Inflammatory cell numbers in the stomach of Japanese subjects with endoscopically normal mucosa without H. pylori infection

2021 ◽  
Author(s):  
Naoki Sumi ◽  
Ken Haruma ◽  
Tomoari Kamada ◽  
Mitsuhiko Suehiro ◽  
Noriaki Manabe ◽  
...  
Keyword(s):  
Inflammatory Cells ◽  
Normal Mucosa ◽  
Mucosal Inflammation ◽  
Upper Gastrointestinal Endoscopy ◽  
Fundic Gland ◽  
Eosinophilic Gastritis ◽  
Pyloric Mucosa ◽  
Sydney System ◽  
Updated Sydney System ◽  
H Pylori

Introduction: Since inflammatory cells, such as lymphocytes and plasma cells, normally inhabit the stomach, the border between normal and mild inflammation is difficult to visually determine using the updated Sydney system scale of gastritis. Additionally, eosinophils in the gastric mucosa must be counted to diagnose eosinophilic gastritis. We aimed to determine the normal number of inflammatory cells in patients with endoscopically normal mucosa and without H. pylori infections. Methods: We assessed patients aged 20–79 years, who had undergone upper gastrointestinal endoscopy at Kawasaki Medical School Hospital between January 2010 and December 2014. Inflammatory cells were counted in 1,000 μm2 fields of pyloric and fundic gland mucosal biopsy specimens. We finally included 325 (male, n = 141; female, n = 184; average age = 49.3 years) patients without inflammation who had H. pylori-negative endoscopic results and negative histological findings interpreted based on the updated Sydney System and the Kyoto classification of gastritis. Results: The average numbers of nucleated cells were 83.3 ± 14.2/mm2 and 65.4 ± 12.6/mm2 in the pyloric and fundic gland mucosae, respectively. Inflammatory cells were significantly more abundant in the pyloric mucosa than the fundic gland mucosa (p < 0.05). Age and sex distribution did not significantly differ. Eosinophils were absent or scanty in the gastric mucosae of both glands in all patients. Conclusion: We determined the absolute values of inflammatory cells, including eosinophils, in normal mucosae of pyloric and fundic glands. These findings could be important in defining gastric mucosal inflammation, including eosinophilic gastritis diagnosis.

scholarly journals Distribución de estadios de OLGA y OLGIM según edad y estado del Helicobacter pylori en un hospital público nivel III en Lima, Perú

2021 ◽  
Vol 51 (1) ◽  
Author(s):  
Andrea Carlin Ronquillo ◽  
Alex Ventura León ◽  
Jorge L Espinoza Ríos ◽  
Eduar A Bravo Paredes ◽  
Paúl Gómez Hinojosa ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
High Risk ◽  
Upper Gastrointestinal Endoscopy ◽  
Gastric Intestinal Metaplasia ◽  
Endoscopic Control ◽  
Staging Systems ◽  
Sydney System ◽  
Group 5 ◽  
Updated Sydney System ◽  
H Pylori

Introduction. The operative link for gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia assessment (OLGIM) staging systems have been suggested to provide risk of assessment for gastric cancer. Objective. To evaluate the distribution of OLGA and OLGIM staging by age and Helicobacter pylori status. Material and methods. We studied 197 subjects undergoing elective upper gastrointestinal endoscopy. The presence of the H. pylori and histological changes were evaluated using the updated Sydney system. Stages III and IV of OLGA/OLGIM were considered high risk stages. Results. The H. pylori rate was 56.85% (112/197). High-risk OLGA/OLGIM cases were rare: 7/112 (6.5%) cases of OLGA in the H. pylori positive group and 6/85 (7%) in the H. pylori negative group; 5 (4.4%) cases of OLGIM in the H. pylori positive and 6 (7%) in the H. pylori negative. The proportion of advanced stages of OLGA and OLGIM increased with age (p < 0.001). High-risk OLGA was not found before age 40 regardless of the presence of H. pylori, but increased to 16.2%, 10.3%, 17.3% and 40.8% in subjects in the fourth, fifth, sixth and seventh decade of life respectively. The OLGIM high risk showed a similar trend: 0% before 40 years and up to 22.6% in people of 70 years. Conclusions. High-risk OLGA/OLGIM cases are infrequent before age 40 and increase significantly with age. No relation was found with the presence of the H. pylori. According to these protocols, only a fifth of the patients would strictly require endoscopic control.

