tumor invasion showed that most carcinomas underwent surgery when the tumor invaded the serosa (pT3) or even the perigastric tissues (pT4). In our research, we chose Goseki’s microscopic classification because of its best coverage of the histological heterogeneity of the gastric carcinomas, providing information about the percentage of the cellular and secretory differentiation with direct impact on the invasion of the tumor. In more than 70% of the cases, the patients showed lesions of severe chronic atrophic gastritis of the non-tumor mucosa. Lately, the incidence of Helicobacter pylori has been 5.5%, lower than indicated by mainstream literature. We observed that the incidence of type 3 incomplete intestinal metaplasia, as the most commonly involved factor in the etiopathogenesis of gastric neoplasms, was encountered in 36.3% of the cases, this percentage rising proportionally with age and being frequently associated with antrum tumors. In conclusion, the permanent analysis of the relation between epidemiological data and some histological features might be relevant for the characterization of the tumoral process or the non-tumor gastric mucosa, leading to an evaluation of the prognosis.

Gastric Polyps and Atrophic Gastritis

Aim. A study of atrophic gastritis severity and rate in patients with gastric polyps (GP).Materials and methods. The study enrolled 61 patients with hyperplastic (HGP) and 41 — with adenomatous GP (AGP). All patients had 24-h gastric pH-metry, control of the pepsinogen I, II and gastrin-17 levels, in addition to a general clinical, endoscopic, histological examination and testing for Helicobacter pylori.Results. GP patients had benign manifestations prevailed with epigastric heaviness and overflow, and a scarce history of H. pylori testing at no control of rendered eradication therapy. A symptomatic proton pump inhibitor treatment in GP was either prescribed or voluntary. Focal atrophic gastritis in endoscopy was revealed in 12 (19.7 %) HGP and 16 (39.0 %) AGP patients, diffused atrophic gastritis — in 49 (80.3 %) HGP and 25 (60.9 %) AGP patients. Low-grade chronic gastritis in histology prevailed in HGP, moderate — in AGP, and severe — in 21.9 % cases. Moderate (27.9 %) to severe (65.6 %) atrophy of gastric mucosa was registered in HGP, with 53.7 and 39.0 % respective AGP cases. Polyp dysplasia was detected in 20 % HGP and 75.6 % AGP cases. Pepsinogen I <25 µg/L at a pepsinogen I/II ratio ><3 was observed in 38 (62.3 %) HGP and 18 (43.9 %) AGP patients. Hypo- and anacidic were 65.6 % HGP and 31.7 % AGP patients. >H. pylori-positive were 52.5 % HGP and 70.7 % AGP cases.Conclusion. A largely similar aetiopathogenesis of gastric polyps and chronic atrophic gastritis warrants the H. pylori diagnosis and a more detailed patient control for chronic gastritis grading and staging, functional insufficiency of gastric mucosa and the severity of hyperplastic and dysplastic change. The H. pylori eradication, in contrast to anti-secretory therapy, allows the containment of chronic gastritis and is a critical measure in gastric cancer prevention.

The Relationship between Primary Duodenogastric Reflux and Helicobacter pylori Gastritis in Children

Background: Most studies of the relationship between duodenogastric reflux (DGR) and Helicobacter pylori have reported that the presence of DGR decreases H. pylori colonization, while H. pylori infection increases the frequency of DGR by impairing antroduodenal motility. The present study aimed to investigate the relationship between primary DGR and the prevalence of H. pylori in children, as well as the degree of colonization and the presence and severity of gastritis. Methods: Included in the study were 410 patients between the ages of 2 and 18 years, referred to the pediatric gastroenterology clinic with complaints of dyspepsia, abdominal pain, and nausea/vomiting, who underwent upper gastrointestinal system endoscopic examination and stomach biopsy. The study group included 60 patients with DGR, while 350 non-DGR patients formed the control group. Results: The mean age of patients with DGR was 15.7 ± 2.1 years, while the mean age of the control group was 14.2 ± 3.8 years (p = 0.02). Of those with DGR, 50 (83.3%) were girls, while in the control group, 215 (61.4%) were girls (p = 0.001). Of patients with DGR, 16 were H. pylori (+) (26.7%), while in the control group, 168 were H. pylori (+) (48%) (p = 0.002). There was no significant difference between the 2 groups with respect to H. pylori degree of colonization (p = 0.08). Gastritis was present in 56 (93.3%) patients in the DGR group and 322 (92%) patients in the control group (p = 0.72). A significant difference was found between the 2 groups in terms of gastritis severity (p = 0.01). Conclusions: The mean age of patients with DGR was significantly higher than that of patients without DGR, and DGR was found to be more common in girls. In patients with DGR, H. pylori prevalence was significantly lower than in those without DGR; however, no significant difference was found between the 2 groups with respect to the colonization degree.

