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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional dyspepsia covers various symptoms associated by the physician with the upper gastrointestinal tract without an identifiable organic cause. The existence of dyspepsia subgroups according to different symptom complexes, e.g. so-called "ulcer-like dyspepsia", has not been proved. Gastro-esophageal reflux disease is a distinguishable independent entity. Little is known about the pathogenesis of this common syndrome. Disturbances of gastric motility, especially postprandial antral hypomotility, are found in 50% of these patients but offer no explanation of the dyspeptic symptoms. Neither abnormal gastric acid secretion nor abnormal acid sensitivity has been proved in these patients. Furthermore, no relation between the symptoms and a Helicobacter pylori infection or a functional disturbance of the biliary tract has been established. In some cases fatty foods can provoke dyspeptic symptoms. Unfavorable psychosocial factors can influence the decision to consult a physician for dyspepsia. Recently, a lowered threshold of perception of stomach and small intestine distension in dyspepsia has been demonstrated. This disturbance of perception offers a new basis for further understanding and for possible treatment. Prokinetic agents can be of help in the treatment of functional dyspepsia. H2-receptor antagonists are most effective in patients presenting symptoms of gastro-esophageal reflux disease. Empiric therapeutic trials in this disease entity, which shows a high placebo response rate (between 30% and 60%), are not of proven value.
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PMID:[Functional dyspepsia. Old wine in new bottles?]. 815 99

One hundred and ninety-six symptomatic Saudi patients with dyspepsia underwent gastroscopy, and multiple biopsies were taken from the antrum of the stomach for identification of Helicobacter pylori. Three methods were studied for diagnosis of Helicobacter pylori, including urease test, culture and histopathology. The commonest gastroscopic findings were gastritis in 82 patients (41.84%) and duodenal ulcer in 40 patients (20.41%). Among the 196 patients, Helicobacter pylori was identified by histopathology in 145 patients (73.98%), the urease test was positive in 126 patients (64.29%), and a positive culture was obtained in 102 patients (52.04%). These results show that there is a high incidence of Helicobacter infection among Saudi patients with peptic ulcer disease or non-ulcer dyspepsia. Helicobacter pylori identification was more successful by histopathology than by the urease test or culture.
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PMID:Helicobacter pylori: incidence and comparison of three diagnostic methods in 196 Saudi patients with dyspepsia. 817 15

Helicobacter pylori infection of the stomach is associated with gastritis and peptic ulceration and may be causative. A noninvasive test for this organism might be useful in managing some patients with dyspepsia without the need for further investigation. We have evaluated a new commercially available serological test (Helico-G ELISA, Porton Cambridge, UK) for this infection to assess its diagnostic accuracy in a retrospective study of 115 patients with non-ulcer dyspepsia. Sixty-three of these patients (55%) were found to have H. pylori infection and gastritis on histology. A sensitivity of 81% and specificity of 90% were obtained. No significant fall in the antibody titres was found in a subgroup of 15 patients who were selected to complete a course of triple therapy despite significant improvement in their dyspepsia score and confirmed eradication of H. pylori organism in 80% of these patients. We conclude that the test has limited value in aiding clinical decision of managing patients with dyspepsia.
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PMID:Evaluation of a commercial enzyme-linked immunosorbent assay (ELISA) kit for serological diagnosis of Helicobacter pylori infection in a group of non-ulcer dyspepsia sufferers. 820 42

The prevalence of Helicobacter pylori infection was determined in peptic ulcer patients, in non-ulcer dyspepsia (NUD) patients, and in the general adult population. The H. pylori infection rate ascertained by microbiologic examination of multiple gastric antral biopsy specimens was 50% (17 of 34) in duodenal ulcer (DU), 5% (1 of 22) in gastric ulcer, and 9% (15 of 159) in NUD patients. A seroepidemiologic survey showed a prevalence of only 4.2% among 496 blood donors and 4.8% among 921 subjects who attended health screening clinics. H. pylori infection is relatively uncommon and does not appear to be the predominant factor in the pathogenesis of peptic ulcer disease in the area. The incidence of peptic ulcer perforations in the area in 1991-92 was 1.5 per 100,000 person-years, reflecting a relatively low frequency of peptic ulcers, which might be due to the low prevalence of H. pylori infection in the population.
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PMID:Helicobacter pylori infection in north-eastern peninsular Malaysia. Evidence for an unusually low prevalence. 820 78

