Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated gastrointestinal (GI) infiltrate is unusual at presentation or relapse of acute myelogenous leukemia (AML). We report a case of acute myelogenous leukemia (FAB-M4) whose isolated relapse presented as a bleeding gastric ulcer. The patient was a 30-year-old male who had been diagnosed to have AML in June 1988. While in third complete remission, he underwent a sibling allogeneic HLA-matched bone marrow transplant. Five months after transplantation, he was readmitted for pneumonia. While in the hospital, he had an episode of upper GI bleeding. The endoscopy revealed a leukemic gastric ulcer, with morphology and immunophenotyping identical to his initial AML. There was no evidence of leukemia in the blood or bone marrow. Although different types of leukemic infiltrates have been recognized at post-mortem examination, our case is unique because AML presenting as an isolated malignant ulcer has not been described previously. We conclude that relapsing AML may present as an isolated gastric ulcer and suggest that any suspicious lesion on upper GI endoscopy should be biopsied after aggressive platelet support.
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PMID:Isolated relapse of acute myelogenous leukemia presenting as a gastric ulcer. 185 86

The aim of this study was to investigate the association of HLA antigens with chronic duodenal and gastric ulcer. 104 patients with chronic peptic ulcer, 52 with duodenal ulcer, and 52 with gastric ulcer were studied, and HLA antigens of the A, B and DR series were sought using the microlymphocytotoxicity test. In duodenal-ulcer patients, no significant differences were observed. In the gastric-ulcer group, Bw49 was increased in both sexes, with an adjusted odds ratio of 10.2. However, when corrected for the number of comparisons made, this difference failed to reach statistical significance. It is concluded that if HLA antigens make any contribution to the aetiology of ulcer disease, this contribution is small and the proportion of cases of gastric ulcer that can be explained by the presence of HLA antigen Bw49 is less than 10%.
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PMID:HLA antigens and peptic ulcer disease. 657 85

The association of duodenal ulcers with antigens AIO and combinations of antigens B18B40, B35B40, A10B5, A10B40 and others and the association of gastric ulcer with antigens A3B7, A3B40, B14B15 were revealed by an investigation of HLA antigens in 46 patients with ulcer disease of the duodenum and 25 patients with ulcer disease of the stomach. It was concluded that the ulcer disease had a hereditary predisposition characterized by genetic heterogeneity with different etiopathogenetic mechanisms of the development of ulcers of different localizations. The HLA antigens may be used as immunogenic markers of ulcer disease if observing the population method in the investigations.
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PMID:[The association of HLA antigens with gastric and duodenal peptic ulcer]. 770 31

This 35-year-old housewife was initially treated with vincristine, prednisolone and L-asparaginase for acute lymphoblastic leukemia (ALL, L1 by FAB classification) in 1988 and entered into complete remission. Ten months later she underwent bone marrow transplantation (BMT) from her HLA-identical and MLC-negative sister. The conditioning regimens consisted of busulfan 4 mg/kg/day for 4 days orally and cyclophosphamide 60 mg/kg/day for 2 days intravenously followed by cyclosporine and prednisolone for graft-versus-host disease prophylaxis. Fifty days after BMT, she suffered interstitial pneumonitis and a gastric ulcer, and was treated with a high dose of methylprednisolone and cimetidine. She experienced transient improvement, but soon cough, dyspnea and epigastralgia became worse. The specimens obtained by transbronchial alveolar lavage (BAL) and endoscopic gastric biopsy showed many giant cells containing inclusion bodies which were identified as cytomegalovirus (CMV). This time ganciclovir was started in addition to prednisolone. Then she gradually improved and after repeated BAL and the gastric biopsy after treatment showed no inclusion body in the specimen. Although leukocytopenia was significant for this patient, ganciclovir is considered to be useful for controlling CMV infection in both the lungs and stomach.
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PMID:[Good response to ganciclovir in a patient of cytomegalovirus (CMV) interstitial pneumonitis and gastric ulcer following allogeneic bone marrow transplantation for acute lymphoblastic leukemia]. 774 99

A total of 55 gastric ulcer patients and 1045 healthy persons were investigated for 36 HLA antigens (A, B, C loci). The study revealed that HLA B12, B15, B35, Cw4 were more common in the patients (34.55, 18.18, 27.27 and 25.45%, respectively). HLA A3 (10.9% in the patients and 25.74% in those healthy) is found to be protective against gastric ulcer. The data obtained are considered with regard to heterogeneity of the disease.
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PMID:[HLA antigens in stomach ulcer]. 801 13

