Cases reported "Gastritis, Atrophic"

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1/37. 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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2/37. Primary biliary cirrhosis associated with type A gastritis and chronic thyroiditis.

    We report a patient with primary biliary cirrhosis (PBC) associated with type A gastritis, chronic thyroiditis, and iron deficiency anemia. The patient was a 45-year-old Japanese woman who was admitted to our hospital with severe microcytic and hypochromic anemia, abnormal results for liver function tests, and a diffuse goiter. The diagnosis of PBC (Scheuer's stage II) was confirmed by the presence of specific anti-mitochondrial antibody in high titers and histological examination showing chronic non-suppurative destructive cholangitis with bridging fibrosis. Additionally, marked atrophic mucosa throughout the body and fundus of the stomach was observed endoscopically, and there was positivity for intrinsic factor antibody, an extremely low ratio of serum pepsinogen a to C, and hypergastrinemia, indicating coexisting type A gastritis. The severe anemia was thought to be caused by failure of dietary iron absorption related to achlorhydria with this gastritis. However, the serum level of vitamin B12 was normal. She also had autoimmune thyroiditis. PBC is frequently associated with extrahepatic autoimmune diseases, including ductular lesions. However, the association of PBC with type A gastritis is quite rare, although the stomach is also an exocrine glandular structure. This particular case, in addition to previous reports, leads to a discussion of whether type A gastritis should be regarded as a possible, although uncommon, component disorder of so-called dry gland syndrome.
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ranking = 1.2857142857143
keywords = gastritis
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3/37. Relationship between pernicious anaemia and gastric neuroendocrine cell disorders.

    The incidence of gastric carcinoid tumours is increasing. This rise is probably due to the number of gastroscopies and improved histological techniques. The majority (65%) of these gastric tumours is associated with chronic atrophic gastritis and pernicious anaemia. In this article two patients are presented, one with pernicious anaemia and gastric neuroendocrine cell hyperplasia and one with pernicious anaemia and multiple gastric carcinoids. These neuroendocrine cell disorders have a relatively favourable prognosis. Therefore, a wait-and-see policy was preferred. The pathogenesis, clinical symptoms, diagnosis, prognosis and treatment of these different neuroendocrine cell manifestations are discussed. We recommend performing a gastroscopy at the time of diagnosis for young patients with pernicious anaemia, and whenever abdominal problems, unexplained weight loss or aggravation of the anaemia arise.
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ranking = 0.14285714285714
keywords = gastritis
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4/37. Expression of Cdx1 and Cdx2 mRNAs and relevance of this expression to differentiation in human gastrointestinal mucosa--with special emphasis on participation in intestinal metaplasia of the human stomach.

    BACKGROUND: The caudal-type homeobox genes, Cdx1 and Cdx2, are candidates for directing intestinal development, differentiation, and maintenance of the intestinal phenotype. The aims of this study were: (1) to assess the normal tissue expression patterns of Cdx1 and Cdx2 in the human gastrointestinal tract and (2) to ascertain levels in intestinal metaplasia (IM) of the stomach associated with gastritis. methods: Fresh human tissues were collected by surgical resection from 39 patients after informed consent had been received. RNAs were extracted from 11 distinct sites in the gastrointestinal mucosa (gastric body, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, transverse colon, descending colon, sigmoid colon, and rectum), and Northern hybridization was performed for Cdr1 and Cdx2 mRNAs. In addition, RNAs were also extracted from normal gastric mucosa, and gastric mucosa with mild to severe IM, confirmed histopathologically. Reverse-transcriptase polymerase chain reaction (RT-PCR) was then carried out for Cdx1 and Cdx2. RESULTS: The expression of Cdx1 mRNA increased gradually from the duodenum to the distal colon, with no expression detected in the stomach. Compared with the distribution of Cdx1 mRNA in the mouse gastrointestinal tract, the expression of Cdr1 mRNA in the human gastrointestinal tract showed greater predominance in the jejunum and ileum. The expression of Cdx2 mRNA increased gradually from the duodenum to the proximal colon and decreased from the ascending colon to the rectum. Compared with the expression pattern of Cdx2 mRNA in the mouse gastrointestinal tract, the expression of Cdx2 mRNA in the human gastrointestinal tract showed greater predominance in the ileum. By RT-PCR, both Cdx1 and Cdx2 mRNAs were detected in the mild and severe types of IM. However, neither of these mRNAs was identified in normal gastric mucosa without IM. CONCLUSIONS: Cdr1 and Cdx2 mRNAs are widely present in the human intestinal and colonic mucosae, but not in the gastric mucosa, suggesting that their expression may contribute to the intestinal phenotype. The high levels of these mRNAs in IM mucosa associated with chronic atrophic gastritis point to an association with this phenotypic shift in the gastric mucosa.
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ranking = 0.28571428571429
keywords = gastritis
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5/37. A female with asymptomatic primary biliary cirrhosis associated with pernicious anemia.

    We experienced a female case with asymptomatic primary biliary cirrhosis that was associated with pernicious anemia after 16 years from the onset. She was 52 years old when she first visited a clinic in 1981 for liver dysfunction treatment. Antimitochondrial antibody was negative and antipyruvate dehydrogenase complex antibody was positive in a low titer in its immunoglobulin (Ig)M type. Histological examination of her liver revealed a presence of definite chronic non-suppurative destructive cholangitis with numerous epithelioid cell granuloma. She had been given 600 mg of the oral daily dose of ursodeoxycholic acid since 1992. Macrocytic anemia incidiously appeared in September 1999. An immunological examination detected negative antiparietal cell antibodies and positive anti-intrinsic factor antibodies. Her bone marrow smear showed numerous megaloblasts and serum vitamin B12 in her blood was low at 99 pg/mL. Severe reversed atrophic-type gastritis (type A gastritis) was demonstrated by the use of dye-endoscopy with congo red. Her macrocytic anemia dramatically improved after intramuscular administration of vitamin B12. In conclusion, attention should be given to the association of pernicious anemia during the follow up of primary biliary cirrhosis.
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ranking = 0.28571428571429
keywords = gastritis
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6/37. A patient with autoimmune hepatitis type I, Addison's disease, atrophic thyroiditis, atrophic gastritis, exocrine pancreatic insufficiency, and heterozygous alpha1-antitrypsin deficiency.

