1/8. Eradication of helicobacter pylori heals atrophic corpus gastritis caused by long-term treatment with omeprazole.Long-term treatment with proton pump inhibitors in patients with helicobacter pylori gastritis can lead to atrophic changes in the corpus mucosa. What is still unclear, however, is whether this atrophy can regress in response to helicobacter pylori eradication. We report on a male patient with helicobacter pylori gastritis receiving long-term treatment (4 years) with omeprazole for gastrooesophageal reflux disease, who developed autoaggressive gastritis with progressive atrophy, hypochlorhydria, hypergastrinaemia and nodular ECL-cell hyperplasia. To determine whether these changes might be induced to regress, helicobacter pylori eradication therapy was administered. Ten months after helicobacter pylori eradication autoaggressive lymphocytic infiltrates were no longer detectable, and the glands in the corpus mucosa had normalised despite continued treatment with omeprazole - a finding that was confirmed at two further follow-up surveys performed at 6-month intervals. This case report shows that atrophy of the corpus mucosa developing under long-term treatment with a proton pump inhibitor can be cured by eradicating helicobacter pylori.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
2/8. Primary biliary cirrhosis associated with type A gastritis and chronic thyroiditis.We report a patient with primary biliary cirrhosis (PBC) associated with type A gastritis, chronic thyroiditis, and iron deficiency anemia. The patient was a 45-year-old Japanese woman who was admitted to our hospital with severe microcytic and hypochromic anemia, abnormal results for liver function tests, and a diffuse goiter. The diagnosis of PBC (Scheuer's stage II) was confirmed by the presence of specific anti-mitochondrial antibody in high titers and histological examination showing chronic non-suppurative destructive cholangitis with bridging fibrosis. Additionally, marked atrophic mucosa throughout the body and fundus of the stomach was observed endoscopically, and there was positivity for intrinsic factor antibody, an extremely low ratio of serum pepsinogen a to C, and hypergastrinemia, indicating coexisting type A gastritis. The severe anemia was thought to be caused by failure of dietary iron absorption related to achlorhydria with this gastritis. However, the serum level of vitamin B12 was normal. She also had autoimmune thyroiditis. PBC is frequently associated with extrahepatic autoimmune diseases, including ductular lesions. However, the association of PBC with type A gastritis is quite rare, although the stomach is also an exocrine glandular structure. This particular case, in addition to previous reports, leads to a discussion of whether type A gastritis should be regarded as a possible, although uncommon, component disorder of so-called dry gland syndrome.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |
3/8. Two cases of gastric cancer-bearing double choledochus with ectopic drainage into the stomach.Two cases of double choledochus with ectopic drainage into the stomach associated with gastric carcinoma were reported. The stomachs were resected because of the presence of cancer, and the orifices of the ectopic bile duct were found in the oral side of the lesions. In these two cases, hyperplasia of gastric foveolas and atrophy of fundic gland, with its cystic dilatation, were observed around the orifices. A possible correlation between direct flow of bile juice into the stomach through the ectopic bile duct and the development of gastric cancer was discussed. The literature regarding double choledochus was reviewed.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
4/8. Gastric pseudopolyposis: a new clinical manifestation of type A gastritis.Three cases of type A gastritis associated with multiple polypoid lesions of the body of the stomach are presented. The endoscopic congo-red test showed the red to black color changes of the sprayed congo-red only on the top of the polypoid lesions. The endoscopic methylene-blue test revealed no dye absorption on the antral mucosa or on the top of the polypoid lesions, while the dye was absorbed on the flat mucosa surrounding the top of the polypoid lesions. Histological examinations revealed well-preserved oxyntic glands on the top of the polypoid lesions. The flat mucosa showed marked atrophy or intestinal metaplasia. There have been several reports of experimental models of type A gastritis, where chief and parietal cells decreased in considerable number. These findings and the experimental models suggest that the polypoid lesions resulted from atrophic changes of type A gastritis. The top of the polypoid lesions is the residual oxyntic glands. The lesions, therefore, should be called "gastric pseudopolyposis." The spontaneous disappearance of the polypoid lesions seen in one case is thought to be a result of a further progression of the atrophic gastritis. A pronounced G-cell increase was noted in the antrum and lower body of the stomach. This is considered a secondary phenomenon following the marked reduction of acid secretion.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |
5/8. Primary sjogren's syndrome associated with chronic atrophic gastritis and pernicious anemia.sjogren's syndrome (SS) is a systemic, autoimmune exocrinopathy in which destructive, inflammatory-cell infiltration can affect any gland. Although chronic atrophic gastritis is the most common form of gastrointestinal involvement in SS, pernicious anemia develops in rare cases. We therefore report a patient with these three associated diseases.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
6/8. Antigenic mimicry between helicobacter pylori and gastric mucosa in the pathogenesis of body atrophic gastritis.BACKGROUND & AIMS: The majority of patients with helicobacter pylori infection have autoantibodies cross-reacting with gastric antigens. In this study, the relation between autoantibody status, histopathology of body mucosa, and antigenic profile of H. pylori was investigated. methods: One hundred patients were examined for H. pylori infection, body gastritis, and gastric autoantibodies. Balb/c mice were analyzed for serum autoantibodies after immunization with H. pylori from patients with and without atrophic gastritis. RESULTS: immunoglobulin g autoantibodies were detected in 57 of the 87 infected patients (65.5%) but in none of the 13 patients without infection and gastritis. The autoreaction involved mainly the luminal surface of glandular cells and secretory canaliculi of parietal cells. The autoantibody status correlated with the presence and degree of inflammation and atrophy of the glands. H. pylori from patients with atrophic gastritis showed a higher capacity to induce autoantibodies than H. pylori from patients with a minimal superficial gastritis. Monoclonal antibodies showed differences in the bacterial expression of cross-reacting determinants. CONCLUSIONS: H. pylori-mediated autoimmunity is involved in the pathogenesis of chronic atrophic gastritis. The grade of antigenic mimicry of the infecting H. pylori strain plays a role in the progression of chronic gastritis to atrophy.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |
7/8. Autoimmune enteropathy with severe atrophic gastritis and colitis in an adult: proposal of a generalized autoimmune disorder of the alimentary tract.BACKGROUND: We describe the case of an adult with autoimmune enteropathy consistent with both severe atrophic gastritis accompanying antral stenosis and colitis. methods AND RESULTS: The patient, positive for anti-intrinsic factor antibody, had intractable diarrhea and protein-losing enteropathy. In the ileum inflammatory cells were observed infiltrating the lamina propria along with villus atrophy, and similar inflammation was also found in the lamina propria of the colon and stomach, with complete loss of specialized glands. The myenteric ganglion cells of the hypertrophied muscularis propria in the stenosed antrum showed degeneration with surrounding T-lymphocyte infiltration. There were more CD8 than CD4 lymphocytes in the lamina propria of the stomach and colon. CONCLUSIONS: The CD8 (suppressor-cytotoxic) T lymphocytes may have played an important role in the production of lesions in the stomach, small intestine, and colon, so we propose this case as an example of a generalized autoimmune disorder of the alimentary tract.- - - - - - - - - - ranking = 1keywords = gland (Clic here for more details about this article) |
8/8. Immunohistochemical analysis of a case of gastritis cystica profunda associated with carcinoma development.We report a rare case of gastritis cystica profunda (GCP) accompanied by carcinoma that developed in a 51-year-old Japanese man without antecedent gastric surgery. The polypoid tumor was located in the upper body of the resected stomach. Histologically, it was characterized by herniation of surface epithelium and cystic glands in the submucosa, muscularis propria, and subserosa. Marked chronic atrophic gastritis was found throughout the stomach, and dysplastic epithelia and a few adenocarcinoma cells were found in the deeper parts of the GCP. The Ki-67, p53, and p21WAF1/CIP1 labeling indices for the deeper part of the GCP were higher than those for the superficial parts or the surrounding mucosa, suggesting that both epithelial cell proliferation and p53-dependent p21WAF1/CIP1 expression in dna-damaged cells, which might be associated with gastritis, are enhanced in line with penetration of glands. The underlying mechanisms might be linked in a chain of factors leading to malignancy.- - - - - - - - - - ranking = 2keywords = gland (Clic here for more details about this article) |