Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter pylori is now known to be the most common and important cause of gastritis, and C. pylori infections have been associated with duodenal ulcer, gastric ulcer, nonulcer dyspepsia, and gastric cancer. Although it has been only possible to culture C. pylori for about 5 yr, there are already sufficient data available to allow us to develop the basic framework that relates C. pylori gastritis to the causation of peptic ulcer disease. We review the data and propose mechanisms that implicate C. pylori as an important factor in the pathogenesis of peptic ulcer disease and consider the therapeutic implications. What we now know about C. pylori begins to unravel some of the mysteries surrounding peptic ulcer disease.
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PMID:Campylobacter pylori and peptic ulcer disease. 226 88

Dyspepsia associated with arthritis and non-steroidal anti-inflammatory drugs (NSAIDs) is a common clinical problem. Up to 80% of deaths attributable to peptic ulceration may be associated with NSAID usage. The problem is foremost in the elderly population, in which there has been an increase both in the incidence of peptic ulcers and in the use of NSAIDs. Although the development of duodenal ulceration is not clearly associated with NSAIDs, it is accepted that these drugs increase the risk of gastric ulceration and the occurrence of peptic ulcer complications. Asymptomatic peptic ulceration is common, and patients taking NSAIDs are often asymptomatic prior to presentation with life-threatening complications. The key principle in management of this problem is prevention through careful selection of patients for NSAID use, adequate treatment of peptic ulceration and maintenance of remission. A variety of effective drugs are available for the treatment of peptic ulcers, including H2-receptor antagonists, pirenzepine, sucralfate and colloidal bismuth subcitrate. However, it is recognised that peptic ulceration is a chronic disease with a relapsing-remitting course, often with asymptomatic ulcer episodes. The knowledge that current ulcer-healing strategies do not significantly alter this natural history has lead to increasing efforts to prevent relapse with effective 'maintenance' therapy.
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PMID:Treatment of peptic ulcer disease in the arthritic patient. 268 Apr 37

Campylobacter pylori is an organism living under mucus layer in the stomach and on the places of gastric mucosa metaplasia. It is known to be responsible for the development of gastritis, probably also it participates in the pathogenesis of dyspepsia without ulcer, while its role in the development of gastric and duodenal ulcer has not yet been explained completely. The authors present a characteristics of the organism and the methods of its detection. A number of investigations are discussed which demonstrate its clinical importance. In summary, it is shown that the present state of knowledge on Campylobacter pylori is insufficient for serving as a rationale for antibacterial treatment of peptic ulcer.
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PMID:[Campylobacter pylori in diseases of the stomach and duodenum]. 270 Oct 41

Of 1,100 patients checked by at least two diagnostic tests (urease, histology, culture) 574 (52.1 p. 100) were found to have Campylobacter pylori (C. pylori) in their antral mucosa. Significantly different frequencies of C. pylori (p less than 0.005) were evidenced in the group of patients with active gastroduodenal ulcer (212/298, 71 p. 100), in non-ulcer dyspepsia (NUD) with a previous history of GD ulcer (108/177, 61 p. 100) and NUD without antecedent history of GD ulcer (254/625, 41 p. 100). Whatever the group, males and immigrants were significantly at risk. Chronic alcoholism (greater than 60 g/day) and non-steroid anti-inflammatory drug (NSAID) intake were not predictive for the presence of C. pylori but smokers were significantly at risk when the total (n = 1,100) population was taken into consideration. C. pylori was found in 29 p. 100 of asymptomatic controls (n = 31). There was no significant difference in the frequency and intensity of symptoms when comparing C. pylori+ and C. pylori- patients. The macroscopic aspect of the antral mucosa was not predictive since 51 p. 100 of patients with normal endoscopy were C. pylori+. A strong correlation was observed between the incidence of C. pylori and the severity of gastritis at histology (p less than 0.001) and C. pylori was found in 7 p. 100 of patients with normal histology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical, endoscopic and histologic findings in 1,100 patients of whom 574 were colonized by Campylobacter pylori]. 274 27