Ménétrier Disease; 2-Year-Old Boy Presenting With Prolonged Emesis, Generalized Edema and Chance Histopathological Finding of Cytomegalovirus Gastritis: A Case Report

Ménétrier disease (MD) is characterized by enlarged gastric folds with associated protein losing gastropathy. In children it is a rare and self-limited cause of protein losing gastropathy. We report a case of a 2-year-old male who presented with prolonged, refractory emesis and peripheral edema. Workup revealed severe hypoalbuminemia, hypoproteinemia, iron deficiency anemia, and high stool alpha-1 antitrypsin. Hepatic protein synthesis was normal with no urinary protein loss. Endoscopy showed antrum sparing, severe erosive gastritis in body and fundus, characteristic of MD. Histologic examination displayed inflammation with eosinophilia, foveolar hyperplasia, atrophic oxyntic epithelium, and rare CMV inclusions. Patient received antiviral therapy, intravenous albumin, diuretic and was discharged on high protein diet. Follow-up revealed clinical recovery, with endoscopy and histology showing normal gastric mucosa throughout the stomach. It is important to remain vigilant of this condition in pediatric population and to include it in the differential diagnosis in cases of protein losing gastroenteropathy.

Ménétrier Disease; 2-Year-Old Boy Presenting With Prolonged Emesis, Generalized Edema and Chance Histopathological Finding of Cytomegalovirus Gastritis: A Case Report

Ménétrier disease (MD) is characterized by enlarged gastric folds with associated protein losing gastropathy. In children it is a rare and self-limited cause of protein losing gastropathy. We report a case of a 2-year-old male who presented with prolonged, refractory emesis and peripheral edema. Workup revealed severe hypoalbuminemia, hypoproteinemia, iron deficiency anemia, and high stool alpha-1 antitrypsin. Hepatic protein synthesis was normal with no urinary protein loss. Endoscopy showed antrum sparing, severe erosive gastritis in body and fundus, characteristic of MD. Histologic examination displayed inflammation with eosinophilia, foveolar hyperplasia, atrophic oxyntic epithelium, and rare CMV inclusions. Patient received antiviral therapy, intravenous albumin, diuretic and was discharged on high protein diet. Follow-up revealed clinical recovery, with endoscopy and histology showing normal gastric mucosa throughout the stomach. It is important to remain vigilant of this condition in pediatric population and to include it in the differential diagnosis in cases of protein losing gastroenteropathy.

Hsp60 Quantification in Human Gastric Mucosa Shows Differences between Pathologies with Various Degrees of Proliferation and Malignancy Grade

Background: Stomach diseases are an important sector of gastroenterology, including proliferative benign; premalignant; and malignant pathologies of the gastric mucosa, such as gastritis, hyperplastic polyps, metaplasia, dysplasia, and adenocarcinoma. There are data showing quantitative changes in chaperone system (CS) components in inflammatory pathologies and tumorigenesis, but their roles are poorly understood, and information pertaining to the stomach is scarce. Here, we report our findings on one CS component, the chaperone Hsp60, which we studied first considering its essential functions inside and outside mitochondria. Methods: We performed immunohistochemical experiments for Hsp60 in different samples of gastric mucosa. Results: The data obtained by quantitative analysis showed that the average percentages of Hsp60 were of 32.8 in normal mucosa; 33.5 in mild-to-moderate gastritis; 51.8 in severe gastritis; 58.5 in hyperplastic polyps; 67.0 in intestinal metaplasia; 89.4 in gastric dysplasia; and 92.5 in adenocarcinomas. Noteworthy were: (i) the difference between dysplasia and adenocarcinoma with the other pathologies; (ii) the progressive increase in Hsp60 from gastritis to hyperplastic polyp, gastric dysplasia, and gastric carcinoma; and (iii) the correlation of Hsp60 levels with histological patterns of cell proliferation and, especially, with tissue malignancy grades. Conclusions: This trend likely reflects the mounting need for cells for Hsp60 as they progress toward malignancy and is a useful indicator in differential diagnosis, as well as the call for research on the mechanisms underpinning the increase in Hsp60 and its possible roles in carcinogenesis.

