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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is presented of ascites infected with candida in a cirrhotic patient. Candida infection of the ascitic fluid and candidemia were found 24 hours after perforation of a gastric ulcer. Combined intravenous therapy with Amphotericin B and 5-Fluorocytosine eradicated the infection within two weeks. The need for comprehensive therapeutic approach in the debilitated patient prone to fungal and bacterial infection is emphasized.
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PMID:Candida infected ascites caused by perforated ulcer. 44 Apr 6

We aimed to produce a unifying hypothesis to explain the different locations of peptic ulcer and gastritis observed in different populations. The pre-Helicobacter pylori literature on patterns of gastroduodenal disease was reviewed and compared with recent human and animal findings on H. pylori infection. Early observations revealed that duodenal and non-pre-pyloric ulcers tend to be mutually exclusive. In duodenal ulcer patients, gastritis is usually restricted to the antrum, while gastric ulcer patients experience more severe pangastritis. The manipulation of acid output by surgery or acid suppressive therapy alters the distribution of gastritis. Recent experimental evidence in humans and animals has shown that these changes parallel changes in the distribution and cellular responses to H. pylori infection. We propose that the most important factor in the ecology of the H. pylori-infected stomach is local acid production. Local acid production determines the location and severity of inflammation and the clinical outcome of this bacterial infection. Priority research areas should be the investigation of the in vivo behaviour of H. pylori in the acid and the non-acid producing areas of the stomach and the measurement of acid output in populations known to have different patterns of gastroduodenal disease.
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PMID:Local acid production and Helicobacter pylori: a unifying hypothesis of gastroduodenal disease. 761 9

Helicobacter pylori is probably the commonest bacterial infection worldwide and is now accepted as the cause of chronic active type B gastritis. It is increasingly accepted as having a critical role in duodenal ulcer, where the prevalence of infection is 90 to 100%. 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 whose ulcers have been healed but in whom the infection persists. There is increasing evidence that what is now clear for duodenal ulcers may also hold true for patients with a gastric ulcer who are infected with H. pylori. Moreover, evidence is accumulating that the risk of a duodenal ulcer complication, such as, bleeding, is reduced following successful eradication of H. pylori. The treatment of duodenal ulcer patients with H. pylori eradication treatment has been advocated by an international working party who met first in Sydney at the 1990 World Congress and subsequently in Athens during the First European Gastroenterology Week. The most recent recommendation suggests that the infection should be treated in any duodenal ulcer patient after the first recurrence, and that a triple therapy regimen or a proton pump inhibitor combined with either amoxicillin or clarithromycin may be prescribed. The combination of a proton pump inhibitor and an antibiotic can eradicate H. pylori in over 80% of cases and simultaneously offers the advantage of rapid symptom relief and the highest rates of duodenal ulcer healing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The current role of Helicobacter pylori eradication in clinical practice. 777 4

Helicobacter pylori is probably the most common bacterial infection worldwide and the accepted cause of chronic active gastritis. It has a critical role in duodenal ulcer, where the prevalence of infection is 90-95%. There is a dramatic reduction in the rate of ulcer recurrence after successful eradication of the organism to about 4% per annum compared with up to 80% when the infection persists. What is true for duodenal ulcers is also true for patients with gastric ulcer who are infected with H. pylori. The risk of recurrent ulcer complications with bleeding is virtually abolished following successful eradication of H. pylori; in contrast, the risk of rebleeding is about 33% in patients still harboring the organism. The treatment of H. pylori infection in patients with confirmed peptic ulcer on first presentation or recurrence has been advocated by a Consensus Conference of the National Institutes of Health. The most evaluated regimens include dual therapy with a proton pump inhibitor and either amoxicillin or clarithromycin, and bismuth-based triple therapy with metronidazole and tetracycline. The use of a proton pump inhibitor-containing regimen offers the advantage of rapid symptom relief and the highest rates of duodenal ulcer healing. Moreover, combinations of a proton pump inhibitor and clarithromycin show more predictable and higher eradication rates than amoxicillin combinations. Newer triple therapies with a proton pump inhibitor plus two antibacterial agents given for 7-1O days are being increasingly described and may become the treatment of choice if initial results are confirmed. However, the optimum dosage regimen needs to be established. A new combination of ranitidine bismuth citrate and clarithromycin has also recently been shown to be effective. At this time it is reasonable to consider all patients with confirmed duodenal or gastric ulcer for eradication of H. pylori, and no patient should be considered for elective surgery without first being offered eradication therapy.
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PMID:Eradication of Helicobacter pylori infection. 864 82

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

One of the most common bacterial infections of human involves Helicobacter pylori, a spiral, gram-negative bacterium that is now thought to be a dominant factor in the development of peptic ulcer disease and may be significant in causing certain forms of gastric cancer. Almost 100% of patients with duodenal ulcer and 70 to 90% affected with gastric ulcer are infected with H. pylori. In order to achieve cure of H. pylori--induced ulcer disease, it is necesary to eradicate the bacterial infection. Mere suppression or clearance infection without eradication is associated with a >80% recurrence of the ulcer. The epidemiology, microbiology, and pathogenesis of H. pylori infections are reviewed. Diagnostic methods and optimal treatment strategies for H. pylori infections are examined. The most current diagnostic and treatment algorithms for peptic ulcer disease are discussed critically, and future directions for drug development aimed at eradication of H. pylori infection are considered.
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PMID:New Therapeutic Approaches to Peptic Ulcer Disease: The Role of Helicobacter Pylori. 1186 95