The etiology of peptic ulcer disease is completely unknown. However, gastric acid secretion plays an important role in the pathogenesis of the disease. Acetylcholine, gastrin and histamine are recognized as the main stimulators of the acid secretion. Extensive studies on blood gastrin have not incriminated this hormone in the pathogenesis of the disease. The present study was done to evaluate the role of circulating histamine in peptic ulcer disease using a sensitive and specific radioimmunoassay method. Since gastrin at least in some species seems to exert its stimulatory effect by releasing histamine, serum gastrin was also determined. There was no significant difference in plasma histamine between patients with duodenal or gastric ulcer, nonulcer dyspepsia or ulcer patients after proximal gastric vagotomy. However, patients taking a histamine-2 blocker (cimetidine or ranitidine) had significantly higher plasma histamine than those not taking these drugs. This effect was not due to interference in the histamine assay. There was no correlation between plasma histamine and plasma gastrin. Plasma gastrin was significantly increased in patients having been operated on with a proximal gastric vagotomy. In conclusion, plasma histamine is similar in patients with different upper gastrointestinal disorders. However, histamine-2 blockers may increase plasma histamine.
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PMID:Histamine and gastrin in plasma of patients with upper gastrointestinal diseases. 276 43

Campylobacter pylori causes type B gastritis and C. pylori infection has been associated with duodenal ulcer, gastric ulcer, non-ulcer dyspepsia, and gastric cancer. Although we have been able to culture C. pylori for only about 5 years, what we now know about this organism can explain many mysteries surrounding peptic ulcer disease. Whenever one investigates a population of ulcer patients for the presence of any accepted potentially important pathogenetic factors, one finds that the population of patients with duodenal ulcer disease differs (statistically) from those without duodenal ulcer disease, but that to a large degree they also overlap. None of the traditional factors can be considered essential and characteristic of chronic duodenal ulcer. The exception is the presence of a C. pylori infection, the presence of which is almost invariable. Several properties of C. pylori have been identified that might be virulence factors, including (a) provoking a marked acute and chronic inflammatory response, (b) rapid motility through gastric mucus, (c) urease activity, (d) a fibrillar adhesin(s), (e) several putative exotoxins, and (f) microinvasion. We can now add to the old dictum "no acid-no ulcer," "no C. pylori-no ulcer" at least as far as chronic duodenal ulcer disease in adults is concerned.
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PMID:Campylobacter pylori. The organism and its clinical relevance. 280 38

Dyspepsia stands for a constellation of symptoms referrable to the upper gastrointestinal tract. However, the term dyspepsia is too vague to be useful in scientific work unless critically defined. In many cases dyspepsia coincides with the irritable bowel syndrome. An increased use of endoscopy and the possibility of prompt symptom relief in peptic ulcer by treatment with H2-receptor antagonists have focused the interest on patients with ulcer-like dyspepsia but in whom there is no evidence of ulcer disease. This large group of patients deserves further nosologic classification and there is a strong need of pathophysiologic and interventional studies.
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PMID:Dyspepsia. Definition and discussion of nomenclature. 286 94