At the turn of the century, duodenal ulcer rose from rarity to affect 10% of males in their life time, subsequently declining in some countries such as UK, levelling off in others such as Germany, and continuing to increase in still others such as Hong Kong. The annual incidence per 1000 population varies from about 1 in Japan to 1.5 in Norway, 1.8 in USA and 2.7 in Scotland, and the frequency also varies within many individual countries, such as Australia, China and India, and among races such as a higher prevalence among whites than blacks in USA and among Chinese than Javanese in Indonesia. Ulcer frequency is higher in winter months, and this appears universal, being true in cold as well as in warm countries. Most places report a rise of ulcer rates among the elderly in recent decades. The male to female ratio also varies geographically, for example from 1:1 in USA to 18:1 in India, and with time such as moving from 2:1 to 1:1 in the last two decades in USA, and the duodenal ulcer to gastric ulcer ratio varies widely from place to place, for example from 0.8 in Japan to 19:1 in Africa and 32:1 in India. Placebo healing rates also differ geographically, ranging from 5% in Philippines to 78% in Mexico. These epidemiological data can only be explained by the presence of multiple aetiological factors, including analgesics, society stress, cigarette smoking, Helicobacter pylori, dietary factors, and genetic factors. Three lines of evidence support a genetic role: family studies, twin studies and blood group studies. Family aggregation occurs more commonly in patients with early-onset (< 30 yr) of symptoms. Blood group O prevalence is more associated with late-onset of symptoms. Other genetic markers include nonsecretor status, HLA antigens, phenylthiocarbamide taste sensitivity, and alpha-1-antitrypsin. Genetic syndromes such as MEN I also support a genetic role and give insight into pathogenetic mechanisms. The best physiological marker is still hyperpepsinogenemia I, which is transmitted by autosomal dominance, despite recent report of lower serum pepsinogen 1 after healing of Helicobacter pylori associated gastritis.
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PMID:Epidemiology and genetics of peptic ulcer. 835 24

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. Most patients continue through life with a chronic superficial gastritis while some develop either duodenal or gastric ulcer. In a very small proportion the lymphoid reaction to H. pylori infection appears to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma, while in others the evidence suggests that chronic superficial gastritis progresses to atrophy, the loss of gastric acid secretory capacity and the development of gastric cancer. The mechanisms involving H. pylori infection in peptic ulceration are increasingly well understood and H. pylori is now accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 95%. More important is the dramatic reduction in duodenal ulcer recurrence after successful eradication of the organism to about 4% in a year compared to recurrences of up to 80% in those who ulcers have been healed but in whom the infection persists. There is also increasing evidence for the involvement of H. pylori in gastric ulcer, where infection is seen in between 60 and 80%, and there is a similar dramatic reduction in recurrence following cure of H. pylori infection. The progression of H. pylori gastritis from the acute infection to chronic superficial gastritis, predominantly antral gastritis or a pangastritis with increasing atrophy appears to be associated with the differing outcomes seen in this disease. Moreover, there is increasing data on the roles played by bacterial heterogeneity and the virulence of the organism, host factors such as the HLA genotype and immune response, environmental factors and the age of acquisition of infection play in determining these clinical outcomes of the disease.
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PMID:The role of Helicobacter pylori in pathogenesis: the spectrum of clinical outcomes. 889 29

Helicobacter pylori infection is associated with duodenal and gastric ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. Although more than half the world's population harbors H. pylori, only a proportion will develop clinically significant disease. The specific clinical outcome of an individual can be examined as the modulation of host factors by H. pylori infection. Host acid-secretory status and sensitivity to gastrin can be modulated by H. pylori infection. Once H. pylori has established itself in the stomach, virtually everyone develops gastritis, and variations in gastritis patterns have been associated with different gastric acid responses to H. pylori infection. The patterns of gastritis are important because they seem to determine disease outcome. Blood group antigens have been implicated in studies of ulcer disease. Receptors to Lewis antigens in gastric mucosa indicate that host mucosal factors influence H. pylori attachment. Conversely, H. pylori strains express Lewis antigen-like molecules, suggesting an autoimmune component for some H. pylori-associated diseases. HLA genotypes may influence the host response to H. pylori infection, and those of H. pylori-infected individuals have been correlated with histological features. The clinical outcome of H. pylori infection is most likely a result of complex interactions among host, bacterial, and environmental factors. The mechanisms by which these diverse factors influence the pathogenesis of different clinical outcomes remain under investigation.
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PMID:What are the host factors that place an individual at risk for Helicobacter pylori-associated disease? 939 54

The (re)discovery of the gastric pathogen Helicobacter pylori almost one and a half decade ago completely changed our conception on gastroduodenal ulcer disease and gastric cancer. The most important issue is that Helicobacter pylori induces a mild, antrum dominant chronic pangastritis without increased risk of severe diseases in most of the cases. A smaller part of the infected develops antrum dominant gastritis with increased risk of duodenal ulcer. In a few cases the corpus is also affected, pangastritis occurs with increased risk to develop gastric ulcer and gastric cancer. Until now it is not quite obvious why some of the infected patients get ill while others not, and why different diseases develop in different patients. 1. From the bacterial point of view it is ascertained that toxin-producing strains (VacA, CagA positive) are more likely to induce ulcer formation and gastric carcinoma. 2. Genetic phenotype of the infected patients (blood-group and HLA antigens) may also be of importance. 3. Environmental factors may affect (promote or inhibit) disease development. All of these factors determine the complex immunological, functional and morphological changes characteristic for the developing disease.
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PMID:[Pathophysiology of Helicobacter pylori infection]. 1046 31