scholarly journals Association of Helicobacter pylori infection with nodular antritis and follicular gastritis

2006 ◽  
Vol 63 (3) ◽  
pp. 313-315 ◽  
Author(s):  
Ratko Tomasevic ◽  
Gradimir Golubovic ◽  
Miroslav Kiurski ◽  
Dragana Stankovic ◽  
Radoje Doder ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Case Report ◽  
Chronic Gastritis ◽  
Upper Gastrointestinal Endoscopy ◽  
Antral Mucosa ◽  
Urease Test ◽  
Sydney System ◽  
H Pylori ◽  
The Relationship ◽  
Upper Gastrointestinal

Introduction. Helicobacter pylori (H. pylori) infection is known to be the must common cause of chronic gastritis having some endoscopic and pathologic characteristies as determinated by the Sydney System for Gastritis Classification. The aim of our case report was to point out the relationship between an endoscopic finding of nodular antritis and the presence of H. pylori infection and active chronic gastritis. Case report. Our patient underwent upper gastrointestinal endoscopy for dyspeptic complaints and was diagnosed as having nodular antritis, but also underwent urease test and hystopathologic examination of antral mucosa, to determine the presence and density of H. pylori infection and the presence and severity of gastritis. After a course of anti H. pylori treatment, dyspepsia improved and new biopsy specimens obtained two months and six months afterwards revealed no pathological findings. Conclusion. The case report supported the association of H. pylori infection of lymphoid follicles with nodular gastric mucosis.

Clue of Diagnosis for Autoimmune Gastritis

Digestion ◽  
2021 ◽  
pp. 1-8
Author(s):  
Toshihiro Nishizawa ◽  
Shuntaro Yoshida ◽  
Hidenobu Watanabe ◽  
Akira Toyoshima ◽  
Yosuke Kataoka ◽  
...  
Keyword(s):  
Detection Rate ◽  
Pathological Diagnosis ◽  
Autoimmune Gastritis ◽  
Detection Rates ◽  
Pathological Evaluation ◽  
Sydney System ◽  
Updated Sydney System ◽  
Greater Curvature ◽  
H Pylori ◽  
Parietal Cell Antibody

<b><i>Background:</i></b> The diagnostic clues for autoimmune gastritis (AIG) can be classified into 2 categories: endoscopic findings and pathological diagnosis. We believe that research on the AIG detection rate by endoscopists could provide a better understanding of the diagnosis of AIG. This study aimed to clarify the ratio of the endoscopic and the pathological diagnoses of AIG. <b><i>Methods:</i></b> We retrospectively reviewed consecutive patients who underwent esophagogastroduodenoscopy (EGD). During their first EGD, the gastric mucosa with C2 atrophy or more was biopsied for pathological evaluation based on the updated Sydney system. A gastric biopsy was also performed after <i>Helicobacter pylori</i> eradication, obtaining specimens from at least 2 sites, the greater curvature of the corpus and the antrum. We enrolled patients who were positive for the anti-parietal cell antibody and were diagnosed with AIG, histologically and/or endoscopically. The detection rates of AIG were compared between endoscopic diagnosis and pathological diagnosis. <b><i>Results:</i></b> A total of 10,822 patients underwent EGD during the study period. Finally, 41 patients with AIG were enrolled, leading to an AIG prevalence of 0.38% in this study. As for the clue leading to AIG detection, 31.7% (13/41) were diagnosed through endoscopy (proximal-predominant atrophy), and 68.3% (28/41) were diagnosed pathologically. The AIG detection rate by endoscopists in the posteradication group was significantly lower than in <i>the H. pylori-negative</i> group (<i>p</i> &#x3c; 0.05). <b><i>Conclusion:</i></b> Endoscopists frequently overlooked AIG, especially in posteradication cases. Pathological assessment using the updated Sydney system after <i>H. pylori</i> eradication might be a promising strategy to detect AIG better.

