Multispectral imaging detects gastritis consistently in mouse model and in humans
Thomas BazinSergio Ernesto Martinez‐HerreraAude Jobart‐MalfaitYannick BenezethMatthieu BoffetyCatherine JuliéJean‐François EmileValérie MichelFrançois GoudailEliette TouatiFranck MarzaniDominique Lamarque
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Abstract Gastritis constitutes the initial step of the gastric carcinogenesis process. Gastritis diagnosis is based on histological examination of biopsies. Non-invasive real-time methods to detect mucosal inflammation are needed. Tissue optical properties modify reemitted light, i.e. the proportion of light that is emitted by a tissue after stimulation by a light flux. Analysis of light reemitted by gastric tissue could predict the inflammatory state. The aim of our study was to investigate a potential association between reemitted light and gastric tissue inflammation. We used two models and three multispectral analysis methods available on the marketplace. We used a mouse model of Helicobacter pylori infection and included patients undergoing gastric endoscopy. In mice, the reemitted light was measured using a spectrometer and a multispectral camera. We also exposed patient’s gastric mucosa to specific wavelengths and analyzed reemitted light. In both mouse model and humans, modifications of reemitted light were observed around 560 nm, 600 nm and 640 nm, associated with the presence of gastritis lesions. These results pave the way for the development of improved endoscopes in order to detect real-time gastritis without the need of biopsies. This would allow a better prevention of gastric cancer alongside with cost efficient endoscopies.Keywords:
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The authors analyze results of a study of 100 patients with chronic gastritis showing secretory insufficiency with a dubious diagnosis. Endoscopy and intragastric pH-metry were used. The diagnosis of chronic gastritis was confirmed in 35 patients and of them with secretory insufficiency only in 21 patients that evidences inadequate attention to the complaints, anamnesis, incomplete examination and use of laboratory and other data.
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The aim of this study was to evaluate the prevalence of chronic gastritis in pet dogs, to determine the histopathologic changes of gastric mucosa and, to determine its relationship with canine gastric Helicobacter infection. Sixty percent (n = 18), 27% (n = 8) and 13% (n = 4) of the examined stomachs showed normal, congested and erosive gastric mucosa respectively. Histopathologic examination was confirmed the presence of chronic gastritis in 40% of dogs (n = 12). Lymphocytic-plasmacytic gastritis was the most common type of chronic gastritis. Gastric Helicobacter was detected in cytological examination of 26 out of 30 dogs (86.6%) but in the PCR analysis, 93% of gastric samples were positive for GHLO. There was no significant relation between the presence of Helicobacters and chronic gastritis (p>0.05). Follicular gastritis was detected in 12 cases (40%) and there was also no significant correlation between its presence and GHLO's infection (p>0.05). In conclusion, chronic gastritis can be considered as a prevalent disease especially in dogs. Nutritional and environmental factors as well as individual immune response may have role in induction of chronic gastritis, but the clinical significance of these histopathologic changes should be evaluated.
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The authors propose the definition of chronic gastritis with a brief overview of the history of investigation of this diseases and its prevalence with special reference to (1) the bacterial profile and its role in the development of infectious and inflammatory process in gastric mucosa, (2) the modern state of and new trends in the classification of chronic gastritis including their advantages and disadvantages, (3) the relationship between chronic gastritis and functional gastroduodenal dyspepsia syndrome. It is concluded that mucous microflora plays an important factor in the development ofpathology but H.pylori is not its predominant component. Modern classifications of chronic gastritis provide a basis for a deeper insight into evolution of chronic gastritis and its transformation into cancer. The diagnosis of ‘chronic gastritis with functional gastroduodenal dyspepsia syndrome‘ is invalid.
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Altogether 31 children with chronic gastritis were examined. Three diagnostic tests were employed for detecting Campylobacter pylori. The clinical signs of the disease and the endoscopic features of the gastric mucosa are described.
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Aim: To analyze the role of tumor necrosis factor (TNF)-α in the pathogenesis of Helicobacter pylori (HP)-associated chronic gastritis.Methods:Nineteen patients with HP-associated chronic gastritis, eighteen patients with HP-negative chronic gastritis, and 11 healthy controls were subjected. Sixteen patients with HP-associated chronic gastritis accepted treatment against HP infection for a week. Antral biopsies were taken and cultured for 48 h, and TNF-α mRNA levels were assessed using RT-PCR assay and supernatants were collected to detect TNF-α using ELISA. Results: The level of TNF-α protein in the supernatants and the expression of TNF-α mRNA in antral biopsies were higher in patients with HP-positive chronic gastritis than those in HP-negative chronic gastritis and healthy controls (P0.05). TNF-α level was decreased in the supernatants from patients with HP-associated gastritis after the treatment against HP infection (P 0.05). Conclusion: TNF-α is highly expressed in antral mucosa after HP infection, which may play an important role in the pathogenesis of chronic gastritis.
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Chronic gastritis
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AbstractChronic (atrophic) gastritis is a progressive disease which in a small proportion of patients leads to severe (total) atrophy (severe grade of chronic gastritis) of the antral or body mucosa or both. Chronic gastritis is a premalignant condition which favours the development of gastric cancer. Chronic gastritis precedes gastric cancer and shows a severalfold increase in the risk of gastric cancer compared to subjects with histologically normal stomachs. Several tentative modifications to the estimate of the risks may be presented: (i) a severe risk of developing gastric cancer is restricted to subjects with a severe grade of chronic gastritis (ii) the risk of gastric cancer is increased in subjects who have either severe antral or body chronic gastritis, the risk being approximately three to five times higher in the antral chronic gastritis (B-type of gastritis) than in the body chronic gastritis (A type of gastritis); (iii) the antral and body chronic gastrites are independent risk factors for gastric cancer, the joint risks being multiplicands of the marginal risks i.e., the estimated risk is highest in those subjects who show severe chronic gastritis in both the antrum and the body (AB type of gastritis); (iiii) the chronic gastritis mediated gastric cancer risk is limited to gastric cancers of the intestinal type, and thus covers only a proportion of all cases of gastric cancer. In the highest risk groups it may be estimated that the probability of a subject developing gastric cancer in subsequent decades is up to 30% if the subject is a young man who has severe chronic gastritis in his antrum, or who has it coexistently in the antrum and body.Key Words: gastric cancerchronic atrophic gastritiscancer risk.
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The isolation of Helicobacter pylori from the human stomach has changed the insights into the mechanisms of chronic gastritis. The altered concepts are reflected in newly developed classification systems. In 1989 distinction of the types A, B and C of chronic gastritis was proposed as a working formulation. In this classification type A gastritis is an autoimmune disease with antibodies against parietal cells and intrinsic factor. It is limited to the body of the stomach and may be complicated by pernicious anaemia. Type B gastritis is related to bacterial infection by Helicobacter pylori and predominantly affects the antrum. It is associated with peptic ulcer disease. Type C gastritis is caused by chemical injury due to bile reflux and drugs. Especially NSAIDs are implicated. Each of these forms of gastritis has its histological counterpart. In 1990 the A, B, C terminology was overruled by the Sydney system, which recognises three forms of gastritis: acute, chronic and special forms and is otherwise mainly descriptive. The different classification systems are briefly discussed. It is concluded that uniformity in classification is most important since it will facilitate epidemiologic research of the natural history and long-term outcome of these diseases.
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