Cases reported "Gastritis"

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1/12. CD4/CD8 double-positive adult T cell leukemia with preceding cytomegaloviral gastroenterocolitis.

    We present a rare case of adult T cell leukemia (ATL) in which leukemic T cells simultaneously expressed CD4 and CD8 surface antigens and refractory cytomegalovirus (CMV)-induced gastroenterocolitis preceded its clinical onset. A 40-year-old male was admitted to our hospital with abdominal pain and bloody stool. biopsy specimens of the gastric and rectal mucosa indicated CMV-induced gastroenterocolitis. The patient also proved to be seropositive for human T lymphotropic virus type I (HTLV-I). While being administered gancyclovir for CMV infection, he presented hepatomegaly and systemic lymphadenopathy. Monoclonal expansion of lymphoid cells integrated with HTLV-I genome was observed. He underwent a LSG15 regimen and hepatomegaly and lymphadenopathy improved markedly. Gastroenterocolitis also improved, but the symptoms did not disappear completely. CMV-induced diseases are prevalent among immunosuppressed patients. Although there was no evidence that this patient had ATL on admission, it is likely that he was severely immunodeficient. CMV can easily infect damaged mucosa. ATL cells often infiltrate gastrointestinal mucosa and may have triggered CMV gastroenterocolitis in this case.
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2/12. 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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3/12. Eosinophilic gastritis due to anisakis: a case report.

    BACKGROUND: the parasite anisakis simplex is a helminth included in the nematode class. When man eats raw or rare fish and cephalopods infested by anisakis larvae, he can acquire the parasitic disease (anisakidosis). The parasite can also originate manifestations of immediate IgE mediated hypersensitivity in patients with sensitisation to it. methods AND RESULTS: we present the case of a 14 year old boy diagnosed of eosinophilic gastritis after endoscopic examination and biopsy associated to recurrent abdominal pain. After allergologic study, a type I hypersensitivity mechanism against anisakis simplex is confirmed by means of prick test, antigen specific IgE determination and antigen specific histamine release test. Sensitisation against fish proteins is ruled out as well as parasitic infestation. CONCLUSIONS: in this case report we demonstrate a type I hypersensitivity mechanism against anisakis simplex in a patient diagnosed of eosinophilic gastritis. This can be suspected in cases of gastritis or non filiated enteritis with a torpid evolution following the conventional treatment and especially if the onset of the symptoms is related with the intake of fish. The therapeutic success was reached when fish and shellfish were taken out of the diet. After two years without seafood ingestion our patient is asymptomatic and the allergologic study has been normalised.
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4/12. Acute measles gastric infection.

    We describe the case of a 44-year-old man who was referred for gastroscopy because of abdominal pain. During endoscopy, inflammatory changes of the antrum and corpus mucosa were clearly visible, and biopsy samples from the antrum and corpus mucosa were taken. At histology, routine hematoxylin and eosin staining showed characteristics indicative of so-called ex-helicobacter pylori-gastritis that had developed after antibiotic treatment 2 years ago. Additional large, bizarre inclusion bodies and clusters of multinucleated giant cells were located in the surface epithelium and within the lamina propria. These giant cells had an appearance similar to that of Warthin-Finkeldey cells, which can be found during the prodromal phase of measles infection. Anti-measles virus immunochemistry showed a strong positivity for measles virus antigen within the giant cells. Based on these results, the final diagnosis of morbilliform gastritis was made. To our knowledge, no case of measles gastritis has been described in the literature. Our case report confirms the systemic character of measles virus infection and confirms that measles viral replication can involve the gastric mucosa in addition to the conjunctiva, lung, and intestina.
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5/12. helicobacter pylori-negative gastric ulcerations associated with celiac disease at first presentation.