scholarly journals The Difference of Serum Gastrin-17 Level Based on Gastritis Severity and Helicobacter Pylori Infection

2019 ◽  
Vol 7 (8) ◽  
pp. 1266-1269
Author(s):  
Dumawan Harris Parhusip ◽  
Gontar Alamsyah Siregar ◽  
Leonardo Basa Dairi
Keyword(s):  
Serum Gastrin ◽  
Demographic Data ◽  
Cross Sectional Study ◽  
Mucosal Inflammation ◽  
P Value ◽  
Cross Sectional ◽  
Significant Difference ◽  
Sydney System ◽  
The Difference ◽  
H Pylori

BACKGROUND: Gastritis was defined as the histological presence of gastric mucosal inflammation. One of the most common aetiology was H. pylori. Gastrin-17 was a hormone that was secreted by G cells. H. pylori infection induced increased in gastrin-17 in gastritis. Therefore, this study was to investigate the relationship of gastrin-17 with gastritis severity and H. pylori infection. AIM: To determine the difference in serum Gastrin-17 level based on gastritis severity and H. pylori infection. METHODS: A cross-sectional study enrolling 45 patients with gastritis was conducted in Haji Adam Malik General Hospital between April and July 2018. Endoscopy and biopsy examinations were performed to confirm the diagnosis of gastritis. Gastritis severity was assessed using the Updated Sydney System. The presence of H. pylori infection was detected by a Campylobacter-like organism (CLO) examination. Gastrin-17 level and demographic data were also gathered. The analysis was done using Mann Whitney and Kruskal-Wallis test. P-value of < 0.05 was considered statistically significant. RESULTS: Serum Gastrin-17 level was significantly different based on gastritis severity (P = 0.001 according to neutrophils infiltration and P = 0.023 according to degree of atrophy), H. pylori infection (P = 0.038), and combined gastritis severity and H. pylori infection (P < 0.001). Serum Gastrin-17 level was higher in subjects with severe neutrophils infiltration, without atrophy, and with H. pylori infection. CONCLUSION: There was a significant difference in serum Gastrin-17 level based on gastritis severity and H. pylori infection.

scholarly journals Rebamipide Improves Chronic Inflammation in the Lesser Curvature of the Corpus afterHelicobacter pyloriEradication: A Multicenter Study

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tomoari Kamada ◽  
Motonori Sato ◽  
Tadashi Tokutomi ◽  
Tetsuo Watanabe ◽  
Takahisa Murao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Chronic Inflammation ◽  
Epidemiologic Studies ◽  
Untreated Group ◽  
Primary Endpoints ◽  
Sydney System ◽  
Updated Sydney System ◽  
H Pylori ◽  
Lesser Curvature

Background and Aim. Although many epidemiologic studies have shown thatHelicobacter pylorieradication has prophylactic effects on gastric cancer, it does not completely eliminate the risk of gastric cancer. We aimed to investigate the changes in histological gastritis in patients receiving rebamipide treatment afterH. pylorieradication.Methods. 206 patients who had undergoneH. pylorieradication were evaluated. Of these, 169 patients who achieved successful eradication were randomly allocated to 2 groups: the rebamipide group (n= 82) and the untreated group (n= 87). The primary endpoints were histopathological findings according to the updated Sydney system at the start of the study and after 1 year.Results. Final assessment for histological gastritis was possible in 50 cases from the rebamipide group and 53 cases from the untreated group. The activity and atrophy improved in both the rebamipide and untreated groups, and no significant intergroup differences were observed. Chronic inflammation affecting the lesser curvature of the corpus was significantly improved in the rebamipide group compared to in the untreated group (1.12±0.08versus1.35±0.08;P= 0.043).Conclusions. Rebamipide treatment afterH. pylorieradication alleviated chronic inflammation in the lesser curvature of the corpus compared to that in the untreated group. This trial is registered withUMIN000002369.

