Cases reported "Gastritis, Hypertrophic"

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1/16. Primary gastric plasmacytoma: a rare cause of hypertrophic gastritis in an adolescent.

    BACKGROUND: This report describes a 16-year-old patient with gastric rugal hypertrophy caused by a primary gastric plasmacytoma. She had a 3-month history of nausea and burning abdominal pain. Radiographic studies showed giant rugal hypertrophy. Superficial endoscopic gastric biopsies showed mild inflammation with plasma cells of polyclonal origin in the mucosa. When symptoms persisted, she underwent laparoscopic full-thickness gastric biopsy. There was monoclonal plasma cell infiltration histologically diagnostic of plasmacytoma and inconsistent with helicobacter pylori-associated mucosa-associated lymphoid tissue (MALT) lymphoma. There was no evidence for involvement of the bone marrow or regional lymph nodes. The tumor did not respond to radiotherapy, necessitating total gastrectomy. methods: blood samples were analyzed for interleukin (IL)-6 by enzyme-linked immunosorbent assay. Gastric biopsy and gastrectomy specimens were subjected to immunophenotyping for kappa and lambda light chains, CD45, CD20, and LN1 and to polymerase chain reaction analysis for herpes virus HHV8. RESULTS: There was no elevation in circulating IL-6 levels, militating against a pathogenesis akin to that of Castleman's disease. There was no evidence for infection with the Kaposi's sarcoma-associated herpes virus HHV8, which has recently been found in patients with multiple myeloma. CONCLUSIONS: This diagnosis and the characteristics of the tumor are very unusual, if not unique, for a patient of this age. The diagnostic evaluation of this patient also demonstrates the importance of deep endoscopic or full-thickness biopsies in some children with hypertrophic gastritis.
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2/16. Menetrier's disease: evolution of disease under histamine-2 receptor antagonists.

    A 33-yr-old man, with known peptic disease, developed giant thickening of the gastric mucosa and hypoproteinemia. Serial endoscopic and x-ray examinations of the upper gastrointestinal tract were available before and after the development of Menetrier's disease. In a 1-yr interval, erosive gastritis developed in a normal gastric mucosa, which was followed a few months later by hypoproteinemia. The patient developed the disease while being treated with histamine-2 receptor antagonists.
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3/16. Giant fold gastritis with consecutive gastric carcinoma in a patient with peutz-jeghers syndrome.

    We describe the case of a 36-year-old patient with peutz-jeghers syndrome and a very unusual gastric morphology resembling giant fold gastritis. The latter lacked additional features of Menetrier's syndrome, was not influenced by eradication of helicobacter pylori and persisted for more than ten years under regular endoscopic surveillance. Histologically, foveolar hyperplasia was found in the enlarged folds. Endoscopic ultrasound documented a hyperechoic widening of the gastric mucosa without involvement of the deeper layers. However, despite annual control gastroscopies, an adenocarcinoma developed between the folds and was in an already advanced stage at diagnosis (UICC III). We suggest that a variant of peutz-jeghers syndrome may be characterised by marked foveolar hyperplasia similar to Menetrier disease, and that not conventional endoscopy alone, but rather endoscopic ultrasound may be considered in such patients.
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4/16. Early gastric cancer arising from localized Menetrier's disease.

    A case of early gastric cancer arising from Menetrier's disease in the stomach is described. The patient was a 53-year-old man, who suffered from epigastralgia. Radiological and endoscopic examination demonstrated giant mucosal folds along the greater curvature of the stomach. On the distal margin, signet-ring cell carcinoma was demonstrated by biopsy. The coexistence of Menetrier's disease and early gastric cancer has rarely been reported. Cases reported in the literature were reviewed and the increased malignant potential of Menetrier's disease was discussed.
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5/16. Menetrier's disease: an excellent response to octreotide. A case report from the middle east.

