Hypergastrinemia after Helicobacter pylori infection is associated with bacterial load and related inflammation of the oxyntic corpus mucosa (original) (raw)
2004, Journal of Gastroenterology and Hepatology
Helicobacter pylori infection causes hypergastrinemia. This study aimed to determine the association between serum gastrin and the severity of H. pylori-related gastric histology. A total of 458 dyspeptic patients were included in this study after the absence of gastric malignancy was confirmed using endoscopy. The gastric specimens of each patient were collected from the antrum and corpus for the analysis of H. pylori-related histology changes by updated Sydney's system. Before endoscopy, the fasting blood samples were collected for gastrin analysis. The H. pylori-infected patients had higher gastrin levels than those without infection (P = 0.01). Gastrin levels were related to H. pylori density and acute and chronic inflammation scores in the corpus mucosa (P < 0.05), but not in the antral mucosa (P = NS). Gastrin levels were also not related to the presence of gastric atrophy. Multivariate regression showed that the gastrin level was only related to acute corpus inflammation. However, in the patients without infection, the gastrin level was also associated with acute corpus inflammation. Nevertheless, the patients with denser H. pylori infection were more likely to have acute corpus gastritis than those with lighter H. pylori infection, and thus presented with higher gastrin levels (P < 0.05). The increased level of gastrin of serum after H. pylori infection was associated with acute inflammation in the gastric corpus mucosa, but not in the antral mucosa. Denser H. pylori infection causes more severe corpus gastritis and thus may lead to a higher fasting level of gastrin of serum.
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Pattern of gastritis as manipulated by current state of Helicobacter pylori infection
wseas.us
Helicobacter pylori (H. pylori) infection prevails from 60-80% in patients with gastric ulcer and 90-100% in those having duodenal ulcer. Patients with such type of chronic infection are at increased risk to develop peptic ulcers or gastric adenocarcinomas. The present work aims mainly to identify the pattern of chronic gastritis and potential effect of H. pylori infection using certain biomarkers, histological and immunochemical tests. Fifty eight individuals, clinically diagnosed as having chronic gastritis, were participated in the present study. They were categorized into 2 groups, the first one (31%) demonstrated positive reaction to IgM antibodies of Helicobacter pylori (H. pylori) (>40u/ml) and the second group (69%) demonstrated negative reaction. Blood and antral biopsy samples were collected, directed to determination of serum gastrin, pepsinogen I (PgI), pepsinogen II (PgII), prostaglandin E 2 (PGE 2) and interlukin-6 (IL-6). Immunohistochemistry technique was also done in antral biopsy to demonstrate the expression of inducible nitric oxide synthase (iNOS), nitrotyrosine, DNA fragmentation, myeloperoxidase and histopathological examination. Serum gastrin, PgI, PgII, PGE 2 , IL-6 demonstrated significant increase in gastritis patients as compared to normal group. PgI, PgII showed significant increase joined with slight increase of IL-6 in IgM positive group as compared to negative one. Immunostaining testes in antral biopsy showed strong positive reactions for the above mentioned markers as compared to IgM negative group (mild positive reaction). In conclusion, gastritis patients who express IgM antibodies for H. pylori infection showed higher gastrinaemia and more pronounced atrophic, inflammatory and apoptotic damage than those not expressing IgM antibodies.
Helicobacter pylori related hypergastrinaemia is the result of a selective increase in gastrin 17
Gut, 1993
Helicobacter pylon infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylon. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that >90% of the circulating gastrin consisted ofgastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmolIl (8-39) (p<0-05), entirely because of a fail in G17 from 6 pmol/l (<2.4-25) to <2-4 pmoil/ (<2.4-23) (p<0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmolll (38-114) to 33 pmol/ (19-88) (p<0 005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmolfl (<2-4-52) (p<0-001).
Mucosal gastrin cells and serum gastrin levels in children with Helicobacter pylori infection
Advances in Medical Sciences
Purpose: Impaired control of gastric juice secretion is observed in chronic gastritis due to Helicobacter pylori (H. pylori) infection. G cells are stimulated by such cytokines as tumor necrosis factor (TNF-alpha), interferon gamma (IFNgamma) and interleukin-8 (IL-8). The number of D cells producing somatostatin decreases simultaneously. An increase in gastrin levels could also depend on alkalization in G cell environment caused by bacterial urease. The aim of the study was to evaluate G cell counts in the antrum and gastrin levels in the serum of children with H. pylori infection and after bacterium eradication. Material and methods: The study was performed in 106 patients. Children were divided into 3 groups with regard to the presence and course of H. pylori infection. Fifty nine children (55.7%) had chronic gastritis in the course of H. pylori infection with a positive titre of antibodies in IgG class against H. pylori; 29 children (27.3%) with past H. pylori infection, without bacterium colonization and gastritis but with a positive titre of antibodies in IgG class against H. pylori; 18 children (17%) with functional disorders of the gastrointestinal tract but without H. pylori infection. Results: The quantitative analysis of gastrin cells in the antral mucosa of children performed by immunohistochemical method showed the highest gastrin cell count in group I with H. pylori infection (112.1±58.9 cell/mm 2 ) and in group II with past H. pylori infection (105.3±73.1 cell/mm 2 ). The serum gastrin level (92.9±41.6 U/ml) was the highest in children with H. pylori infection. In controls, it was 70.0±15.3 U/ml and could be compared to the results of children with past H. pylori infection.