scholarly journals Evaluation of chronic gastritis with Helicobacter pylori using updated Sydney system

2021 ◽  
Vol 9 (9) ◽  
pp. 2728
Author(s):  
Anjana M. L. ◽  
Kavitha Yevoor
Keyword(s):  
Helicobacter Pylori ◽  
Chronic Gastritis ◽  
Histological Evaluation ◽  
Statistical Association ◽  
Histopathological Changes ◽  
Biopsy Specimens ◽  
Sydney System ◽  
Updated Sydney System ◽  
H Pylori ◽  
Significant Statistical Association

Background: Helicobacter pylori has been established as a major etiological factor in the pathogenesis of chronic gastritis. The aim of the study was to interpret the histopathological changes in chronic gastritis using updated Sydney system and the association with H. pylori infection.Methods: This was a 3 years study in which 62 gastric endoscopic mucosal biopsies taken from patients presenting with dyspepsia were included. Slides were stained with routine H and E and Giemsa for H. pylori detection in chronic gastritis cases. Grading of the variables were done with reference to Sydney system of classification.Results: Out of 62 gastric biopsy specimens, 55 cases (88.7%) were histopathological diagnosed as chronic gastritis. Among chronic gastritis, 21 (38%) cases showed H. pylori and majority of these being moderately (2+) positive. 27 (49%) cases showed neutrophilic activity with most of them showed mild (1+) activity. Chronic inflammation was seen 52 (94.5%) with majority of these graded as moderate (2+). Intestinal metaplasia was seen in 8 (14.5%) of cases with majority being mild (1+). Atrophy was seen only in 3 (5.4%) of cases with majority being mild (1+). Significant statistical association was found between H. pylori and neutrophilic activity (p<0.001).Conclusions: Histological evaluation of chronic gastritis using updated Sydney system of classification helps in detection of H. pylori infection and prevents further progression of the disease. 

RAD51 G135C genetic polymorphism and their potential role in gastric cancer induced byHelicobacter pyloriinfection in Bhutan

2015 ◽  
Vol 144 (2) ◽  
pp. 234-240 ◽  
Author(s):  
T. T. H. TRANG ◽  
H. NAGASHIMA ◽  
T. UCHIDA ◽  
V. MAHACHAI ◽  
R.-K. VILAICHONE ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Genetic Polymorphism ◽  
Intestinal Metaplasia ◽  
Polymorphism Analysis ◽  
Genotype Distribution ◽  
High Prevalence ◽  
The Status ◽  
Sydney System ◽  
Updated Sydney System ◽  
H Pylori

SUMMARYIn order to evaluate the role of the RAD51 G135C genetic polymorphism on the risk of gastric cancer induced byHelicobacter pyloriinfection, we determined allele frequency and genotype distribution of this polymorphism in Bhutan – a population documented with high prevalence of gastric cancer and extremely high prevalence ofH. pyloriinfection. The status of RAD51 G135C was examined by restriction fragment length polymorphism analysis of PCR amplified fragments and sequencing. Histological scores were evaluated according to the updated Sydney system. G135C carriers showed significantly higher scores for intestinal metaplasia in the antrum than G135G carriers [mean (median) 0·33 (0)vs.0·08 (0),P= 0·008]. Higher scores for intestinal metaplasia of G135C carriers compared to those of G135G carriers were also observed inH. pylori-positive patients [0·3 (0)vs.0·1 (0),P= 0·002] andH. pylori-positive patients with gastritis [0·4 (0)vs.0·1 (0),P= 0·002] but were not found inH. pylori-negative patients. Our findings revealed that a combination ofH. pyloriinfection and RAD51 G135C genotype of the host showed an increasing score for intestinal metaplasia. Therefore, RAD51 G135C might be the important predictor for gastric cancer ofH. pylori-infected patients.