The costs of peptic ulcer disease to society are very high. Costs can be expressed as either direct or indirect. Direct costs include hospitalization or clinic visits, physicians' fees, and medication. Indirect costs are loss of productivity due to absenteeism from work or loss of income from death of an employee. The daily cost of different ulcer drugs such as the histamine (H2)-receptor antagonists for intravenous treatment, acute healing, and maintenance can easily be compared. As newer anti-ulcer drugs such as H2-receptor antagonists have been introduced into the marketplace, the number of prescriptions and medication costs have increased rather than decreased. In part, this may be accounted for by the high frequency with which H2 antagonists are prescribed for patients with non-ulcer dyspepsia. Some patients have chronic peptic ulcer disease with multiple painful recurrences or complications such as hemorrhage, perforation, or obstruction. They may require long-term care or drug maintenance, hospitalization, or surgery. For patients with chronic ulcer disease or complications, randomized controlled trials to compare the efficacy, safety, and costs of different forms of therapy (maintenance drugs, surgery, or placebo) have not been reported. However, based upon good efficacy and safety for acute healing and long-term drug maintenance for painful duodenal ulcer disease, long-term maintenance with H2-receptor antagonists is now prescribed for many patients. No controlled randomized trials have been reported to document that long-term maintenance with H2-receptor antagonists actually reduces peptic ulcer complications. However, by current cost estimates, long-term H2-receptor antagonist therapy is less expensive than ulcer surgery for uncomplicated ulcer disease for up to eight years. However, maintenance drug therapy after eight years may be more expensive than elective ulcer surgery in patients with chronic peptic ulcer disease who are good surgical candidates. Patients with complications of peptic ulcer disease seem to represent a different subset than patients with symptomatic ulcer disease. Further studies in these subsets are needed to ascertain the most effective, safest, and least expensive management such as surgery, long-term drug maintenance, or intermittent drug therapy to prevent recurrent ulceration or complications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Economic and health aspects of peptic ulcer disease and H2-receptor antagonists. 287 74

After infradiaphragmatic radiotherapy the cancer-related 10 year survival was 99% in 365 patients with seminoma Stage I referred to the Norwegian Radium Hospital between 1970 and 1982. Thirteen patients relapsed, 11 of them within the first 3 years after treatment. Nine of the recurrent patients were cured by radiotherapy alone (4) or in combination with chemotherapy (5). There is no need to include the inguinal lymph nodes into the irradiation field or to give scrotal irradiation, not even to patients with tumor infiltration beyond the testicular tissue, or to those with prior scrotal or inguinal surgery. At least 1 year after radiotherapy moderate or more severe dyspepsia was observed in 16 patients. Nine patients developed a peptic ulcer. In general, there was no increased risk for development of a second non-germ cell cancer after radiotherapy. However, 4 patients developed a pulmonary cancer indicating a border-line significance of increased risk for this type of malignancy. (p:0.05). In conclusion, infradiaphragmatic radiotherapy remains the optimal routine treatment in seminoma patients with Stage I.
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PMID:Radiotherapy for testicular seminoma stage I: treatment results and long-term post-irradiation morbidity in 365 patients. 292 Nov 42

Campylobacter pylori has been associated with gastritis, duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Evidence that C. pylori may be the causative agent or at least a major contributory factor in peptic ulcer disease has generated intense interest in the development of reliable methods for detecting C. pylori infections. We have developed a specific and sensitive enzyme-linked immunosorbent assay (ELISA) that detects serum immunoglobulin G antibodies directed against high molecular weight cell-associated proteins (HM-CAP) of C. pylori. In a blinded fashion we tested sera from 300 individuals and found that all of 147 HM-CAP ELISA-negative individuals were also negative for C. pylori, as documented by a negative urea breath test; also, 151 of 153 C. pylori-positive (by urea breath test) individuals were HM-CAP ELISA-positive. Campylobacter pylori was cultured from the two ELISA-negative but infected patients and these isolates did possess HM-CAP antigens, showing that these two individuals had failed to seroconvert. Thus, the specificity and positive predictive value of the HM-CAP ELISA were each 100%; the sensitivity of the assay was 98.7%, and the negative predictive value was 98.6%. The HM-CAP ELISA and the urea breath test both proved valuable for detecting C. pylori infection, the urea breath test being a more direct method whereas the ELISA is less expensive and easier to perform. Furthermore, the results of a serologic test such as the HM-CAP ELISA would not be influenced by recent ingestion of bismuth compounds or antimicrobial therapy, which might suppress C. pylori and cause a transient false-negative result in the urea breath test.
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PMID:A sensitive and specific serologic test for detection of Campylobacter pylori infection. 277 37


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