3,489 research outputs found

    Endoscopic findings of gastric neoplasms in familial adenomatous polyposis are associated with the phenotypic variations and grades of dysplasia

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    Patients with familial adenomatous polyposis (FAP) are at increased risk of developing gastric neoplasms. However, endoscopic findings have not been sufficiently investigated. We investigated the phenotypic expression of gastric adenoma (low-grade dysplasia) and gastric cancer (high-grade dysplasia or carcinoma) in patients with FAP and clarified their relationships to endoscopic findings. Of 29 patients with FAP who underwent esophagogastroduodenoscopy between 2005 and 2020, 11 (38%) had histologically confirmed gastric neoplasms, including 23 lesions of gastric adenoma and 9 lesions of gastric cancer. The gastric neoplasms were classified into 3 phenotypes (gastric, mixed, or intestinal type) according to the immunostaining results and evaluated for location (U or M region: upper or middle third of the stomach or L region: lower third of the stomach), color (same as the background mucosa, whitish, or reddish), macroscopic type (elevated, flat, or depressed), background mucosal atrophy (present or absent), fundic gland polyps in the surrounding mucosa (present or absent), and morphologic changes in tumor size. Elevated whitish gastric adenomas were further subdivided by macroscopic type (flat elevated, protruded, or elevated with a central depression) and color (milky- or pinkish-white). The gastric adenomas included gastric (11/23, 48%), mixed (4/23, 17%), and intestinal (8/23, 35%) phenotypes. In contrast, no lesions of gastric cancers showed a gastric phenotype (0/9, 0%), while 5 (56%) and 4 (44%) lesions were intestinal and mixed phenotypes, respectively. Gastric cancers were significantly more likely than gastric adenomas to present as reddish depressed lesions with gastric atrophy. All gastric-type adenomas occurred in non-atrophic mucosa, in mucosa with fundic gland polyps in the periphery, in the U or M region, and as flat elevated or protruded lesions with a milky-white color. Half of the lesions increased in size. Meanwhile, the typical endoscopic features of intestinal-type adenomas included occurrence in the L region and elevated pinkish-white lesions with central depression. None of the intestinal-type adenomas increased in size during the observation period. We believe that these endoscopic features will be useful for the prompt diagnosis and appropriate management of gastric neoplasms in patients with FAP

    Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.

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    Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells

    Correlation between the ABO blood group system and gastritis

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    Introdução: A infecção pelo Helicobacter pylori (HP) e fatores ambientais são importantes fatores de risco para gastrite. Estudos apontam correlação entre o sistema ABO e doenças gastrointestinais. Objetivos: caracterizar o perfil sociodemográfico de portadores de gastrite e HP e sua correlação com o sistema do grupo sanguíneo ABO. Materiais e métodos: Estudo prospectivo e descritivo, realizado em Aracaju, Sergipe, Brasil, de abril/2018 a maio/2019. Amostra constituída por 133 pacientes que realizaram endoscopia digestiva alta, análise histopatológica e tipagem sanguínea. Foram diagnosticados com gastrite 93 pacientes. Utilizou-se questionário sociodemográfico e clínico. Os dados foram analisados pelo RCore Team 2019 e submetidos a análises descritivas e inferenciais. Nível de significância 5%. Resultados: Idade média 53,7 anos (DP 17,4) sendo 48 (51,6%) do sexo masculino (p=0,018), 56 (65,9%) pardos, 45 (52,9%) casados e 33 (35,5%) tinham empregos fixos. Dos portadores de gastrite, 59 (63,4%) eram do tipo sanguíneo O. Dentre os tipos de gastrite, 31(33,4%) eram enantematosa leve e 16 (51,6%) desses eram do tipo O. Houve prevalência do tipo O em todos os graus de atividade inflamatória. Foi detectado H. pylori em 29 (31,2%) pacientes, sendo o fenótipo O mais prevalente nos graus moderado e severo da infecção. Conclusão: Os homens foram mais acometidos de gastrite, independente do tipo segundo a classificação de Sydney. O fenótipo sanguíneo O foi mais prevalente nos portadores de gastrite, naqueles que apresentaram atividade inflamatória à histologia e em portadores de H. pylori grau moderado e severo.Introduction: Helicobacter pylori (HP) infection and environmental factors are important risk factors for gastritis. Studies show a correlation between the ABO system and gastrointestinal diseases. Aims:  To characterize the sociodemographic profile of patients with gastritis and HP and its correlation with the ABO blood group system. Materials and methods: Prospective and descriptive study, carried out in Aracaju, Sergipe, Brazil, from April / 2018 to May / 2019. Samples were collected from 133 patients who underwent upper digestive endoscopy, histopathological analysis, and blood typing. Out of which, 93 patients were diagnosed with gastritis. A sociodemographic and clinical questionnaire was also used. Data analyzed by RCore Team 2019 and submitted to descriptive and inferential analyzes. Results: Average age 53.7 (SD 17.4) with 48 (51.6%) being male (p = 0.018), 56 (65.9%) brown, 45 (52.9%) married and 33 (35.5%) pursuing permanent jobs. Fifty-nine patients (63.4%) out of those with gastritis were blood type O. Among the types of gastritis, 31 (33.4%) were mild enanthematous and 16 (51.6%) of these were type O. There was a prevalence type O in all degrees of inflammatory activity. H. pylori were detected in 29 (31.2%) patients;  the most prevalent phenotype being the moderate and severe degrees of infection. Conclusion: Men were mostly affected by gastritis, regardless of the type according to the Sydney classification. The blood phenotype O was more prevalent in patients with gastritis, in those who had inflammatory activity at histology and in patients with moderate, and severe H.pylori

