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

Infection with Helicobacter pylori is associated with almost all cases of peptic ulcer. Using Bayes' formula, we evaluated whether testing for H. pylori in a patient with proven ulcer might help in the work-up of a Zollinger-Ellison syndrome (ZE). A negative test for H. pylori in a patient with duodenal ulcer would raise a pretest probability for ZE of 10-20% to a posttest range of 61-78%. The information provided by a negative test result with respect to ZE is greater in younger than in older ulcer patients. It is also greater in duodenal than gastric ulcer. We conclude that testing for H. pylori in ulcer patients, in whom ZE constitutes a possible differential diagnosis, adds substantially to the decision making at relatively low cost and little additional risk to the patient.
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PMID:Testing for Helicobacter pylori in the diagnosis of Zollinger-Ellison syndrome. 202 53

To evaluate the role of Campylobacter pylori in different gastrointestinal disorders, serum IgG antibodies against C. pylori were determined in dyspeptic patients and in a control group of healthy children and adults. Twenty-eight percent of the dyspeptic patients with normal mucosa were seropositive. Among the patients with altered mucosa, the seroprevalence increased from duodenitis (48%) to gastritis (89%) and gastric or duodenal ulcer, gastric stump gastritis and carcinoma (100%, for each group, respectively). The C. pylori detection rate was lowest in patients with duodenitis alone (19%) and highest in patients with duodenal ulcers (95%). Therefore, C. pylori does not play an important role in patients with duodenitis alone. About 30% of patients with gastritis, active duodenal or gastric ulcer had antibody levels as low as the seroconverted dyspeptic patients but with normal gastroduodenal mucosa. C. pylori was not considered a causative factor for mucosal damage in these patients.
Infection
PMID:The role of Campylobacter (Helicobacter) pylori in disorders of the gastrointestinal tract. 231 73

Desoxyfructo-serotonin (DFS) has shown good results in clinical trials of LL patients. After clinical trials in Bamako (Mali) reported in three articles, clinical trials began in India, at Bombay. Acute toxicity tests done in Paris and chronic toxicity tests done in India had shown absence of side effects. This was also confirmed after pre-clinical pharmacology. In vitro tests show that DFS enhances cellular immune response. Receptors for anti-erythrocyte antibody on LL macrophages are demonstrated by erythrocyte rosetting. Infection with M. leprae markedly reduces rosetting. But in the presence of DFS this reduction in rosetting is not observed. Patient's peripheral blood lymphocytes, sensitised with leprosy antigen, show a low level of rosetting with patients' macrophages. DFS greatly enhances the lymphocyte-macrophage interaction. DFS has an important anti-stress activity. Gastric ulcer induced in rats by restraint were reduced by 40% (Mester et al.) and 50% (Das Neves). DFS increased the uptake of serotonin by LL patients platelets. HPLC studies were done to see the level of DFS in the plasma, in the serum and in the urine of LL patients and controls. We are synthetising new lyposoluble derivatives in order to make easier the penetration of DFS and a long time effect.
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PMID:[Desoxyfructo-serotonin: its therapeutic effect in the treatment of leprosy]. 250 90

A great deal of information about the spiral bacteria of the stomach has accumulated in the past 5 years. These bacteria, currently named Campylobacter pylori but likely to be renamed as a new genus, have adapted to living beneath the mucus layer and above the gastric surface mucous cells. When metaplastic gastric mucous cells are also present in the duodenal bulb, C. pylori may also get a foothold in this latter location. Observations of the high prevalence of C. pylori in patients with gastritis and with duodenal ulcers, and the slightly lower prevalence in patients with gastric ulcer, have led to the hypothesis that the bacteria play an aetiological role in these three conditions. There is now fairly convincing evidence that the organisms can cause active chronic gastritis. The most persuasive of this comes from reports of the rapid development of gastritis and symptoms in two volunteers who swallowed the organism, plus two other series of accidental challenges. Other evidence is provided by the waning and waxing of gastritis, which has been correlated in several studies with clearance followed by recrudescence of the organisms. The role of the bacterium in peptic ulcer is less certain. The present data do not provide strong evidence for a causal role in gastric ulcer, although we cannot rule out that it may be important in some. The very high prevalence in patients with duodenal ulcer, including one series in children (who rarely harbour the organism), raises the distinct possibility that the bacteria play an aetiological role in this form of ulcer. Reports of ulcer healing with antibiotics and of lower recurrence rates in those cleared of the organism, increase the possibility, However, methodological flaws in some studies, plus the usual need for confirmation of key studies, indicate that we should await more definitive evidence before accepting that duodenal ulcer can be an infectious disease.
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PMID:Bacteria in ulcer pathogenesis. 304 51