Changes of 18 F-fluoro-2-deoxyglucose position-emission tomography findings by the eradication of Helicobacter pylori in the stomach.

Helicobacter pylori (HP) infection is reported to increase 18 F-fluoro-2-deoxyglucose (FDG) accumulation in the stomach. The accumulation of FDG by positron-emission tomography (FDG-PET) in the stomach for the voluntary health examinees of cancer checkup was examined before and after the HP eradication. From March 2013 to October 2015, eighty-one subjects were performed FDG-PET to detect cancer at the health checkup. All of them were also surveyed by esophagogastroduodenoscopy. Subjects were classified as the 33 cases of HP positive (group A), 38 cases of originally negative (group B), and the 10 negative cases by HP eradication therapy (group C). Group A was treated by combination of amoxicillin, clarithromycin, and proton pump inhibitor for a week, and all of them eradicated HP. A part of group A (n=7) was serially performed FDG-PET one to five years after the treatment and compared the maximum standard uptake value of FDG (SUV) around the fundic gland region. SUV of group A (3.55±0.69) was significantly higher than those of both group B (2.96±0.72) and group C (2.89±0.51) (p<0.01, respectively). Groups B and C are almost comparable and showed no significant difference during the course. In group A, HP eradication significantly decreased the SUV to 3.1±0.43 (P<.01). SUV after the eradication was significantly reduced (P<.01) in the mild to moderate atrophy (C1-C3) group according to Kimura and Takemoto classification of chronic gastritis of group A. Although SUV in the advanced atrophy group (O1-O3) tended to decline after the eradication, the change was not significant. HP-infected stomach showed higher FDG uptake in the fundic gland region and HP eradication decreased the uptake in the mild to moderate atrophic gastritis but not in the severe atrophic gastritis.

&lt;i&gt;Helicobacter pylori&lt;/i&gt; infection and inflammatory bowel diseases

Helicobacter pylori is detected in the human intestine on average in 35% of clinical cases, but the question about its etiopathogenetic role in intestinal diseases has not been fully investigated. Many scientists study a relationship between the H. pylori persistence and development of various bowel diseases. Diverse viewpoints have been proposed regarding a potential link between H. pylori and inflammatory bowel diseases (IBD). Here we review the data from domestic and foreign studies aimed at examining potential role of H. pylori both as a trigger and protector resulting in the pathogenetic alterations leading to developing Crohn‘s disease and ulcerative colitis. The former is favored by the hypothesis wherein H. pylori may trigger IBD due to potential connection between extragastric infection and its direct damaging action as well as indirect effects contributing to the initiation of oxidative stress, autoimmune aggression and development of intestinal dysbiosis. In addition, the effects of enterohepatic Helicobacter spp. promoting IBD pathogenesis are discussed. The mechanisms underlying the protective role of H. pylori infection may be driven via differentially expressed acute and/or chronic local inflammatory mucosal response able to downmodulate systemic immune responses and suppress autoimmune reactions, as well as skewing host immune response from a pro-inflammatory Th1/Th17 cell-mediated towards regulatory T-cell response. Moreover, it was found that H. pylori may induce production of antibacterial peptides counteracting potentially pathogenic bacteria involved in IBD pathogenesis. In particular, it was found that IBD patients are dominated with moderate active antral gastritis coupled to atrophy, with the peak intensity observed in patients under 30 years of age. Intensity of intestinal metaplasia in the gastric mucosa of IBD patients accounted for by the duration of the disease course. Basal IBD therapy with 5-aminosalicylic acid lowers severity and activity of gastritis, degree of atrophy as well as magnitude H. pylori invasion in the gastric mucosa. There is evidence that 5-aminosalicylic acid-containing drugs may result in a so-called “spontaneous eradication” of H. pylori infection. Extended investigations are required to examine a role of H. pylori in IBD pathogenesis.

Could SARS-CoV-2 be associated with emphysematous gastritis?