    Ulcers of the small bowel have repeatedly been described as a late complication of celiac disease and they are considered a signum mali ominis. We report a case of a 53-year-old woman presenting with diarrhea, epigastric pain and abdominal distensions for a period of few weeks. At upper GI endoscopy, biopsies were taken showing complete atrophy of the villi and colonization of the small bowel mucosa. Additionally, uncommon multilocular peptic ulcers were seen in the gastric antrum. These ulcers proved to be helicobacter pylori-negative with no evidence of zollinger-ellison syndrome. Biopsies of gastric ulcers showed signs of a lymphocytic gastritis with an extensive infiltration of the lamina propria by almost exclusively CD3- and CD45R0-positive t-lymphocytes. Intraepithelial t-lymphocytes were found to be increased in the antral as well as the corpus mucosa. Typing the patient for human leukocyte antigens showed a DQA1*0501 and DQB1*0201 phenotype. According to the present report, gastric peptic ulcers seem to be another phenomenon associated with celiac disease. In the case presented here, ulcers were diagnosed together with celiac disease already at first presentation of the patient.
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6/12. osteoporosis with underlying connective tissue disease: an unusual case.

    A 44-year-old male was initially seen by dermatologists, who noted an erythematous rash on sun-exposed areas, the back, shoulders, and upper arms. There was associated muscle weakness and significant weight loss. Investigation revealed mildly raised aspartate and alanine transaminases but normal creatine kinase. Inflammatory indices and antinuclear antibodies (ANAs) were normal. biopsy of the rash was reported as consistent with either dermatomyositis (DM) or acute lupus erythematosus. A diagnosis of DM was made, and prednisolone was given with improvement of the rash but deteriorating myopathy. The patient was referred to the rheumatology department, and further history revealed multiple vertebral fractures after falling from standing height; these had occurred six months prior to starting steroids. Besides smoking he had no other risk factors for osteoporosis. Examination showed normal muscle strength, no muscle tenderness, and no joint abnormality. Repeat muscle enzymes were normal, and ANAs were now 1 : 100, but dsDNA antibodies and extractable nuclear antigens were normal. Investigations for osteoporosis revealed a hypergonadotrophic hypogonadism picture. Further examination indicated scanty pubic and auxiliary hair, small testicles, and mild gynecomastia. He is married, though has no children of his own. The hormonal profile raised the possibility of Klinefelter's syndrome, which was subsequently confirmed with karyotyping of 47 XXY. hypogonadism has been established as a cause of osteoporosis in males, and in this case would explain the occurrence of fractures in the absence of other major risk factors. Systemic lupus erythematosus has been recognized in association with Klinefelter's syndrome; in view of the normal muscle enzymes, his rash is most likely due to acute discoid lupus with androgen deficiency causing muscle weakness.
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7/12. Crystalline plasma cell inclusions in helicobacter-associated gastritis.

    BACKGROUND: Crystalline cytoplasmic inclusions are well documented in B cell lymphomas but have rarely been described in reactive plasmacytic infiltrates. AIM: Three cases of Lelicobacter-associated gastritis are described in which plasma cells focally contained rhomboid and needle-shaped crystalline inclusions. methods: Crystalline inclusions were identified in the gastric biopsy specimens from three patients undergoing routine upper gastrointestinal endoscopy. The cells were characterised immunohistochemically using the following antisera: cytokeratin, leucocyte common antigen, desmin, CD20, CD68, CD79a, CD138, immunoglobulin (Ig)G, IgA and IgM heavy chains, and kappa and lambda Ig light chains. Clinical follow-up data were obtained. RESULTS: All biopsies showed a Lelicobacter-associated active chronic gastritis. Variable numbers of plasma cells with intracytoplasmic crystalline inclusions in the superficial lamina propria were seen. The crystals were not stained with any of the antisera tested, but the cells containing the crystals expressed CD79a and CD138 and, in the two assessable cases, showed IgA and lambda light chain immunoreactivity. The more numerous morphologically normal plasma cells in each patient were polytypic, and there were no histological features to suggest lymphoma. Crystals were not identified in the plasma cells in mucosal biopsy specimens from other sites in any of the patients. CONCLUSIONS: Crystalline inclusions in plasma cells can occur in association with Lelicobacter gastritis. Although light chain restriction was shown in two patients, the overall histological and clinical findings indicated a reactive process. The presence of plasma cell crystals in isolation should not be considered to be diagnostic of lymphoma.
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8/12. monoclonal gammopathy of undetermined significance and Russell body formation in helicobacter pylori gastritis.