Since Marshall's discovery before 20 years, Helicobacter pylori (H. pylori) infection is reportedly to be associated with a variety of clinical outcomes including peptic ulcer disease and gastric cancer. The first step of the H. pylori colonization might be its adhesion to the surface epithelial cells, which evokes gastric inflammatory events initiated by neutrophil recruitment from the microcirculation. Mongolian gerbil is one of the suitable animal models for H. pylori infection, which exerts gastric ulcer and cancer with its bacterial infection. In H. pylori-colonized gerbils, extensive levels of microvascular leukocyte adhesion and migration into the parenchymal side and significant levels of inflammatory cell infiltration are encountered. Bacterial urease not only neutralizes gastric luminal acid, but also plays as an adhesion factor to the surface epithelium. Recently, such an adhesion to the epithelium is reported to be important for bacterial type IV secretory system, which intermediates Cag A injection into the epithelial cells. Then, multiple chemokine and cytokine networks are activated and mucosal inflammatory lesion formation would be completed. In the long-term colonization of H. pylori, gastric mucosal cell turnover would be modified due to persistent inflammation and then such deregulation of cell turnover might link to the precancerous lesion formation.
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PMID:Gastric mucosal response to Helicobacter pylori. 1252 36

Diagnosis and treatment of stomach ulcer associated with helicoid-bacterial infection and with hemorrhage are discussed in the paper. The many-year observations show that the risk of relapsing hemorrhage is high in patients with the above diagnosis. Eradication of the causative agent by using the modern therapeutic schemes cuts significantly the rate of such relapses. The most effective method of monitoring the infection and eradication results is suggested, i.e. urease test combined with microbiological diagnosis involving the method of polymerase chain reaction.
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PMID:[Diagnosis and treatment of Helicobacter infections in patients with stomach ulcer associated with hemorrhage]. 1532 56

Wound healing in the gastrointestinal tract is an orderly process involving orchestrated responses of various cell types. Lipopolysaccharides (LPS) are major components of the outer membrane of Gram-negative bacteria, which are known to impair gastric ulcer healing in animals. The influence of LPS on intercellular communication in wound healing, however, is unknown. We examined the effects of LPS-induced macrophage activation on the proliferative response in cultured rat gastric epithelial cells (RGM-1) and fibroblasts JHU-25. Rat peritoneal resident macrophages were activated with increasing doses of LPS. The supernatant from the activated macrophage preparation, designated as macrophage-conditioned medium, was then used to treat RGM-1 or JHU-25 cells. Cell proliferation and migration were determined by [(3)H]-thymidine incorporation and a monolayer wound-healing assay, respectively. Macrophage-conditioned medium significantly suppressed RGM-1 cell proliferation but had no effect on cell migration. The same medium, however, increased JHU-25 cell proliferation. LPS treatment alone suppressed JHU-25 cell proliferation while it had no effect on RGM-1 cell proliferation, indicating that the differential effects of the macrophage-conditioned medium on cell proliferation were elicited by the factors derived from macrophages. In this regard, tumor necrosis factor (TNF)-alpha stimulated while interleukin (IL)-1beta suppressed RGM-1 cell proliferation, suggesting that IL-1beta but not TNF-alpha may play a part in the mediation of the antiproliferative effect of macrophage-conditioned medium on gastric epithelial cells. In contrast, IL-1beta suppressed while TNF-alpha had no effect on JHU-25 cell proliferation. Collectively, LPS-activated macrophages delay gastric mucosal regeneration but promote fibroblast proliferation in vitro. Such changes may partly elucidate the detrimental effect of bacterial infection on tissue repair in the stomach.
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PMID:Shift of homeostasis from parenchymal regeneration to fibroblast proliferation induced by lipopolysaccharide-activated macrophages in gastric mucosal healing in vitro. 1735 54

Phlegmonous gastritis is an uncommon local or diffuse bacterial infection of the stomach wall. It is an extremely rare disease with a fulminating course and a high mortality rate. A majority of cases are diagnosed only postmortem, and early diagnosis is crucial for survival. This used to be common in the preantibiotic era; a resurgence of cases has occurred of late due to the spread of acquired immunodeficiency syndrome. There are varying local and systemic associations like gastric ulcer, gastric carcinoma, post-therapeutic endoscopy, postsurgery, human immunodeficiency virus infection, malnutrition, Kaposi's sarcoma, myeloma, leukemia, Sjogren's syndrome, and glucocorticoid use. We report a case of phlegmonous gastritis in a 70-year-old lady associated with gastric lymphoma. She succumbed to death on the fifth day of hospitalization despite broad-spectrum antibiotic therapy. She could not be operated upon due to the onset of multiorgan dysfunction syndrome and multiple comorbidities. To our knowledge, gastric lymphoma presenting as phlegmonous gastritis has not been reported in published English literature.
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PMID:Gastric lymphoma presenting as phlegmonous gastritis. 1906 19


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