A 90-year-old patient was admitted to the emergency department with symptomatology of fever, cough, dyspnea, diarrhea, and abdominal pain. Physical examination revealed fever, tachypnea, hypoxemia, bibasal crackles and diffuse abdominal pain. Nasopharyngeal swabs were positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on RT-PCR test. The blood test showed lymphopenia (0.67 × 10³/µL), neutrophilia (7.58 × 10³/µL), lactic acidosis (pH 7.29, lactate 8.7 mmol/L), elevated C-reactive protein (2.50 mg/dL) and procalcitonin (7.32 ng/mL). Chest x-ray revealed bilateral ground-glass opacities that suggested coronavirus disease 2019 (COVID-19) pneumonia. Abdominal CT scan showed diffuse gastric pneumatosis with progression to the esophagus and duodenum (Figs. 1A/B and 2A), associated with hepatic portal venous gas (Fig. 2B). These findings were compatible with COVID-19 pneumonia associated with severe emphysematous gastritis and massive gastric distension. Supportive care and broad-spectrum antibiotic were prescribed. The patient, however, showed respiratory worsening and he died during admission.Fig. 2Contrast-enhanced computed tomography (CT) with sagittal (A) and coronal (B) sections showing hepatic portal venous gas and diffuse gastric pneumatosis.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Emphysematous gastritis is a severe infection caused by gas-forming bacteria, with a high risk of mortality [[1]Singhania N. Bansal S. Singhania G. et al.Emphysematous gastritis.J Emerg Med. 2020; 59: e259-e261Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar]. On the other hand, SARS-CoV-2 is associated with several gastrointestinal disorders due to the invasion of the gastrointestinal angiotensin-converting enzyme 2 (ACE2) receiver and hypercoagulability caused by vascular endothelial cell injury. To our knowledge, this is the first published case of emphysematous gastritis in a patient with SARS-CoV-2 infection. Further research is needed to establish this relationship.

Clinical features and risk factors of gastric cancer detected by esophagogastroduodenoscopy in esophageal cancer patients.

Gastric cancer is the most frequent primary cancer-associated with esophageal cancer and is most commonly detected by endoscopic surveillance. However, the clinical features of synchronous or metachronous gastric cancer that could be detected by esophagogastroduodenoscopy in esophageal cancer patients are unknown. We reviewed the clinical records of all esophageal cancer patients (n = 1379) registered in the cancer registration database who underwent initial treatment between April 2010 and October 2015. We retrospectively analyzed the proportions of synchronous and metachronous gastric cancer cases, the cumulative incidence rate of metachronous gastric cancer in total and by esophageal cancer treatments (endoscopic resection, esophagectomy, and chemoradiotherapy), and the clinical features of esophageal cancer patients with synchronous or metachronous gastric cancer. Overall, 67 (5.3% of 1275) esophageal cancer patients with synchronous gastric cancer and 40 (5.1% of 791) esophageal cancer patients with metachronous gastric cancer were analyzed. The 5-year cumulative incidence rate of metachronous gastric cancer was 5.6% in total, 7.8% after endoscopic resection, 4.7% after esophagectomy, and 4.1% after chemoradiotherapy for esophageal cancer. From the results of multivariate analysis, the risk factors for synchronous gastric cancer were male (odds ratio 13.3) and moderate/severe atrophic gastritis (odds ratio 17.9), and the risk factor of metachronous gastric cancer was moderate/severe atrophic gastritis (hazard ratio 27.6) in patients with esophageal cancer. The incidence rates of synchronous and metachronous gastric cancer with esophageal cancer were both over 5%. Careful endoscopic observation is required for moderate and severe atrophic gastritis at detecting concomitant gastric cancer in esophageal cancer patients.

Prevalence and associated risk factors of gastritis among patients visiting Saint Paul Hospital Millennium Medical College, Addis Ababa, Ethiopia.

