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

This study investigates whether patients who take nonsteroidal antiinflammatory drugs are more likely to have Helicobacter pylori gastritis than age-matched individuals who do not take nonsteroidal antiinflammatory drugs, and whether patients who take nonsteroidal antiinflammatory drugs who are also infected with H. pylori are more likely to have dyspepsia, mucosal damage, or ulcers than those who are not infected. Two studies were performed, one serological and the other endoscopic, both in arthritis patients receiving nonsteroidal antiinflammatory drugs chronically. The presence of H. pylori was identified with a sensitive enzyme-linked immunosorbent assay test. One hundred eighty-three patients participated in the serological study and 75 patients in the endoscopic study. The frequency of H. pylori infection increased with age, independent of nonsteroidal antiinflammatory drug use; the age-adjusted frequency of H. pylori infection in arthritis patients paralleled that of 351 asymptomatic individuals without arthritis. The frequency of H. pylori infection increased from 30.7% in age group 21-30 years to 73.4% in age group 61-75 years. Nonsteroidal antiinflammatory drug-induced mucosal injury, either hemorrhages or erosions, was more frequent in those without H. pylori infection than with infection (61% vs. 32% for hemorrhages and 57% vs. 34% for erosions for those without and with H. pylori infection; only the difference in the frequency of hemorrhages was significant, P less than 0.05). No difference was observed in the presence of dyspeptic symptoms between those with and without H. pylori infection. These data suggest that nonsteroidal antiinflammatory drug-induced damage to the gastroduodenal mucosa does not increase the susceptibility to H. pylori infection.
 ...
PMID:Long-term nonsteroidal antiinflammatory drug use and Helicobacter pylori infection. 201 71

At the present, Helicobacter-associated gastritis is not considered to be an important cause of dyspeptic symptoms. Therefore, patients with dyspeptic symptoms and proven Helicobacter-gastritis are diagnosed as having functional dyspepsia, provided that Helicobacter-associated lesions like ulcers or malignancies are absent. It is controversial whether or not to treat a patient with functional dyspepsia with Helicobacter gastritis. Conclusive controlled clinical trials are lacking. If it is assumed in a given patient, that Helicobacter could be responsible for the complaints (an assumption which can never be proven and only suspected when the patient remains asymptomatic during longterm follow-up after cure of the infection) and if the patient has not responded to a standard treatment (antisecretory or prokinetic agents), we recommend Helicobacter therapy. Presently, in spring 1995, the following treatment is, in our view, the best choice during seven (to ten) days: The patient takes 20 mg omeprazol in the morning, 250 mg clarithromycin in the morning and in the evening and 500 mg metronidazole in the morning and in the evening.
 ...
PMID:[Functional dyspepsia: approaches to Helicobacter pylori eradication therapy]. 760 89

Functional dyspepsia (or 'non-ulcer') is usually defined as chronic or intermittent upper abdominal symptoms for which no organic cause can be found. Division of functional dyspepsia into subgroups such as reflux-like, ulcer-like, dysmotility-like and non-specific dyspepsia has been proposed, but lacks a scientific basis. Gastric acid hypersecretion, Helicobacter pylori-associated gastritis, gastric and small intestinal motor disorders, psychological and neurohormonal factors all might play a role in the pathogenesis. The heterogeneity of the underlying abnormalities makes it unlikely that one single treatment modality will ever be beneficial to all patients. In general practice, a therapeutic trial, with either a prokinetic or an acid secretion inhibiting drug, is usually carried out before diagnostic procedures are performed to exclude organic abnormalities. In the choice of the initial therapy, some guidance can be derived from the prominent symptoms. In a study in 30 H. pylori-negative patients with functional dyspepsia ranitidine (150 mg bid) significantly reduced the severity of heartburn. The effect was most pronounced in patients of the reflux-like subgroup.
 ...
PMID:Pathophysiology and treatment of functional dyspepsia. 801 77

