Cases reported "Gastritis, Atrophic"

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1/16. 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.
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2/16. 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.
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3/16. Expression of Cdx1 and Cdx2 mRNAs and relevance of this expression to differentiation in human gastrointestinal mucosa--with special emphasis on participation in intestinal metaplasia of the human stomach.

    BACKGROUND: The caudal-type homeobox genes, Cdx1 and Cdx2, are candidates for directing intestinal development, differentiation, and maintenance of the intestinal phenotype. The aims of this study were: (1) to assess the normal tissue expression patterns of Cdx1 and Cdx2 in the human gastrointestinal tract and (2) to ascertain levels in intestinal metaplasia (IM) of the stomach associated with gastritis. methods: Fresh human tissues were collected by surgical resection from 39 patients after informed consent had been received. RNAs were extracted from 11 distinct sites in the gastrointestinal mucosa (gastric body, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum), and Northern hybridization was performed for Cdr1 and Cdx2 mRNAs. In addition, RNAs were also extracted from normal gastric mucosa, and gastric mucosa with mild to severe IM, confirmed histopathologically. Reverse-transcriptase polymerase chain reaction (RT-PCR) was then carried out for Cdx1 and Cdx2. RESULTS: The expression of Cdx1 mRNA increased gradually from the duodenum to the distal colon, with no expression detected in the stomach. Compared with the distribution of Cdx1 mRNA in the mouse gastrointestinal tract, the expression of Cdr1 mRNA in the human gastrointestinal tract showed greater predominance in the jejunum and ileum. The expression of Cdx2 mRNA increased gradually from the duodenum to the proximal colon and decreased from the ascending colon to the rectum. Compared with the expression pattern of Cdx2 mRNA in the mouse gastrointestinal tract, the expression of Cdx2 mRNA in the human gastrointestinal tract showed greater predominance in the ileum. By RT-PCR, both Cdx1 and Cdx2 mRNAs were detected in the mild and severe types of IM. However, neither of these mRNAs was identified in normal gastric mucosa without IM. CONCLUSIONS: Cdr1 and Cdx2 mRNAs are widely present in the human intestinal and colonic mucosae, but not in the gastric mucosa, suggesting that their expression may contribute to the intestinal phenotype. The high levels of these mRNAs in IM mucosa associated with chronic atrophic gastritis point to an association with this phenotypic shift in the gastric mucosa.
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4/16. Combined adenocarcinoma and carcinoid tumor in atrophic gastritis.

    The development of adenocarcinoma or carcinoid tumors in atrophic gastritis is widely documented. We report the simultaneous occurrence of gastric adenocarcinoma and carcinoid (composite tumor) in atrophic gastritis, a finding reported only twice before in the literature. This 52-yr-old man with rectal bleeding, epigastric pain, and iron deficiency anemia was noted to have multiple polypoid masses on upper endoscopy. biopsy revealed features of both adenocarcinoma and carcinoid tumor in a background of atrophic gastritis, leading to a total gastrectomy, lymph node dissection, and liver biopsy. The gastrectomy specimen was characterized by a 6 cm pedunculated polyp and multiple sessile nodular masses between 0.4 and 2.5 cm in the background of a granular mucosa. On microscopic examination, the large polypoid mass corresponded to a well-differentiated adenocarcinoma, intestinal type, infiltrating the wall. The smaller nodules were composed of carcinoid tumors, restricted to the mucosa, or infiltrating the gastric wall. carcinoid tumor was also seen in the large polypoid mass closely intermingled with adenocarcinoma.The carcinoid tumor metastasized to the liver. lymph nodes showed both adenocarcinoma and carcinoid tumor. The gastric mucosa was characterized by atrophic gastritis with intestinal metaplasia, neuroendocrine hyperplasia, and microcarcinoids. The adenocarcinoma stained strongly for CK7, CK 20, MIB-1, and focally for chromogranin and synaptophysin. The carcinoid tumor was negative for CK7, CK 20 and MIB-1, and was positive for chromogranin and synaptophysin. Overexpression of p53 was noted only in the adenocarcinoma. Electron microscopy revealed neurosecretory granules in the carcinoid characteristic of a neuroendocrine tumor. Composite tumor can occur in the setting of atrophic gastritis. The findings in this patient reinforce the concept that the epithelial and neuroendocrine cells of the gastrointestinal tract both result from multidirectional differentiation of a primitive cell.
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5/16. Simultaneous EBV-positive lymphoepithelioma-like carcinoma and EBV-negative intestinal-type adenocarcinoma in a patient with helicobacter pylori-associated chronic gastritis.