BackgroundThe health of individuals is not only the absence of disease checked medically, but also encompasses social and psychological aspects. Any departure from the state of physiological, psychological, or social well-being was affected by different factors. However, all contributory factors were not equally responsible for affecting disease. This study was undertaken as a search for the relative effects of sociocultural and individual behavioral factors contributing to acute and chronic gastritis patients visiting Saint Paul Hospital Millennium Medical College (SPHMMC).MethodsA cross-sectional study was carried out on 364 patients visited SPHMMC in the study. Primary data were collected through an interview schedule tool with an exit approach by validating questions pertaining to sociocultural and individual behavioral factors. The status of gastritis was measured as whether patients had Helicobacter Pylori infection, signs and symptoms indicated gastritis that occurred, and persisted for less than a month, greater than a month, or none of the signs and symptoms. Descriptive statistics, bivariate analysis, and multivariable ordinal logistic regression model were used to identify the predictors of gastritis severity. P-value ≤ 0.05 was declared as an indicator of statistically significant.ResultsThe prevalence of gastritis in the study area was 78.8%. Specifically, 48.9% and 29.9% had acute and chronic gastritis, respectively. The study found that low income and taking medicinal drugs was slightly significantly contributed to higher gastritis status; however, being younger age was slightly significantly contributed to lower gastritis status. Furthermore, the results indicated that eating spiced foods (Adjusted Odds Ratio (AOR) = 1.508; 95% CI: 1.046, 2.174), lack of physical exercise regularly (AOR = 1.780; 95% CI: 1.001, 3.168), stress (AOR = 2.168; 95% CI: 1.379, 3.4066), and substance use (AOR = 1.478; 95% CI: 1.093, 1.999) were significantly contributed to higher gastritis status.ConclusionsThe findings suggested that women should take enough rest and sleep well, men refrain from involvement in any risky behaviors, young people and those who earn low income per month should equip with knowledge and understanding on how to practice good health behaviors, eating foods on time, avoiding eating spiced food frequently, doing physical exercise regularly, and taking medicinal drugs according to physician advice are recommended.

Helicobacter pylori eradication prevents secondary gastric cancer in patients with mild-to-moderate atrophic gastritis.

Whether Helicobacter pylori eradication prevents metachronous recurrence after endoscopic resection (ER) of early gastric cancer remains controversial. This multicenter retrospective study aimed to evaluate the long-term (>5years) effects of H.pylori eradication by stratifying patients' baseline degrees of atrophic gastritis. A total of 483 H.pylori-positive patients who had undergone ER for early gastric cancer were divided into two groups-(i) those having undergone successful H.pylori eradication within 1year after ER (eradicated group, n=294) and (ii) those with failed or not attempted H.pylori eradication (non-eradicated group, n=189). The cumulative incidences of metachronous gastric cancer between the two groups were compared for all patients, for patients with mild-to-moderate atrophic gastritis (n=182), and for patients with severe atrophic gastritis (n=301). During a median follow-up of 5.2years (range 1.1-14.8), metachronous cancer developed in 52 (17.7%) patients in the eradicated group and in 35 (18.5%) patients in the non-eradicated group (P=0.11, log-rank test). In patients with mild-to-moderate atrophic gastritis (111 and 71 in the eradicated and non-eradicated groups, respectively), the cumulative incidence of metachronous cancer was significantly lower in the eradicated group than that in the non-eradicated group (P=0.03, log-rank test). However, no significant intergroup difference was observed in patients with severe atrophic gastritis (P=0.69, log-rank test). Helicobacter pylori eradication had a preventive effect on the development of metachronous gastric cancer in patients with mild-to-moderate atrophic gastritis.

Gastric histopathological features after the administration of omeprazole, amoxicillin, and clarithromycin in gastritis Helicobacter pylori rat model.

Objective:This research work aimed to assess the histopathological features and degree of gastritis severity in a rat model, induced by Helicobacter pylori infection after administering omeprazole, amoxicillin, and clarithromycin as the standard first-line eradication regimen.Material and Methods:Twenty-one male rats were adapted for 7 days and randomly divided into three equal groups. Group 1 was considered a negative control. Group 2 and Group 3 were treated as H. pylori-inoculated groups. Group 2 was set as a positive control. Group 3 was administered omeprazole, amoxicillin, and clarithromycin as a first-line eradication regimen. Gastric histopathological examination was conducted. The difference in the severity of gastritis among the groups was examined using the one-way analysis of variance test. The significance was determined to be p < 0.05.Results:Gastritis was found in all inoculated groups. The severity of gastritis was highest in Group 2 (p < 0.05). We could see a refinement in gastritis severity after administering omeprazole, amoxicillin, and clarithromycin as a first-line eradication regimen (Group 3 vs. Group 2; p <0.05).Conclusion:Gastritis, induced by the H. pylori rat model, was found in all inoculated groups. There was a refinement in the degree of gastritis severity after the administration of omeprazole, amoxicillin, and clarithromycin as a first-line eradication regimen.