Fifty-three patients with previously uninvestigated chronic dyspepsia symptoms in the absence of gastrointestinal or extra-gastrointestinal disease (functional dyspepsia) underwent antral and duodenal mucosal biopsies to detect the role of such samplings in the presence of normal endoscopic findings. Patients were enrolled in a randomized, placebo-controlled, double-blind trial, receiving either eradicating treatment (colloidal bismuth subcitrate plus metronidazole) or placebo if they had Helicobacter pylori-associated gastritis (20 patients), or cisapride or placebo if they had normal antral mucosa (28 cases). Unsuspected celiac sprue was found in one patient. Eradicating treatment ameliorated histological gastritis (p = 0.01). However, owing to great placebo efficacy, symptom remission rates following a 1-month wash-out period in both treatment groups were no higher than that in controls. Independent of the initial randomization, an extremely low symptom recurrence rate was observed during a drug-free follow-up study equivalent to the mean duration of symptoms before enrollment. We conclude that in functional dyspepsia, bulbar and antral biopsies are not useful in clinical management, equivalent symptom relief can be achieved in patients randomly assigned to both drugs and placebos, and such improvement can be long lasting in the absence of any maintenance treatment. We believe the prevalence of unsuspected villous atrophy and the therapeutic role of investigation-based reassurance deserve further assessment.
 ...
PMID:Are routine duodenal and antral biopsies useful in the management of "functional" dyspepsia? A diagnostic and therapeutic study. 840 29

Nonulcer dyspepsia (NUD) is an enigmatic disorder which likely has heterogeneous etiologies. Helicobacter pylori-associated gastritis has been identified in a large number of patients with NUD, raising speculation that chronic infection with this organism may cause dyspepsia in some patients. Prospective case-control and cohort studies however do not suggest that H. pylori prevalence is greater in NUD than in asymptomatic controls. Limited therapeutic trials of H. pylori-eradication therapy have not shown a convincing symptomatic improvement compared with placebo treatment. Definition of the role of H. pylori in NUD awaits further well-designed, well-controlled epidemiologic and therapeutic studies. Until such information is available, routine endoscopic gastric biopsies looking for H. pylori in patients with NUD should be abandoned.
 ...
PMID:Endoscopy-negative dyspepsia. Hold those forceps! 840 11

Approximately 50% of patients with nonulcer dyspepsia harbor Helicobacter pylori gastritis, yet there is no convincing evidence that H. pylori is causally linked to chronic dyspepsia. The prevalence of H. pylori is probably not higher in patients with nonulcer dyspepsia than in the asymptomatic general population, and H. pylori is not associated with a specific symptom profile. Moreover, no plausible mechanisms to explain how histologic gastritis could induce intermittent symptoms have been identified. Finally, there is a lack of cogent experimental evidence linking H. pylori to nonulcer dyspepsia. On the basis of the available data, it must be concluded that H. pylori is unlikely to play an important role in most patients with nonulcer dyspepsia.
 ...
PMID:The role of Helicobacter pylori in nonulcer dyspepsia. A debate--against. 844 64

Gastritis is a histopathologic diagnosis, which correlates poorly with both clinical symptoms of non-ulcer dyspepsia and endoscopic abnormalities. Worldwide, most cases of gastritis are due to Helicobacter pylori and are characterized by a diffuse superficial antral gastritis. Chronic inflammatory cells and lymphoid follicles are present in the lamina propria. Neutrophils are present in the surface and pit-lining epithelium. In North America and Western Europe, reactive gastropathy due to duodenal reflux or non-steroidal anti-inflammatory agents is also common. In this condition, there is no increase in inflammatory cells, but the pit-lining cells become hyperplastic, and the pits have a corkscrew appearance. Most examples of multifocal atrophic gastritis are the result of long standing Helicobacter gastritis, although there may be other causes as well. It is characterized by loss of glands in both pyloric and corpus mucosae with intestinal metaplasia of the surface epithelium. A subtype of intestinal metaplasia, in which sulphomucin (large bowel mucin) is present, has been associated with the development of distal gastric cancer. However, this association is relatively weak and is not considered useful for screening purposes. Gastric dysplasia may develop in areas of the stomach affected by intestinal metaplasia. High-grade dysplasia is a significant finding, with up to 60 percent of cases having coincident carcinoma and a further 25 percent of cases likely to develop an invasive malignancy within fifteen months.
 ...
PMID:The morphology of gastritis. 904 89