Demonstration of Helicobacter pylori infection receives more and more importance in nowadays gastroenterological practice. The authors have compared culture and histology from 69 antral biopsy specimens for their ability to document Helicobacter pylori infection. Infection ratios in the context of clinical and histological diagnoses resulted in a distribution pattern similar to that described by others: 85-69% of duodenal ulcer patients, 67-67% of gastric ulcer patients, 62-54% of patients with gastritis and/or erosion(s) and 33-60% of endoscopically negative patients were found to be Helicobacter pylori positive with culture and histology respectively. Normal or atrophic mucosa showed no bacteria with either methods, but one must also consider the small number of such cases in this study. Chronic gastritis with no signs of activity proved to be infected only in a minority of cases, while chronic active gastritis cases were Helicobacter pylori positive in 72 and 61% histologically and with culture respectively. The modified Giemsa stain used in this study grave a relative specificity of 0.74 and sensitivity of 0.79 as compared with culture. There was a good association between the two methods tested, and this could be further improved by doing the two tests simultaneously. The association was weaker when the tests were done asynchronously, this is why it is not recommended to use such a diagnostic schedule. Comparison of the traditional haematoxylin-eosin stain with the modified Giemsa stain resulted in a very strong association between the two.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Detection of Helicobacter pylori in biopsy specimens, methodical studies]. 747 65

Gastroduodenal infection by Helicobacter pylori is a known cause of many gastric and duodenal disorders. Infection by H. pylori is very frequent ant its prevalence increases with age by about 1% per year. Human-to-human transmission appears probable. H. pylori lives under the mucous layer of gastric-type epithelium. It is the main causal agent of chronic diffuse superficial gastritis (type B). After several decades lesions of superficial gastritis can evolve to atrophic gastritis. Spontaneous short- or long-term disappearance of H. pylori from the antral mucosa is rare. H. pylori infection appears to be necessary for the recurrence of duodenal as well as gastric ulcer. Eradication decreases the frequency of relapses, but its long-term effect remains to be evaluated. The presence of H. pylori, however, is not itself sufficient for ulcer development. Why only some patients infected with H. pylori develop ulcer has not been elucidated. The role of H. pylori infection in the gastrotoxicity of non-steroid anti-inflammatory agents is still debated. It has not yet been determined whether eradication leads to reduction of the high digestive morbidity linked to intake of such agents, but it is known that eradication of H. pylori does not obviate the risk of ulcer and of complication. There is a significant association between H. pylori infection, atrophic gastritis and intestinal type gastric cancer. H. pylori infection appears to be one of the factors in gastric cancerogenesis. Cellular proliferation of gastric lymphomas to low-grade B cells would in most cases be secondary to chronic H. pylori infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Helicobacter pylori and gastroduodenal disease]. 793 99

Infection with Helicobacter pylori is the main etiological factor in duodenal and gastric ulcer disease, and eradication of the organism cures peptic ulcer disease. Cure of the infection therefore has become the ultimate treatment goal in ulcer patients. Only therapies that achieve a > 90% cure rate should be used in clinical practice and, as in any other disease, the therapy with the highest cure rates should be used. Bismuth-based triple therapy is considered the gold standard; it has been used successfully in many studies, usually with good tolerability on the part of patients. Many physicians have been hesitant to prescribe this therapy. The regimen is complex, and it is thought to have many side effects. Several groups have shown that concomitant therapy with a proton pump inhibitor increases efficacy and lessens side effects. Moreover, it has become clear that the duration of treatment can be decreased to just 7 days. With this adjustment it now seems sensible to use this short 7-day quadruple therapy, which at present has superior cure rates when compared with any other anti-Helicobacter therapy. This article is a plea for the use of this regimen and gives practical advice about how to employ therapy in general practice. Suggestions are made about how to motivate a patient to comply with the therapy prescribed. If these suggestions are followed, good compliance seems possible, and a near 100% cure rate will be within reach.
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PMID:How to achieve a near 100% cure rate for H. pylori infection in peptic ulcer patients. A personal viewpoint. 877 31