    This report describes a 60-yr-old white male presenting with decompensated liver cirrhosis. He had a history of Addison's disease for 36 yr, primary hypothyroidism for 5 yr, and moderate alcohol consumption. His laboratory studies and a liver biopsy supported the diagnosis of autoimmune hepatitis. Furthermore, he was found to be heterozygous for the piZ allele of the alpha1-antitrypsin gene with normal serum alpha1-antitrypsin levels and absence of pulmonary affection. Mucosal biopsies revealed moderately severe atrophic gastritis; however, signs of pernicious anemia were missing. An association of autoimmune hepatitis with endocrine disorders and atrophic gastritis has been described. Long term hydrocortisone therapy for his adrenal insufficiency may have prevented a faster course of the liver disease, whereas the heterozygous alpha1-antitrypsin deficiency and moderate alcohol consumption constituted additional risk factors ultimately leading to the development of cirrhosis.
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ranking = 0.85714285714286
keywords = gastritis
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7/37. Combined adenocarcinoma and carcinoid tumor in atrophic gastritis.

    The development of adenocarcinoma or carcinoid tumors in atrophic gastritis is widely documented. We report the simultaneous occurrence of gastric adenocarcinoma and carcinoid (composite tumor) in atrophic gastritis, a finding reported only twice before in the literature. This 52-yr-old man with rectal bleeding, epigastric pain, and iron deficiency anemia was noted to have multiple polypoid masses on upper endoscopy. biopsy revealed features of both adenocarcinoma and carcinoid tumor in a background of atrophic gastritis, leading to a total gastrectomy, lymph node dissection, and liver biopsy. The gastrectomy specimen was characterized by a 6 cm pedunculated polyp and multiple sessile nodular masses between 0.4 and 2.5 cm in the background of a granular mucosa. On microscopic examination, the large polypoid mass corresponded to a well-differentiated adenocarcinoma, intestinal type, infiltrating the wall. The smaller nodules were composed of carcinoid tumors, restricted to the mucosa, or infiltrating the gastric wall. carcinoid tumor was also seen in the large polypoid mass closely intermingled with adenocarcinoma.The carcinoid tumor metastasized to the liver. lymph nodes showed both adenocarcinoma and carcinoid tumor. The gastric mucosa was characterized by atrophic gastritis with intestinal metaplasia, neuroendocrine hyperplasia, and microcarcinoids. The adenocarcinoma stained strongly for CK7, CK 20, MIB-1, and focally for chromogranin and synaptophysin. The carcinoid tumor was negative for CK7, CK 20 and MIB-1, and was positive for chromogranin and synaptophysin. Overexpression of p53 was noted only in the adenocarcinoma. Electron microscopy revealed neurosecretory granules in the carcinoid characteristic of a neuroendocrine tumor. Composite tumor can occur in the setting of atrophic gastritis. The findings in this patient reinforce the concept that the epithelial and neuroendocrine cells of the gastrointestinal tract both result from multidirectional differentiation of a primitive cell.
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ranking = 1.2857142857143
keywords = gastritis
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8/37. Gastric carcinoid in a young woman with systemic lupus erythematosus and atrophic autoimmune gastritis.

    BACKGROUND: Gastric carcinoid is a rare tumour that is associated with chronic atrophic gastritis in the majority of cases. It usually occurs in the 6th or 7th decade of life and is rarely diagnosed in patients under 30 years of age. methods: We describe a case of multiple gastric carcinoids in a 23-year-old woman with systemic lupus erythematosus and atrophic autoimmune gastritis--an association that has not been reported previously. RESULTS: The combination of atrophic autoimmune gastritis and gastric carcinoid with other autoimmune disorders has rarely been reported in the English medical literature. CONCLUSION: The fact that it mostly concerns (relatively) young patients may suggest a potential causative relation between those autoimmune disorders and the early development of atrophic gastritis with hypergastrinaemia, which subsequently leads to the occurrence of gastric carcinoid tumours at a young age.
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ranking = 1.1428571428571
keywords = gastritis
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9/37. Co-existence of hyperparathyroidism, hypergastrinaemia and multiple gastric carcinoids is not always due to incomplete expression of the men-1 syndrome.

    Until recently, the association of primary hyperparathyroidism and gastric carcinoid, with or without hypergastrinaemia, had been considered an incomplete form of multiple endocrine neoplasia type 1. This is because it seemed unlikely that the rare joint appearance of these diseases could occur only by chance. It is now possible to evaluate the pathogenetic involvement of the multiple endocrine neoplasia type 1 gene in many, apparently sporadic, clinical conditions. This is a case report of a female mimicking multiple endocrine neoplasia type 1 due to the presence of hyperparathyroidism, gastric carcinoid, and hypergastrinaemia. However, involvement of the men-1 gene (exons 2-10) was not detected, whereas hypergastrinaemia was attributed to a chronic atrophic gastritis.
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ranking = 0.14285714285714
keywords = gastritis
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10/37. 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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ranking = 0.71428571428571
keywords = gastritis
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