Iron-deficiency and gastric mucosa: Especially the experimental atrophic lesion of the gastric mucosa in iron-deficient rats
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Surgical oncology
Atrophic gastritis
Colorectal Surgery
Intestinal mucosa
AbstractTo diagnose fundic atrophic (type A) gastritis as part of the clinical investigation of various diseases or for epidemiologic purposes, a simple and reliable diagnostic test would be of great value. We studied circulating levels of pepsinogen A (PGA) and pepsinogen C (PGC) in 179 patients with fundic atrophic gastritis, 29 unselected patients with gastric adenocarcinoma, 15 totally gastrectomized patients, and 50 gastroscopically examined normal controls. Of 147 patients with severe atrophic gastritis, 42 (29%) had serum PGA and 22 (15%) serum PGC values within the range of those in totally gastrectomized patients. The most sensitive test for fundic atrophic gastritis was the PGA/PGC ratio in serum, the sensitivity and specificity being 99% and 94%, respectively (discrimination limit, 5.5). Correspondingly, the positive predictive value was 98%, and the negative predictive value 98%. Of 29 unselected patients with gastric adenocarcinoma 22 (76%) had serum PGA/PGC values lower than the discrimination limit for atrophic gastritis. We conclude that the relatively simple analysis of PGA and PGC in serum is a powerful test for fundic atrophic gastritis with several potential areas of application.Key Words: Atrophic gastritisgastrectomygastric cancerintestinal metaplasiapepsinogenpernicious anemiascreening
Atrophic gastritis
Pepsin
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The antioxidative properties of pig urinary bladder mucosa were compared with those of gastric and intestinal mucosa using nitroxide radicals. Electron paramagnetic resonance (EPR) method was used to monitor the metabolic processes of nitroxides in mucosae. The reduction of nitroxides was measured on intact luminal surfaces of gastric, intestinal, and urinary bladder mucosa, as well as in homogenates of mucosa surface layer. Furthermore, N-ethylmaleimide and ascorbate oxidase have been used to characterize the reducing agents in urinary bladder mucosa homogenates. The nitroxide concentration decrease on intact mucosa of the urinary bladder was significantly different from those of the gastric and the intestinal mucosa. The concentration decrease was the largest for intestinal mucosa and the smallest for bladder mucosa. On the other hand, homogenates exhibit the largest nitroxide reduction rates for the bladder mucosa and the smallest for the gastric mucosa. In the bladder surface layer homogenates ascorbate and thiol-containing reducing agents were found and their coupled action in the nitroxide reduction process was established. The mucosa of urinary bladder is protected against nitroxide free radicals by a relatively low permeability and very active endogenous reducing agents. The gastric and intestinal mucosa are more permeable and/or have greater antioxidant activity on their surface. The reduction of nitroxides in the urinary bladder mucosa occurs via the ascorbate-thiol coupled reducing system.
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Objective Atrophic gastritis, as a pre-cancerous condition of gastric cancer, is developed from non-atrophic gastritis.The aims of this study was to compare the gene expression profiles between atrophic gastritis and non-atrophic gastritis using cDNA microarray and to explore the molecular mechanisms in the development of atrophic gastritis. Methods Endoscopy and biopsy were performed consecutively in 227 patients (143 male, 84 female, age range between 16-72 years, with average age 48.6 years). Diagnosis of non-atrophic gastritis and atrophic gastritis was made according to histological examination, and 120 patients were in non-atrophic group and 107 in atrophic group. The total RNA was extracted from the biopsy specimens of two groups with Trizol reagent. cDNA microarray consisting 8 464 human genes (HGEC-80s kit) was used, and labeled cDNA with fluorescence probes were hybridized to microarray, and then the comparison of gene expression profiles was made between atrophic and non-atrophic gastritis. Results It was identified that in gene expression profiles of atrophic gastritis there were 165 genes showing a greater than 2-fold increase and 460 genes showing a greater than 50% decrease as compared to non-atrophic gastritis. RT-PCR analysis revealed similar results as in DNA microarray. Conclusions There is different expression in many genes between the gastric mucosal cells of non-atrophic and atrophic gastritis mucosa. Many genes expression profiles are involved in atrophic gastritis that would be of help in further understanding the development of atrophic gastritis.