A major role for Helicobacter pylori gastritis in nonulcer dyspepsia (NUD) is controversial. Gastroduodenal dysfunction may be associated with H. pylori infection, but there is little evidence for a causal link with dyspepsia. Population-based studies with appropriate methodology have generally failed to confirm an association between H. pylori and NUD. Furthermore, no definite association between subgroups of NUD (ulcer-like, dysmotility-like, reflux-like, and nonspecific) and H. pylori has been identified however the subgroups have been defined, and no specific symptom pattern characterizes patients with H. pylori infection. Whether H. pylori-induced alterations of gastric physiology can explain NUD remains open to debate while we await the results of more specific experiments. Although acid secretion in response to gastrin-releasing peptide may be increased in a subset of NUD patients who are infected with H. pylori, uninfected patients with NUD have not been assessed and the results require confirmation. Most studies suggest no association between H. pylori and gastroduodenal motor or sensory dysfunction in NUD. Treatment trials have been unconvincing. The trials with bismuth therapy have not been adequately blinded. Furthermore, some studies suggest that H. pylori-negative patients with NUD may respond to bismuth treatment, although the results have not been uniform. Therapies aimed at curing H. pylori infection have produced mixed results, with small positive and negative trials. The trials that have used adequate outcome measures have more often than not been negative. Based on current evidence, H. pylori is not established to be of causal importance in NUD.
 ...
PMID:What role does Helicobacter pylori play in dyspepsia and nonulcer dyspepsia? Arguments for and against H. pylori being associated with dyspeptic symptoms. 939 64

Nonulcer dyspepsia or chronic dyspepsia (defined as upper gastrointestinal symptoms of at least 3-weeks duration) is a common problem in Western countries. Up to 30% of the general population suffer from dyspepsia and the dyspepsia-related work-load of the general practitioner is considerable. The general practitioner has to formulate a management approach: what therapy, if any, and which patient should be investigated? A considerable overlap of symptoms make a precise diagnosis without additional investigations difficult, but empirical acid inhibition is an attractive option. Disturbances of gastrointestinal motility and, perhaps, Helicobacter gastritis are additional possible pathogenetic mechanisms. At present, conclusive, controlled clinical trials are lacking and it remains controversial which strategy is most cost-effective but at the same time optimal for the patient.
 ...
PMID:[Nonulcer dyspepsia]. 978 56

Helicobacter pylori gastritis (i.e. H. pylori infection and complications) is a focus of tremendous research activity today. Besides peptic ulcer disease, a large number of reports suggest that other diseases are associated with H. pylori. The International Agency for Research on Cancer sponsored by the World Health organization classified the bacterium as a group I carcinogen in 1994. Population-based studies of H. pylori and gastric cancer in 1991 showed an increased odds ratio, of 3-6, in infected patients, and a calculation of odds ratios in different age groups showed a markedly increased odds ratio, to about 20, in younger ages. Studies of non-ulcer dyspepsia and the effect of cure of H. pylori show either none, small, or significant symptom relief, suggesting a positive effect in a subgroup of non-ulcer dyspepsia patients. Mucosa-associated lymphoid tissue-lymphoma caused by H. pylori could be eradicated, at least in its mild forms. Barrett's ulcer is a possible H. pylori-associated disease as well as gastroesophageal reflux disease. Normal feedback in the acid regulation system is changed in infected patients, which may facilitate an increased gastroesophageal acidic reflux. Gastropathy and/or peptic ulcer due to use of nonsteroidal antiinflammatory drugs is probably aggravated by the infection. The infectious disease H. pylori gastritis is associated with a large number of complications, some of which are serious. There are no data showing any advantages of the infection. Giving anti-H. pylori therapy to infected patients should be regarded as essential.
 ...
PMID:Are there more clinically important complications of Helicobacter pylori infection than peptic ulcer disease? A review of current literature. 984 18


1 2 3 Next >>