Helicobacter pylori is firmly established as a human pathogen; it fulfils all of Koch's postulates as the infectious agent causing chronic, active (type B) gastritis. Infection is strongly associated with duodenal and gastric ulcer. Recently, gastric mucosal-associated lymphoid tissue lymphoma has been successfully treated by curing H. pylori infection. Because of the evidence that the organism causes chronic gastritis and an increased risk of gastric cancer, it has been classified as a category 1 carcinogen by the World Health Organization. However, the overwhelming majority of people infected have no symptoms. Current eradication therapy is not ideal; there are treatment failures and substantial side effects. As a result, therapy should be reserved for people with clinical symptoms and complications. The infection, if present, should be treated in patients who have endoscopic evidence of mucosal ulcers in the stomach or duodenum. Current evidence does not support treating the infection to prevent gastric carcinogenesis or to alleviate symptoms of abdominal discomfort in the absence of peptic ulcers.
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PMID:Why guidelines are required for the treatment of Helicobacter pylori infection in children. 888 75

Infection with Helicobacter pylori (H. pylori) causes gastritis, and may be associated with gastric and duodenal ulcers and also with such malignant diseases as MALT lymphoma and gastric carcinoma. In order to determine whether there are differences in the degree and distribution of gastritis, each patient with H. pylori gastritis only (n = 50) was matched for sex and age with four patients, one each with H. pylori-associated duodenal ulcer, gastric ulcer, gastric carcinoma or MALT lymphoma. From each patient, two biopsies were taken from the antrum and two from the corpus for histopathological examination of H. pylori gastritis. The median summed gastritis score decreases in the following order: antrum: gastric ulcer > duodenal ulcer > gastritis alone > carcinoma > MALT lymphoma, and corpus: gastric ulcer > carcinoma > MALT lymphoma > gastritis alone and duodenal ulcer. We conclude that the degree and distribution of H. pylori gastritis differs significantly among H. pylori-associated diseases. These differences may explain some of the underlying pathomechanisms associated with H. pylori infection.
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PMID:Differing degree and distribution of gastritis in Helicobacter pylori-associated diseases. 924 28

We retrospectively evaluated clinical findings and the actual status of management of 69 tuberculosis patients admitted to the Fujita Health University Hospital, a hospital without isolation wards for infectious diseases, between 1991 and 1994. The largest age group was 60s (27.5%) followed by 70s (24.6%), 80s (15.9%) and 50s (13.0%). Eight patients (11.6%) were in the 20s. Forty-nine patients were smear-positive and 22 patients were smear-negative and culture-positive. Fourteen patients (20.3%) had a past history of pulmonary tuberculosis. Twelve patients (17.4%) also had diabetes mellitus, ten patients (14.5%) had cancer, ten patients (14.5%) gastric ulcer and five patients (7.2%) renal failure. Positive skin reaction to PPD was not found in eleven patients (15.9%) and seven of these patients were quite elderly (over 70 years old). Twenty-five cases (36.2%) were classified as type II (cavitary) and 29 cases (42.0%) as type III (non-cavitary) according to the GAKKAI classification of findings on chest X-ray films for pulmonary tuberculosis. Twenty-four patients (34.8%) were not diagnosed as tuberculosis on admission by physicians in charge. Physicians in charge tended not to suspect smear-negative patients of tuberculosis. Most of the patients with cavities on their chest X-ray films were strongly suspected of tuberculosis on admission, but in some of them, tuberculosis was not considered at all. Smear-positive patients with strongly suspected tuberculosis were diagnosed with the disease within three hospital days, while it took about three weeks in patients who were not considered as tuberculosis on admission to be diagnosed as tuberculosis. In the case of smear-negative patients, it took about one month and two months respectively to diagnose the case as tuberculosis. About half (51.1%) of the smear-positive patients were admitted and treated in single-bed rooms while 44.7% were attended in multiple-bed rooms for 11 days before they were transfered to single-bed rooms. When acid-fast bacilli were detected, 57.4% of the smear-positive patients were transfered to hospitals with isolation wards for infectious diseases, while the remaining smear-positive patients were treated in single-bed rooms at the university hospital. About one-third (31.7%) of the smear-negative patients had already left the hospital when specimens were found to be culture positive for tubercle bacilli. In conclusion, it is utmost important for physicians to suspect tuberculosis for the early diagnosis of the disease.
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PMID:[Actual status of the management of tuberculosis patients in a university hospital without isolation wards for infectious diseases]. 924 73


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