Cases reported "Gastritis"

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1/44. Evolution of acute cytomegalovirus gastritis to chronic gastrointestinal dysmotility in a nonimmunocompromised adult.

    A 30-year-old nonimmunocompromised woman developed chronic gastrointestinal dysmotility as a consequence of acute cytomegalovirus infection. The acute nature of the infection was documented by high immunoglobulin m antibody titer to cytomegalovirus (CMV); the chronicity of the infection was shown by persistence of CMV in biopsy specimens of her gastrointestinal tract over a 21/2-year period. Gastrointestinal dysmotility was confirmed by delayed emptying on gastric nuclear scintigraphy, by retrograde propagation of migrating myoelectric complexes on small intestinal manometry, and by presence of tachygastria on cutaneous electrogastrography. The patient's nausea, vomiting, abdominal pain, and early satiety resolved after a short course of treatment with leuprolide acetate but returned after medication was discontinued. Her symptoms persisted despite clearance of CMV from the gastrointestinal tract after a course of treatment with ganciclovir. These observations show that acute CMV infection can cause gastrointestinal dysmotility in nonimmunocompromised individuals and that the disturbance in gastrointestinal motor function may persist for years after viral infection of the gastrointestinal tract has been eradicated.
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2/44. 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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3/44. Long-term prognosis of idiopathic gastric erosions.

    The long-term prognosis of multiple gastric erosions (erosive gastritis) is analyzed in 58 cases observed over 10-17 years, showing the disease to recur through decades. Idiopathic erosions occur mainly in the antrum and can be visualized roentgenologically, whereas "stress" erosions are in the body of the stomach and may only be diagnosed endoscopically.
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4/44. Multiple carcinoids in the stomach with hypergastrinemia and type A gastritis: a case report.

    We have experienced a case of the stomach with hypergastrinemia and type A gastritis with multiple carcinoids in a 37-year-old woman. An upper gastrointestinal series revealed multiple minute polyps in the upper body of the stomach. All polyps were diagnosed as carcinoid using endoscopic biopsies. She had neither symptom or signs of typical carcinoid disease. The serum gastrin level was as high as 725 pg/ml. Total gastrectomy was performed, and the diagnosis of multiple gastric carcinoids (sm, no) with type A gastritis was histologically confirmed. After the operation, the serum gastrin level returned to normal, and the patient has been doing well and is disease-free to date at 7 years after the operation. This case suggested that multiple gastric carcinoid lesions may be precipitated by chronic atrophic gastritis accompanying hypergastrinemia. In the treatment of multiple gastric carcinoids with type A gastritis, total gastrectomy with lymph node dissection should be standard operative procedure, in order to resect the fundic gland area completely which could be the origin of carcinoids and endocrine cell micronest.
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5/44. Extreme hypergastrinemia caused by atrophic gastritis and helicobacter pylori infection--a case report.

    We present a case with extremely high serum gastrin induced by atrophic gastritis and helicobacter pylori infection. The patient, a 95-year-old male, was diagnosed with idiopathic chronic diarrhea. During diagnostic work-up, his fasting serum gastrin was up to 2078 pg/mL. The secretin test was negative for gastrinoma. octreotide scan showed no suspicious lesion except for diffuse faint uptake over the gastric antrum on the 48-hour-delay film. Gastric acidity test revealed achlorhydria. On histology examination, atrophic gastritis with helicobacter pylori infection was found in the gastric body, but the antral mucus was normal with a slight increase in gastrin-secreting cells. To our knowledge, such extremely high serum gastrin induced by atrophic gastritis and helicobacter pylori infection has never been reported before.
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6/44. Topographic mapping of collagenous gastritis.

