Cases reported "Gastritis, Hypertrophic"

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1/33. 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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2/33. Superficial gastric carcinoma developed on localized hypertrophic lymphocytic gastritis: a variant of localized Menetrier's disease?

    Menetrier's disease is a rare premalignant condition that usually involves the entire stomach. Only few cases of localized disease have been reported, rarely with cancer. Lymphocytic gastritis is a newly described entity that may share a common pathogenesis with Menetrier's disease. The authors report the case of a 62 year old woman with known liver cirrhosis in whom endoscopic examination of the stomach showed an antral tumor. Examination of the surgical specimen showed a superficial gastric adenocarcinoma developed on an hypertrophic gastropathy with both Menetrier's disease and lymphocytic gastritis features. This observation strengthens the hypothesis of a common mechanism between Menetrier's disease and lymphocytic gastritis, which may be part of the same disease spectrum. This disease could also correspond to the "hypertrophic lymphocytic gastritis" recently described.
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3/33. ganciclovir treatment in Menetrier's disease.

    A 2-y-old girl with severe edema, oliguria and hypoalbuminemia caused by protein-losing gastritis was diagnosed with cytomegalovirus-associated Menetrier's disease. After almost two weeks, during which the patient required repeated albumin transfusions, she was treated with intravenous ganciclovir. Within five days her condition had improved, and no additional albumin replacement was needed. Complete recovery was observed after several weeks. CONCLUSION: In patients with severe Menetrier's disease, a course of ganciclovir treatment may be of benefit and should be considered.
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4/33. Giant hypertrophic gastritis and acute hepatitis associated with cytomegalovirus infection.

    A 38-year-old man developed prominent hypoproteinemia after acute elevation of serum transaminase levels. Giant hypertrophy of the gastric mucosa, a short serum albumin half-life, and the absence of massive hepatocyte necrosis established the diagnosis of protein-losing gastropathy. The hypoproteinemia, gastric fold hypertrophy and hepatitis remitted spontaneously within 4 months. A high antibody titer against cytomegalovirus suggested an association between the viral infection and the patient's disease.
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5/33. Remission of severe anemia persisting for over 20 years after eradication of helicobacter pylori in cases of Menetrier's disease and atrophic gastritis: helicobacter pylori as a pathogenic factor in iron-deficiency anemia.

    A man with a 20-year history of recurrent iron-deficiency anemia complicated by helicobacter pylori-positive Menetrier's disease was observed over a 10-year clinical course, during which time he was successfully treated for the anemia and a gastric helicobacter pylori (H. pylori) infection through eradication. Considering the satisfactory therapeutic results in this case, we performed eradication therapy on another H. pylori-positive atrophic gastritis case with a 24-year history of iron-deficiency anemia of unknown etiology, and again, complete remission was obtained. The clinical evidence from these two cases suggests that the gastric H. pylori infection was deeply involved in the pathogeneses of the iron-deficiency anemia. We believe that these case reports will provide useful information on H. pylon-involved pathology in the fields of hematology and gastroenterology.
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6/33. Hyperplastic gastropathy as a presenting manifestation of systemic lupus erythematosus.

    A patient is described who had severe hyperplastic gastropathy as the presenting manifestation of systemic lupus erythematosus (SLE). Aggressive immunosuppressive therapy with systemic corticosteroids and immunoglobulins resulted in complete remission of lupus, and a prompt clinical and radiological regression of hyperplastic gastropathy. Hyperplastic gastropathy is an uncommon gastric illness, which is usually idiopathic but rarely is associated with helicobacter pylori infection, cytomegalovirus infection or lymphocytic gastritis. Three previous case reports have noted a response of idiopathic hyperplastic gastropathy to systemic corticosteroid treatment, yet none of the presented patients had a systemic inflammatory disease. The presented case is the first in the medical literature in which hyperplastic gastropathy is directly linked to the development of clinical and laboratory manifestations of SLE. We suggest that hyperplastic gastropathy be added to the list of rare gastrointestinal manifestations of SLE, and that autoimmune disease be considered a possible cause of hyperplastic gastropathy. As such, any patient with symptomatic idiopathic hyperplastic gastropathy accompanied by other evidence of systemic inflammation should be considered for SLE evaluation and immunosuppressive treatment.
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7/33. Resolution of gastrointestinal protein loss after helicobacter pylori eradication in a patient with hypertrophic lymphocytic gastritis.

    BACKGROUND: Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication. CASE REPORT: A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin g and immunoglobulin m levels. A renal cause for protein loss was excluded, liver function was normal. endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal. CONCLUSION: Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.
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keywords = gastritis
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8/33. Menetrier's disease presenting as an acute protein-losing gastroenteropathy in a 27-year-old man with gaucher disease.

    OBJECTIVES: To describe a unique case of a young man with gaucher disease who was diagnosed with Menetrier's disease. BACKGROUND: After an acute episode of severe gastritis, the patient developed hypoalbuminemia and protein-losing gastroenteropathy, and became unwell. STUDY: endoscopy revealed an abnormal stomach, with rigid, thickened folds covered with viscous greyish exudates. Superficial biopsies revealed foveolar hyperplasia, acute and severe gastritis with massive inflammatory infiltrate of neutrophils in the lamina propria with pit abscess formation. Tissue cultures for helicobacter pylori were negative. RESULTS: Snare deep particle biopsy revealed the typical features of Menetrier's disease. enzyme replacement therapy for gaucher disease was started. CONCLUSION: This case poses a dilemma because the patient improved spontaneously, and as such is dissimilar to other adults who develop Menetrier's disease because of an infection; it is hoped that he may also not be at risk of the potential malignancies that are correlated with adult Menetrier's disease. The value of enzyme treatment is considered.
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9/33. 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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10/33. 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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