    Dynamic expression of CEACAM7 in precursor lesions of gastric carcinoma and its prognostic value in combination with CEA

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    <p>Abstract</p> <p>Background</p> <p>The significance of carcinoembryonic antigen-related cell adhesion molecule 7 (CEACAM7) expression in gastric carcinoma and precancerous lesions and its correlation with CEA expression has rarely been previously investigated.</p> <p>Methods</p> <p>CEACAM7 and CEA expression was detected by immunohistochemistry in consecutive sections of 345 subjects with gastric carcinoma and precancerous lesions. Laser confocal analysis was performed to determine CEACAM7 and CEA localization. Correlation between CEACAM7 and CEA expression with clinicopathological parameters was statistically analyzed.</p> <p>Results</p> <p>CEACAM7 expression correlated with pathologic grading (P = 0.006), Lauren's classification (P = 0.023), and CEA expression (Spearman R = 0.605, P < 0.001) in gastric carcinoma. CEACAM7 co-localized with CEA predominantly in the cytoplasmic membrane of cancerous cells. CEA expression was correlated with lymph node metastasis (P = 0.031). CEACAM7 and CEA expression increased progressively from precursor lesions to gastric carcinomas. A combination of CEACAM7 and CEA expression was determined to be an independent predictor for patients with gastric carcinoma by multivariate analysis (P = 0.001).</p> <p>Conclusions</p> <p>CEACAM7 expression correlates with tumor differentiation and CEA expression in gastric carcinoma. CEACAM7 and CEA expression may synergistically promote gastric carcinogenesis. Combined CEACAM7 and CEA expression analysis can be a useful postoperative predictor for patients with gastric carcinoma.</p

    Immunohistochemical Profile of Mucins in Gastric Carcinoma

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    Gastric adenocarcinoma of the fundic gland: A review of clinicopathological characteristics, treatment and prognosis

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    Gastric adenocarcinoma of the fundic gland is a rare, well-differentiated gastric cancer entity, and very few patients transition to poorly differentiated tubular adenocarcinoma during progression. Gastric adenocarcinoma of the fundic gland originates from the mucosa of the gastric fundic gland, usually without chronic gastritis or intestinal metaplasia. Histologically, the tumor cells are closely arranged to form anastomosing tubular glands, and more than 95% of tumor cells differentiate towards chief cells. Most gastric adenocarcinoma of the fundic gland cases are characterized by submucosal involvement, but the tumor volume is usually small, with lymphatic and vascular invasion rarely observed. Therefore, endoscopic submucosal dissection can be an ideal treatment, leading to a favorable prognosis, and recurrence and metastasis of the disease are uncommon

    Site-specific differences in T lymphocyte composition of the gastric mucosa after Helicobacter pylori eradication

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    In our earlier work, we revealed that inflammation of the lesser curvature of the gastric body and antrum could constitute independent risk factors for gastric cancer development, while inflammation of the greater curvature was not. The aims of this study were as follows: first, to reveal the differences between T lymphocyte populations of the gastric antrum and the greater and lesser curvatures of the gastric body in patients after Helicobacter pylori eradication; second, to analyze the correlation between the composition of the stomach-resident T lymphocytes and time from H. pylori eradication; and third, to evaluate the sex differences in T lymphocyte subsets after H. pylori eradication. To investigate site-specific differences in stomach-resident T lymphocytes after H. pylori eradication, we performed flow cytometry analysis on samples taken from the gastric antrum, greater curvature of the gastric body, and lesser curvature of the gastric body of 20 patients. We also analyzed the correlation between the composition of the stomach-resident T lymphocytes and the time from H. pylori eradication. The lymphocyte subsets of the antrum and lesser curvature of the body were similar. In contrast, compared to those in the greater curvature of the gastric body, CD4(+)/CD3(+) lymphocyte subsets (43.8 +/- 19.4% vs 31.7 +/- 14.6%) were elevated in the lesser curvature of the body, whereas CD8(+)/CD3(+) (67.1 +/- 21.3% vs 80.4 +/- 12.0%), CD7(+)/CD3(+) (91.2 +/- 4.6% vs 93.7 +/- 3.8%), CCR4(+)/CD3(+) (7.7 +/- 8.1% vs 10.4 +/- 7.0%), CD45RA(+)/CD3(+)CD4(+) (27.2 +/- 24.8% vs 39.5 +/- 20.8%), and CD45RA(+)/CD3(+)CD4(-) (14.2 +/- 11.1% vs 18.7 +/- 11.5) were lower. Linear regression analysis showed a negative correlation between the time after H. pylori eradication and CD4(+)/CD3(+) (P < .05, R-2 = 0.198). There were no significant differences between men and women with respect to the lymphocyte populations. These results indicate that there are site-specific differences in lymphocyte composition in the stomach after H. pylori eradication
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