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Purpose of the study . Determine the gastric mucosa Structure in patients with different serum pepsinogen levels and ratios. Material and methods . 801 people (387 men, 414 women) underwent clinical examination and determination of pepsinogen-1, pepsinogen-2 and serum anti-Helicobacter pylori antibodies using GastroPanel (Biokhit, Finland). 161 patients with different levels of atrophy determined by serological screening method underwent a fibroesophagogastroduodenoscopy (Olimpus-10) with biopsy and subsequent morphological examination of the gastric mucosa performed using a visual analogue scale according to the Sydney Staging System. 107 patients had morphometry of the gastric mucosa with the determination of the number of central, parietal and mucoid cells. Results . The prevalence of severe atrophic gastritis in the stomach accounted for 10.9%. H. pylori was detected in 90.0% of the subjects. The morphological study showed atrophy in 94.4–95.8% of subjects with atrophic gastritis of the corpus mucosa of the stomach as defined by serological testing. Conclusions. Atrophy of the stomach mucous membrane as determined by morphological examination was prevalent in patients with severe atrophic gastritis of the corpus mucosa of the stomach, diagnosed using the method for determining serum pepsinogen levels.
Atrophic gastritis
Pepsin
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Zusanli
Atrophic gastritis
Moxibustion
Chronic gastritis
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Atrophic gastritis
pernicious anemia
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The relationship between serum PG I, PG II levels and extent of atrophic gastritis was examined. On 64 patients (male: 32, female: 32, 51.9 years old on average) with established diagnosis of either atrophic gastritis or normal. In the X-ray gastric examination, Fuji Computed Radiography (FCR) was used to obtain clear-cut images of the gastric area. Concerning the serum PG I level, patients in the group with atrophic gastritis showed lower levels than those of the people in the group with no atrophic change, but the variation was wide, and no definite tendency was seen in the relationship between the atrophic change and the serum PG I levels. Concerning the serum PG II level, as the atrophic change progresses, the serum PG II level tended to increase gradually. A significant reduction in the PG I/II ratio was seen in the group with atrophic changes (p < 0.01) in comparison with the group with no atrophic changes, and the PG I/II value tended to decrease. In conclusion, as a relationship between the atrophic change and the serum PG levels had a wide variation, we considered to be difficult by to measure the serum PG level to understand the presence and extent of the atrophic gastritis.
Atrophic gastritis
Pepsin
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OBJECTIVE To observe the effect of the point injection method on the gastric mucosa barrier in rats with chronic atrophic gastritis. METHOD Rat models with varying degrees of chronic atrophic gastritis were made using MNNG in different concentrations. Equal amounts of Huangqi Injection and Danggui Injection were mixed and injected into the point Zusanli to observe the effect of the injection on the pathological change, hexosamine of the gastric mucosa and the value of phospholipid. RESULT The indexes of the gastric mucosa damage, atrophy, metatypical hyperplasia, etc. increased with the increase of the concentration in model making. In the point injection group, marked improvement was detected in gastric mucosa damage and other related pathological changes ( P 0.01). With the increase of the concentration in model making, hexosamine and phospholipid of the gastric mucosa assumed negative correlation ( P 0.01). CONCLUSION With the increase of the severity of chronic atrophic gastritis, the values of hexosamine and phospholipid drop significantly and the function of the gastric mucosa barrier is impaired. Point injection can markedly increase the values of hexosamine and phospholipid and prevent the occurrence of chronic atrophic gastritis by reinforcing the gastric mucosa barrier.
Atrophic gastritis
Zusanli
Chronic gastritis
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The content and distribution of immunoglobulins IgA and IgG in gastric mucosa were correlated in 55 individuals with gastric histology, circulating parietal cell antibodies (PCA) and intrinsic factor antibodies (IFA) in serum and the output of intrinsic factor (IF) in the stomach.While a small amount of IgG and IgA is found in normal gastric mucosa, these immunoglobulins (mostly IgA) increase in gastritis, especially in its chronic atrophic form, without metaplasia. The immunoglobulins, mainly IgA, are here contained within the round cell infiltrates. There is a gross parallelism between the amount of round cells infiltrating the gastric mucosa and the content of immunoglobulins therein.No correlation was found between the presence or absence of circulating PCA and IFA in serum and the content of immunoglobulins in the gastric mucosa. No PCA could be detected in the gastric mucosa of patients with chronic atrophic gastritis with or without intestinal metaplasia by the method used.No correlation was found between the decrease in IF output and the content of immunoglobulins in the gastric mucosa. While patients with most advanced atrophic gastritis with intestinal metaplasia showed the greatest impairment of IF output in the stomach, the content of IgA and IgG in their gastric mucosa was lower than that of patients with advanced atrophic gastritis without metaplasia, who also had a higher average output of IF in the stomach, than in the former group.The accumulation of immunoglobulins (mainly IgA) in the atrophic stomach is thus to be considered as a corollary of the inflammatory infiltration of the gastric mucosa, by round cells producing immunoglobulins.
Atrophic gastritis
Intestinal metaplasia
pernicious anemia
Metaplasia
Intrinsic factor
Immunoglobulin A
Foveolar cell
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