    We report the case of a 72-year-old man with 2 simultaneous gastric carcinomas. The larger, ulcerated mass in the antrum was a conventional infiltrating intestinal-type adenocarcinoma. The associated antral-type mucosa showed moderate chronic gastritis, foci with complete and incomplete intestinal metaplasia, and mild to moderate helicobacter pylori infection. The second, smaller tumor was found within fundic-type mucosa and was a lymphoepithelioma-like carcinoma associated with Epstein-Barr virus (EBV) infection shown by the EBV-encoded small rna (EBER) test. The EBER test result was negative in the intestinal type adenocarcinoma. To our knowledge, this is the first report of simultaneous gastric carcinomas with 2 different morphologic phenotypes, in which only one tumor was associated with EBV infection, while the second tumor was related to H pylori-associated chronic gastritis. Our report demonstrates 2 different but simultaneous etiologic pathways of gastric carcinogenesis in the same patient.
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6/16. clofazimine induced enteropathy--a case highlighting the importance of drug induced disease in differential diagnosis.

    A patient on treatment for multibacillary leprosy for the past three years, presented with episodes of abdominal pain. Since the patient improved with conservative management, clofazimine induced enteropathy was considered as a remote possibility. A review of the mucosal biopsies showed macrophages with crystal-storing spaces consistent with clofazimine deposition in the duodenum. This case highlights the need to consider and investigate drug-induced disease as part of the differential diagnosis.
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7/16. The role of gastric resection in the management of multicentric argyrophil gastric carcinoids.

    A patient with pernicious anemia, atrophic non-antral gastritis, hypergastrinemia, and widespread hyperplasia of enterochromaffin-like cells and manifest enterochromaffin-like cell carcinoma was followed up during 39 months, including 15 months after gastric resection. In this case normalization of gastrin levels did not prevent the development of multiple gastric carcinoids in the fundic mucosa, suggesting that factors other than gastrin are of importance in the pathogenesis.
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8/16. New phenotypic aspects in a family with lynch syndrome ii.

    Increasing attention has been given to hereditary nonpolyposis colorectal cancer (HNPCC). This report provides medical genetic/pathologic findings on an HNPCC kindred from southern italy that shows criteria consistent with lynch syndrome ii. An international collaborative effort led to extension of this kindred with disclosure of a potentially new spectrum of phenotypic findings: an excess of gastric carcinoma; complete intestinal metaplasia and chronic atrophic gastritis restricted to the antrum; an apparent excess of colonic mucosal macrophagia, which by special stain appeared to be positive for mucin, with a constant content of both sialo and sulfomucin, a lack of iron, and an inconstant positivity for lysozyme obtained by immunoperoxidase technique; and findings of crypt atrophy of the colonic mucosa. During the relatively short period of investigation of this family, an intensive educational and surveillance program has been mounted in the interest of improving cancer control through direct application of knowledge of natural history and the risk factor evidence through pedigree assessment.
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9/16. 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.
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10/16. Gastric gastrinoma and diffuse G cell hyperplasia associated with chronic atrophic gastritis. Endoscopic detection and removal.

    Chronic atrophic gastritis and a sessile polyp were diagnosed during gastroscopy of a patient with splenomegaly and portal hypertension. The polyp was removed endoscopically. Histologically, it proved to be an endocrine tumour, which was identified as gastrinoma by immunohistochemistry. Then, hypergastrinemia was found and gastrectomy was performed to ensure complete removal of the tumour. The surgical specimen showed G cell hyperplasia of the antro-pyloric mucosa and severe atrophic gastritis with scattered argyrophil micronodules in the corpus-fundus region. 3 years after this treatment the patient is well.
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