Journal of Evidence Based Medicine and Healthcare
BACKGROUND Chronic gastritis is a common condition in general population. Of the many aetiological factors, Helicobacter pylori is one of the primary cause of chronic gastritis. AIMS To study the histopathological features of chronic gastritis associated with H. pylori infection. To find out the relationship between severity of inflammatory reaction in gastritis and intensity of H. pylori. MATERIALS This cross sectional study was carried out in Regional Institute of Medical Sciences (RIMS) Hospital from October 2013 to September 2015. Patients with symptoms suggestive of chronic gastritis attending RIMS OPD were subjected to upper gastrointestinal endoscopy. One of the biopsy specimens was used for rapid urease test using RUT dry test kit and others were processed for histopathological examination as per standard protocol. All the slides were stained with Haematoxylin and Eosin (H&E) stain and Giemsa stain. Histological variable grading was done using the "Updated Sydney System 1994". All the data thus collected were analysed. RESULTS A total of 60 patients (39 males and 21 females) were included in the study with age ranging from 19 to 82 years. Among the 60 patients, maximum endoscopic findings were ulcer (33.3%) followed by erythematous findings (26.7%). The results of Rapid Urease Test (RUT) were positive in 30% (18/60). The histopathology reports for H. pylori detection were positive in 35% (21/60). The majority (81.7%) of the cases were inflammatory on histopathology followed by neoplasia (8.3%), dysplasia (5%) and normal finding (5%). Neutrophilic activity was present in all cases of chronic gastritis, in which 15, 5 and 11 numbers of cases showed mild, moderate and severe grading respectively. Mononuclear cell infiltration also was present in all cases of chronic gastritis and 8, 16, 7 numbers of cases were found to have mild, moderate and severe grading respectively. Only five mild atrophy, four mild Intestinal metaplasia (IM) and one moderate Intestinal metaplasia (IM) were found in gastritis cases. Correlation coefficient of neutrophilic activity with H. pylori density was 0.725 (p=0.000), which was statistically significant. CONCLUSION In our study, histopathological features of H. pylori associated chronic gastritis have shown H. pylori density, neutrophilic activity, mononuclear cell infiltration, glandular atrophy and intestinal metaplasia. We also have observed the association between neutrophilic activity and H. pylori density.
Tropical Journal of Pathology and Microbiology, 2019
Introduction: Helicobacter pylori (H. pylori) is of major concern today and is characterized by mucosal infiltration by neutrophils, mononuclear cells and can cause atrophy and intestinal metaplasia which in long term can predispose to gastric carcinoma or lymphoma. Aims of the study: To evaluate the various histopathological parameters in H. pylori induced gastritis and to correlate with H. pylori density. Materials and Methods: This is a Cross sectional descriptive study conducted in the Department of Pathology and Medicine, which included 50 gastric biopsies that was diagnosed as H. Pylori gastritis for a period of 1 year from January 2017 to December 2017. Histopathological variables like Mononuclear cell infiltration, neutrophilic infiltrate, Atrophy, Density of H. pylori were graded according to updated Sydney system. statistical analysis was done using spearman rank correlation test. Results: There were 50 cases of H. pylori gastritis diagnosed during the study period. The age of the patients ranged from 9 to 75 years with male: female ratio of 2.3:1. Atrophy was seen in 25 cases (50%). Mononuclear cell infiltration was seen in all 50 cases (100%). Neutrophilic activity was seen in all 50 cases (100%). Mild activity was seen in 27 (54%) cases. Moderate activity in 10 (20%) cases and severe activity in 13 (26%) cases. H. pylori density was mild in 29 (58%) cases, moderate in 10 (20%) cases and severe in 11 (22%) cases. H. pylori density showed significant correlation with neutrophilic activity. Conclusion: H. pylori density has significant correlation with severity of neutrophilic activity. Chronic inflammation, metaplasia and atrophy did not show significant correlation with H. pylori density.
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