Isolated Gastric Malakoplakia: A Case Report and Review of the Literature

2004 ◽  
Vol 128 (11) ◽  
pp. e153-e156 ◽  
Author(s):  
Lastra-Camacho Gustavo ◽  
Marie E. Robert ◽  
Laura W. Lamps ◽  
Suzanne P. Lagarde ◽  
Dhanpat Jain
Keyword(s):  
Yersinia Pseudotuberculosis ◽  
African American Woman ◽  
American Woman ◽  
Gastric Body ◽  
Upper Gastrointestinal Endoscopy ◽  
Fundic Gland ◽  
Biopsy Specimens ◽  
Polymerase Chain ◽  
H Pylori

Abstract A 62-year-old African American woman presented with weight loss and dyspepsia. She did not have any clinical evidence of immunodeficiency. Upper gastrointestinal endoscopy revealed multiple small polypoid lesions in the gastric body and fundus that appeared larger and more erythematous than usual fundic gland polyps. Examination of biopsy specimens revealed an infiltrate of large histiocytes with eosinophilic granular cytoplasm located in the lamina propria and containing Michaelis-Gutmann bodies. These histologic findings were diagnostic of gastric malakoplakia. Gastrointestinal malakoplakia is uncommon, and exclusive gastric involvement is extremely rare. Because occult bacterial infection has been postulated as the underlying cause of malakoplakia, the presence of Helicobacter pylori infection was investigated using immunohistochemical and serologic techniques, and the presence of Yersinia enterocolitica or Yersinia pseudotuberculosis infection was investigated by polymerase chain reaction assay. There was no evidence of H pylori, Y enterocolitica, or Y pseudotuberculosis in these biopsy specimens, and there was no evidence of malakoplakia or concurrent malignancy at any other site. Follow-up examination 12 months later revealed no endoscopic or histologic improvement.

scholarly journals Correlation between mast cell density and histological parameters in Helicobacter pylori-associated gastritis

2011 ◽  
Vol 5 (1) ◽  
pp. 163-167 ◽  
Author(s):  
Mana Taweevisit ◽  
Naruemon Klaikaew
Keyword(s):  
Helicobacter Pylori ◽  
Mast Cell ◽  
Mast Cells ◽  
Cell Density ◽  
B Cell Lymphoma ◽  
Inflammatory Cells ◽  
Chronic Inflammatory Cell ◽  
Mast Cell Density ◽  
Sydney System ◽  
H Pylori

Abstract Background: Helicobacter pylori (H. pylori) are a major cause of chronic gastritis and peptic ulcer. This organism plays a role in gastric carcinoma and B-cell lymphoma. However, the exact pathogenesis of gastric inflammation is still unclear. Mast cells, the important inflammatory cells for allergic process, may participate in the pathogenesis of gastritis related to H. pylori infection. Objective: Analyze the relationship between mast cell density, H. pylori intensity, histological alterations, and their severity of biopsy proven gastritis. Methods: One hundred eleven biopsied specimens were collected from Thai patients who were diagnosed H. pylori-associated gastritis of the antrum at King Chulalongkorn Memorial Hospital between 2002 and 2005. All biopsied specimens were examined according to the Updated Sydney System. Mast cell density was evaluated by 0.1% toluidine-stained sections. Results: The higher mast cell density was correlated with increased neutrophilic infiltration (r = 0.220, p = 0.020), chronic inflammatory cell infiltration (r = 0.381, p <0.001), and lymphoid aggregation (r = 0.271, p = 0.004). No relationship was found between mast cell density and intensity of H. pylori, glandular atrophy, or intestinal metaplasia. Conclusion: Mast cells might take part in the pathogenesis of H. pylori gastritis.

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