Cases reported "Helicobacter Infections"

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1/13. 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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2/13. gastric mucosa as an additional extrahepatic localization of hepatitis c virus: viral detection in gastric low-grade lymphoma associated with autoimmune disease and in chronic gastritis.

    The hepatitis c virus (HCV) has been linked to B-cell lymphoproliferation and autoimmunity, and has been localized in several tissues. The clinical observation of an HCV-infected patient with sjogren's syndrome (SS) and helicobacter pylori (HP) positive gastric low-grade B-cell non-Hodgkin's lymphoma (NHL), which did not regress after HP eradication, led us to investigate the possible localization of HVC in the gastric microenvironment. HCV genome and antigens were searched in gastric biopsy specimens from the previously mentioned case, as well as from 9 additional HCV-infected patients (8 with chronic gastritis and 1 with gastric low-grade B-cell NHL). HCV-specific polymerase chain reaction (PCR) and immunohistochemistry procedures were used. The gastric B-cell NHL from the patient with SS was characterized by molecular analyses of B-cell clonality. HCV rna was detected in both the gastric low-grade B-cell NHL and in 3 out of 6 gastric samples from the remaining cases. HCV antigens were detected in the residual glandular cells within the gastric B-cell NHL lesions, in glandular cells from 2 of the 3 additional gastric lesions that were HCV positive by PCR, and in 1 additional chronic gastritis sample in which HCV-rna studies could not be performed. By molecular analyses, of immunoglobulin genes, the B-cell NHL from the patient with SS was confirmed to be a primary gastric lymphoma, subjected to ongoing antigenic stimulation and showing a significant similarity with rheumatoid factor (RF) and anti-HCV- antibody sequences. Our results show that HCV can localize in the gastric mucosa.
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3/13. Sulfomucins in helicobacter pylori-associated chronic gastritis in children: is this incipient intestinal metaplasia?

    BACKGROUND: Little is known about early stages of intestinal metaplastic in chronic gastritis. The purpose of this study was to determine the presence of sulfated mucosubstances hence most probably intestinal metaplasia, in isolated cells of surface gastric pits, and glands in pediatric patients with helicobacter pylori-associated chronic gastritis. methods: Participants were nine patients (nine different biopsies; mean age 11.5 years, range 3-16 years) with sulfomucin-containing cells evident in the gastric biopsy specimen. Eight of the patients were selected from a group of 15 patients with histologically documented H. pylori-associated chronic gastritis in whom the utility of the Sydney system was being tested. RESULTS: Symptoms and endoscopic findings of H. pylori-associated chronic gastritis were the same regardless of the presence or absence of sulfomucin-containing cells. On hematoxylin and eosin stained tissues, neither intestinal metaplasia nor atrophy was apparent. However, periodic acid-Schiff (PAS)-alcian blue (pH 1.0) stain revealed the presence of sulfated mucosubstances in isolated cells of gastric pits and glands in the nine patients. CONCLUSIONS: This finding may represent a "minimal" form of incomplete intestinal metaplasia (type III). Because the nine patients had been untreated, the change is probably reversible. Two follow-up biopsies in patients in whom H. pylori had been treated and eradicated showed absence of sulfated mucins. Although these findings cannot be regarded as fully developed type III intestinal metaplasia, it is possible that left untreated, the alteration may persist and evolve into some other complication. This conclusion justifies follow-up of these patients.
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4/13. Salivary gland MALT lymphoma associated with helicobacter pylori infection in a patient with sjogren's syndrome.

    We report a case of salivary gland MALT lymphoma in sjogren's syndrome associated with localized H. pylori infection. A 76-year-old woman had a history of bilateral cheek masses for two years. Histologically, the parotid glands were invaded by numerous centrocyte-like cells to form lymphoepithelial lesions. The tumor cells showed immunohistological differentiation into B cells. Southern blotting demonstrated immunoglobulin gene rearrangement. These results indicated that the tumors were MALT lymphoma. H. pylori, as assessed by the urease test (CLO test; BML Ltd., tokyo, japan), was positive in the tumor specimen. After wide local excision of the tumors followed by radio therapy and oral administration of antibiotics and proton pump inhibitor, no evidence of recurrence was found during the 24-months of follow up. H. pylori infection in the salivary gland is rare, although the source of infection and transmission of H. pylori organisms has been thought to be the oral cavity. We discussed the association between H. pylori infection and salivary gland MALT lymphoma. The microorganism may play a role as an additional antigenic stimulus for the development of salivary gland MALT lymphoma as well as for the development of gastric MALT lymphoma. This means that H. pylori can play a role in lymphoma progression as booster of B cell lymphoproliferation.
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5/13. Regression of fundic gland polyps following acquisition of helicobacter pylori.