Community-driven research in the canadian arctic: dietary exposure to methylmercury and gastric health outcomes

ABSTRACT Indigenous Arctic Canadians have a higher prevalence of gastric neoplasms relative to North Americans of European ancestry. We investigated the hypothesis that low-dose methylmercury exposure from eating fish/whale increases the risk of gastric cancer in Arctic communities. We used intermediate endpoints from an established model of gastric carcinogenesis: intestinal metaplasia, atrophy, and severe chronic gastritis. During 2008–2012, we obtained gastric biopsies from participants of community-driven projects in 3 communities. In 2016, we collected hair samples to measure methylmercury levels and interviewed them about diet. In cross-sectional analysis, logistic regression estimated odds ratios for the estimated effect of hair-methylmercury concentration on the prevalence of each pathology outcome stratified by selenium intake. Among 80 participants, prevalence of intestinal metaplasia, atrophy and severe chronic gastritis was 17, 29 and 38%, respectively. Adjusted Odds of severe chronic gastritis and atrophy were highest at hair-methylmercury concentrations ≥1μg/g when estimated selenium intake was 0, and approached 0 for all methylmercury levels as estimated selenium intake increased. Gastric pathology increased with methylmercury exposure when selenium intake was low. Though limited by small numbers, these findings suggest selenium ingested by eating fish/whale may counter harmful effects of methylmercury exposure in Arctic populations.

Thrombotic microangiopathy triggered by podocytopathy.

Thrombotic microangiopathy (TMA) is a rare group of diseases characterized by microangiopathic hemolytic anemia, thrombocytopenia, and target organ damage. It can be divided into primary and secondary TMA. Herein we report a case of TMA associated to a primary glomerular disease. We report the case of a 31-year-old Black male from Cape Verde admitted in March 2018 with nephrotic syndrome and upper gastrointestinal bleeding, the latter due to severe erythematous gastritis. He was discharged after clinical stabilization. The patient came to Portugal 8 months later. On admission, he presented with rapid deterioration of kidney function and hyperkalemia. The etiologic study revealed microangiopathic hemolytic anemia, nephrotic syndrome and microscopic hematuria. Immunologic study and viral serology were negative. ADAMTS13 activity and inhibitor testing were within normal range, genetic complement evaluation showed CFH-H3 in homozygosity, functional complement studies revealed decreased function of alternative pathway. Kidney biopsy was consistent with the diagnosis of TMA, and electron microscopy was compatible with minimal change disease. Patient underwent plasmapheresis with resolution of hemolysis, fluid overload and recovery of renal function. Two months later, he presented with nephrotic syndrome and started prednisolone with remission. Six months later, the nephrotic syndrome relapsed, and it became steroid-, MMF-, and rituximab-resistant. Tacrolimus was initiated, achieving partial remission. Atypical hemolytic uremic syndrome is an uncommon disease and is rarely reported as secondary to glomerular diseases. This case showcases the challenges regarding treatment options in a resistant glomerulopathy and the implications of therapeutic choices and kidney outcomes with the coexisting TMA.

Laparoscopic one anastomosis gastric bypass: a revisional procedure for failed open vertical banded gastroplasty in treatment of morbid obesity: a prospective study

Background The main indications for revision of bariatric surgery are inadequate weight loss, weight regain, or complications, so laparoscopic one anastomosis gastric bypass (LOAGB) is a promising bariatric procedure used as a revisional procedure for failed open vertical banded gastroplasty (VBG). Aim The aim was to evaluate LOAGB as a revisional bariatric procedure for failed open VBG regarding technical feasibility, weight loss, improvement in comorbidities, and complications. Patients and methods This prospective cohort study was carried out at the Gastrointestinal and Laparoscopic Surgery Unit, General Surgery Department, Tanta University, between October 2017 and October 2018. It included 20 patients who underwent LOAGB as a revisional bariatric procedure for failed open VBG. Results The study population included 17 females and three males, with a mean age of 38.25±5.36 years. The mean preoperative BMI was 48.15±4.35 kg/m2. The mean operative time was 145.36±25.19 min, and the mean postoperative hospital stay was 3.12 days. Neither conversion to open technique or to other bariatric procedures nor mortality occurred. Early complications were encountered in 3 patients (15%). Late complications included four (20%) patients. Severe biliary gastritis occurred in one (5%) patient, who was managed by side-to-side jejunojejunostomy. The mean postoperative excess body weight loss percent (EBWL%) achieved was 47.14±15.24 at 1 year and 60.85±12.17 at 2 years. The mean BMI achieved was 32.72±5.46 at 1 year and 28.14±4.45 at 2 years. Conclusion LOAGB surgery as a revisional procedure for failed open VBG is an effective bariatric surgical procedure producing significant weight loss and resolution or improvement of comorbidities with low perioperative complications.