    BACKGROUND: infection by helicobacter pylori has been linked to monoclonal gammopathy of undetermined significance (MGUS). MGUS is thought to develop due to chronic antigenic stimulation in people with a specific genetic predisposition. methods AND RESULTS: We describe a patient presenting with dyspepsia associated with H. pylori-related erosive gastritis. Histopathologic findings revealed infiltration with plasma cells containing accumulated condensed intercisternal immunoglobulins, the so-called 'Russell bodies'. In addition, MGUS was present with total immunoglobulins within the normal range but a significantly decreased serum concentration of IgG subtype 3. Molecular analyses demonstrated IgH formation, T-cell receptor gamma rearrangement, and alterations within the IgHG3 gene sequence. Following H. pylori eradication, gastritis and dyspepsia gradually resolved but MGUS persisted for at least 22 months. CONCLUSIONS: This is the first report to demonstrate that upon infection with H. pylori, an impaired secretory capacity of plasma cells due to specific molecular changes can present as Russell body gastritis. The molecular findings question a pathogenetic link between Russell bodies and H. pylori, but suggest genetic alterations in the immunoglobulin locus as the possible cause for both MGUS and Russell body gastritis.
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9/12. Detection of cellular immunity derangements in chronic gastritis by a skin window test.

    An autologous "skin window test," used lately for the study of cellular immunity in cancer, was applied here successfully to 54 patients with upper-gastrointestinal ailments, 48 of whom had a coexistent fundic and/or antral chronic gastritis of varying severity. The diagnoses of gastritis were made by multiple fiber-gastroscopic biopsies. The ether-alcohol-fixed cryostat sections of fundic and antral biopsies were mounted on cover slides and placed on small cutaneous abrasions of the forearm of the same patients for 24--28 hr. The exudates on cover slides and on imprints of the abrasions were read blindly for the mononuclear cell response according to criteria set for this test by Black and Leis (10). A positive reaction was obtained in 8 of the 54 patients using autologous fundic mucosal biopsy. An autologous antral mucosal biopsy gave positive reaction in only 2 of the 26 of the patients in whom it was used. The positive yield of this autologous skin window test in chronic advanced fundic gastritis was somewhat higher than that obtained by other authors using lymphocytes blast transformation or macrophages migration inhibition test in vitro. It was much higher than the yield obtained by others who used skin tests in vivo, with homologous or heterologous gastric mucosal extracts as antigens. The autologous skin window is safe in regard to possible transmission of hepatitis. Its applicability for detection of cellular immunity derangement in chronic gastritis carries promise.
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10/12. Progression of gastritis to monoclonal B-cell lymphoma with resolution and recurrence following eradication of helicobacter pylori.

    OBJECTIVE: To follow a patient with helicobacter pylori-associated gastritis by performing serial endoscopic biopsies to observe the histologic progression of the gastritis to a monoclonal B-cell lymphoma with resolution and subsequent recurrence following eradication of H pylori organisms. DESIGN: A case report of a patient followed over 3 years. MAIN OUTCOME MEASURES: Characteristics of the gastric mucosa as determined by histologic and gene rearrangement studies on multiple random biopsies obtained serially before and after the eradication of H pylori organisms. RESULTS: A progression from H pylori-associated gastritis through lymphoid hyperplasia to a monoclonal B-cell lymphoma was observed. With the techniques used, a resolution of the lymphoma was observed on eradication of H pylori organisms, with a subsequent recurrence of the lymphoma 15 months later, despite the absence of H pylori organisms. CONCLUSION: The observations made of this patient support an association between H pylori and the development of a gastric monoclonal B-cell lymphoma. This lesion appears to develop in the setting of gastritis and progresses through lymphoid hyperplasia followed subsequently by the lymphoma. We speculate that this process is initially antigen driven by the organism and may subsequently become autonomous as genetic damage is accumulated, so that eradication of H pylori organisms will lead to regression of the lesion to the degree that there are autonomously proliferating cells present.
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