    The prevalence of helicobacter pylori infection is very low in patients with fundic gland polyps (FGPs) of the stomach. We report here two cases with multiple FGPs that regressed following new H pylori acquisition. Patient Nos I and II had multiple FGPs in normal fundic mucosa without inflammatory changes or atrophy. Both were not infected with H pylori. Following acquisition of H pylori infection however, all FGPs in both patients completely disappeared except for one FGP in patient No I. Although the size of the remaining polyp in patient No I was greatly reduced after H pylori acquisition, it became enlarged again after eradication. Interestingly, in the remaining polyp, we found an activating beta-catenin gene mutation whereas no such mutations were detected in FGPs of patient No II. Thus H pylori infection may have an inhibitory effect on the development of FGPs.
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6/13. Isolated granulomatous gastritis successfully treated by helicobacter pylori eradication: a possible association between granulomatous gastritis and helicobacter pylori.

    We report two cases of granulomatous gastritis that resolved completely with helicobacter pylori eradication. Two Japanese women, one 61 years old and one 58 years old, presented to our hospital with epigastralgia. endoscopy revealed multiple shallow ulcerative lesions in the gastric corpus of both patients. biopsy specimens demonstrated acute and chronic inflammation with multiple small, noncaseating granulomas at the level of the foveolar isthmi-the junction between the pits and the glands. Both specimens were positive for helicobacter pylori. No other causes of organic granulomatous disease could be found. Both patients were diagnosed as having isolated granulomatous gastritis and were given triple therapy for Helicobacter pylorieradication, with their fully informed consent. The granulomatous gastritis resolved after successful Helicobacter pylorieradication therapy. This report describes a possible association between isolated granulomatous gastritis and Helicobacter pyloriinfection. To our knowledge, this is the first report describing isolated granulomatous gastritis successfully treated by triple therapy ( Helicobacter pylorieradication therapy).
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7/13. Extranodal marginal zone (MALT) lymphoma in common variable immunodeficiency.

    We describe two patients with common variable immunodeficiency (CVID) who developed extranodal marginal zone lymphoma (formerly described as mucosa-associated lymphoid tissue lymphoma or MALT lymphoma). One patient, with documented pernicious anaemia and chronic atrophic gastritis with metaplasia, developed a helicobacter pylori-positive extranodal marginal zone lymphoma in the stomach. Three triple regimens of antibiotics were necessary to eliminate the H. pylori, after which the lymphoma completely regressed. Patient B had an H. pylori-negative extranodal marginal zone lymphoma of the parotid gland, which remarkably regressed after treatment with clarithromycin. Reviewing the literature, we found eight cases of extranodal marginal zone lymphoma complicating CVID, but probably many more cases labelled as non-Hodgkin's lymphoma are hidden in the literature. Until more data are available on the predictive value of noninvasive screening for pathology of the stomach, we recommend endoscopy to assess the gastric status in CVID patients in order to detect these malignancies at an early stage. Elimination of H. pylori infection is the treatment of choice in Helicobacter-positive extranodal marginal zone lymphoma. The possibility of elimination failure, most probably due to frequent and prolonged exposure to antibiotics in this patient group, should be taken into account. Treatment with antibiotics in Helicobacter-negative extranodal marginal zone lymphoma must be considered.
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8/13. Mucosa-associated lymphoid tissue lymphoma of the transverse colon: a case report.

    We herein present a case of a 75-year-old female with mucosa-associated lymphoid tissue (MALT) lymphoma of the transverse colon with the stage IE (Ann Arbor classification). colonoscopy revealed the tumor's appearance as a IIa plus II c-like early colon cancer as defined according to the macroscopic classification of the Japanese research Society for Cancer of Colon, rectum and Anus, measuring less than 2 cm in diameter. Histologically, the tumor was diagnosed as MALT lymphoma because of the presence of lymphoepithelial lesions consisting of diffuse proliferation of atypical lymphocytes and glandular destruction. The majority of these lymphocytes immunohistochemically stained for the B-lymphocyte marker. The patient first underwent H pylori eradication therapy with Lansap. However, the tumor size gradually increased over the next 4 mo and the patient eventually underwent surgical resection. The operative procedure included a partial colectomy with dissection of the paracolic lymph nodes. The tumor measured 45 mm multiply 30 mm in diameter and histological examination showed that the lymphoma cells had infiltrated the muscle layer of the colon without nodal involvement. The patient has had no recurrence postoperatively without any chemotherapy.
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9/13. 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.
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10/13. Synchronous adenocarcinoma and low grade B-cell lymphoma of mucosa associated lymphoid tissue (MALT) of the stomach.

    We describe nine cases of gastric adenocarcinoma (six intestinal and three diffuse type) occurring in the stomach synchronously with primary low grade B-cell lymphoma of mucosa associated lymphoid tissue. In four cases the two neoplasms were admixed to form collision tumours. Where collision was present between lymphoma and adenocarcinoma of intestinal type no lymphoepithelial lesions were seen involving neoplastic glands. helicobacter pylori-like organisms were seen in seven cases (78%) which is consistent with an aetiological role for this organism in both tumours in the stomach.
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