    A 74-year-old woman was investigated for abdominal pain and diarrhea. Endoscopic examinations including biopsies of the stomach and colon demonstrated the typical subepithelial deposits characteristic of collagenous gastritis and collagenous colitis. Histochemical and ultrastructural methods confirmed the presence of collagen in the subepithelial deposits. The topographic distribution of these collagen deposits and their relationship to the inflammatory process in the stomach were then defined by endoscopic mapping and multiple site biopsies of the mucosa in the gastric body and antrum. These studies indicate that collagenous gastritis not only is distinctive, but also is a far more extensive and diffuse inflammatory process than has previously been appreciated.
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7/44. A unique early gastric tubular adenocarcinoma arising from a pre-existent carcinoid tumor in a patient with a more than 20-year history of type A gastritis: an immunohistochemical and ultrastructural study.

    A unique early gastric tubular adenocarcinoma developed from a pre-existent carcinoid tumor in a patient with a more than 20-year history of type A gastritis, multiple endocrine cell micronests, hypergastrinemia, and a high level of serum antiparietal cell autoantibody. The patient was a 60-year-old Japanese man. The background gastric mucosa around the tumor showed marked atrophy with intestinal metaplasia, in which endocrine cell micronests were frequently observed, and was consistent with type A gastritis. The mass was composed of both adenocarcinoma and carcinoid tumor. The adenocarcinoma was restricted to the lamina mucosa and submucosal area, and constituted a minor component of the tumor mass. The carcinoid tumor was the dominant constituent of the tumor, that invaded continuously the subserosa and muscularis propria. Based on this examination together with the detailed immunohistochemical and ultrastructural studies, the adenocarcinoma was presumed to have developed from the pre-existent carcinoid tumor. Ultrastructurally there were no amphicrine cells in the tumor, containing both endocrine granules and mucin droplets.
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8/44. A rare association of primary biliary cirrhosis and pernicious anemia.

    Primary biliary cirrhosis is often associated with autoimmune diseases. However, an association between primary biliary cirrhosis and pernicious anemia has rarely been reported. We report a patient with primary biliary cirrhosis associated with pernicious anemia and autoimmune gastritis. The patient was a 64-year-old Japanese woman who had been diagnosed as having primary biliary cirrhosis 5 years previously. She was readmitted with jaundice and macrocytic anemia. The diagnosis of pernicious anemia was confirmed by the low level of serum vitamin B12 and the presence of anti-parietal cell antibody and anti-intrinsic factor antibody. Pernicious anemia should be regarded as a possible complication of primary biliary cirrhosis.
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9/44. Menetrier's disease and adenocarcinoma of the pancreas.

    A 74-year old woman with abdominal pain and edema was diagnosed to have Menetrier's disease on surgical full thickness gastric wall biopsy. Two months later, she complained of increasing severe abdominal pain radiating to the back, unusual in Menetrier's. work-up showed classic Menetrier's disease with large gastric folds, achlorhydria, gastrointestinal protein loss and hypoalbuminemia. A celiac arteriogram, however, suggested a pancreatic neoplasm and adenocarcinoma of the body of the pancreas was confirmed at laparotomy. This is the first report of the concurrence of these two diseases. The difficulty of differentiating Menetrier's from occult gastrointestinal cancer is discussed.
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10/44. Idiopathic granulomatous gastritis with multiple aphthoid ulcers.

    A 47-year-old woman had idiopathic granulomatous gastritis characterized by serpiginous aphthoid ulcer with satellite aphthous ulcers at the antrum to angulus with noncaseating epithelioid granulomas including giant cells in the gastric mucosa. No definite etiologic factors could be detected; systemic sarcoidosis, Crohn's disease, infections (tuberculosis, syphilis and fungus), neoplasm, and foreign body reaction were excluded by additional investigations. However, the patient was found to be infected with H. pylori. Despite the success of H. pylori-eradication, the granulomatous lesion took a long time to heal for at least 17 months or more. The relation between granulomatous gastritis and H. pylori was discussed. There was no apparent evidence of granuloma in the other organs during clinical and follow-up studies for over three years.
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