    Menetrier's disease is a rare acquired cause of protein losing enteropathy, with premalignant potential. Since its first description in 1888, around 300 cases have been reported. This disease occurs more frequently in males aged 30-50 years. We report here the case of a 31 year- old Sudanese female who presented with generalized edema. Laboratory investigations showed hypoproteinemia and hypoalbuminemia without evidence of renal or liver disease. Upper gastrointestinal endoscopy showed giant gastric folds. The histopathological features of biopsies taken from these folds were consistent with Menetrier's disease. Our patient showed excellent response to treatment with subcutaneous octreotide and this may ameliorate the need for surgery as the definitive treatment of this disease.
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6/16. Hypertrophic gastropathy symptoms responsive to prednisone. A case report and a review of the literature.

    We describe a 33-year-old man with giant hypertrophic gastropathy (Menetrier's disease), which, on operative biopsy of the stomach, showed a significant inflammatory component. The patient was treated with prednisone and quickly responded. Although a review of the literature revealed only two cases similarly treated, with equivocal results, spontaneous remission, does occur. Symptoms associated with this disease may respond to corticosteroids, which may offer effective therapy while awaiting involution of the gastropathy. Thus total gastrectomy may be avoided.
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7/16. Lymphocytic gastritis and giant gastric folds associated with gastrointestinal protein loss.

    Lymphocytic gastritis is a recently described lesion which occurs in a significant proportion of patients with celiac sprue. This paper describes two patients with lymphocytic gastritis and no evidence of celiac sprue. Both patients had markedly enlarged gastric folds and serum hypoproteinemia, which were clinically suggestive of Menetrier's disease. These cases indicate that lymphocytic gastritis may cause a protein-losing gastropathy and should be considered in the differential diagnosis of Menetrier's disease.
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8/16. Familial giant hypertrophic gastritis (Menetrier's disease).

    Familial giant hypertrophic gastritis involving three generations is reported. A review of the literature, where approximately 200 cases are described, showed only few cases of familial occurrence of this disease, and only in siblings. Our findings suggest dominant heredity, but considering the sparsity of familial occurrence reported earlier, heredity seems to be of only minor pathogenetic significance.
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9/16. technetium-99m serum albumin measurement of gastrointestinal protein loss in a subtotal gastrectomy patient with giant hypertrophic gastritis.

    Gastrointestinal protein loss was measured using Tc-99m labeled human serum albumin in a patient with giant hypertrophic gastritis. Gastric secretion was aspirated via a nasogastric tube and measured for radioactivity after intravenous injection of Tc-99m albumin. Assessment of radioactivity of the collected gastric secretion yielded a total radiocount of 98.7 kilocounts per minute within 6 hours, which is equivalent to 1.1% of the total dose. Therefore, at least 1.1% of the circulating albumin was excreted into the gastric cavity within 6 hours, and, since simultaneous abdominal imaging did not demonstrate obvious accumulation of tracer in the gastrointestinal tract, protein loss was thought to be due to giant gastric rugae of the resected stomach. It was concluded that Tc-99m albumin is a valuable means for detection of the site of protein loss in patients with protein-losing gastroenteropathy. This method has several advantages in the clinical setting; it is less time consuming, easy to perform, and provides quantitative and qualitative assessment of protein loss.
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10/16. mucus secretion in hypertrophic, hypersecretory, protein-losing gastropathy.

    A 48-year-old man presented with giant folds of the gastric mucosa, hypoalbuminemia, and hypersecretion of acid. In vivo labeling of plasma proteins by 51CrCl3 disclosed an abnormal gastric protein clearance. mucus secretion, evaluated by the output of dry matter, mucosubstance constituents (hexosamine and fucose), protein (by the method of Lowry), and sodium were five to eight times those in nine healthy volunteers, but were normalized by the histamine-H2-receptor antagonist cimetidine. The proportion of dry matter and protein was the same in the patient and in healthy subjects, indicating that the loss of plasma protein into the stomach probably occurred as part of an abnormally great secretion of mucus.
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