Acid peptic disease is common, and its management is costly. Less than a decade ago, the traditional theories regarding the etiology and pathogenesis of acid peptic disease were upset by the discovery of Helicobacter pylori infection in association with chronic active gastritis. A substantial body of investigation after that discovery has established this infection as the major cause of human chronic active gastritis and has defined a critical role for H. pylori in the etiology, pathophysiology, and treatment of duodenal ulcer disease. Furthermore, evidence is accumulating to link H. pylori to gastric ulcers, non-ulcer dyspepsia, and even gastric carcinoma. Research has clarified some unique features of the organism that have been put to advantage in the development of diagnostic tests, and it has also clarified some features of the infection that make it difficult to treat. Although treatment is decidedly beneficial for certain patient subsets, simpler and more effective therapy is needed.
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PMID:The role of Helicobacter pylori in acid-peptic disease. 826 81

The present study evaluated the effect of a one-day high-dose combined therapy on Helicobacter pylori infection. Thirty-two consecutive patients (suffering from either peptic ulcer or nonulcer dyspepsia) with Helicobacter pylori infection received omeprazole (40 mg) + bismuth subcitrate (240 mg x 4) + amoxicillin suspension (2000 mg x 4) + metronidazole (500 mg x 4), for only one day. Endoscopy, histology, culture, and susceptibility studies were done at entry and 30 and 90 days after the treatment day. Successful eradication was obtained in 23/32 (72%) patients and gastritis had resolved in 95% of these. Side effects were induced by the treatment in 6/32 (19%) patients, but these were all self-limiting, short-lasting, and did not require any specific treatment. Development of bacterial resistance to metronidazole occurred in 6/9 (67%) non-eradicated patients. These data suggest that one-day treatment with high doses of amoxicillin, metronidazole, bismuth, and omeprazole represents an effective, safe, and inexpensive therapeutic approach for the treatment of H. pylori infection.
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PMID:One-day therapy for treatment of Helicobacter pylori infection. 936 53

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output > 10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence of Helicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis). Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P < 0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found among Helicobacter pylori-positive compared to Helicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr were Helicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence of Helicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.
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PMID:Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion. 842 Jul 45

Motor disorders of the upper gastrointestinal tract are a frequent finding in patients with non-ulcer dyspepsia (NUD). In this study we attempted to assess whether Helicobacter pylori infection contributes to gastrointestinal motor disorders in NUD. Interdigestive and post-prandial gastrointestinal motility was studied in 46 consecutive patients with NUD and in eight healthy control subjects. Abdominal complaints were assessed by means of a symptom score. Chronic gastritis and H. pylori infection were assessed and graded by histology. Accordingly, patients with NUD were divided into two sub-groups: 18 patients with H. pylori infection and chronic active gastritis and 28 patients without H. pylori infection. The length of the interdigestive motor cycle was not different in patients with NUD (139 +/- 6 min, mean +/- SEM), compared with controls (128 +/- 5.5 min). There was also no difference in the duration of individual phases I, II, and III, either between NUD and controls or between H. pylori-positive and -negative patients. The motility index (MI) of antral phase II also was not changed in NUD patients. Postprandial antral motility was decreased in patients with NUD (MI 6.96 +/- 0.4 vs. 9.7 +/- 0.3 controls; p < 0.025), with no difference between H. pylori-positive and -negative subgroups. It therefore appears unlikely that H. pylori infection plays a primary role in the pathophysiology of antroduodenal motor disorders in NUD.
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PMID:Gastrointestinal motility in patients with non-ulcer dyspepsia: a role for Helicobacter pylori infection? 843 42

A review is presented on the relationship between Helicobacter pylori infection and gastritis and its possible significance in non-ulcer dyspepsia. Although there is consensus about the pathogenetic role of H. pylori in gastritis, the correlation between H. pylori and gastritis does not appear to be qualitative, as generally thought and accepted, but rather quantitative. It is not a black and white relationship; in other words the microorganism is present in large quantities in inflamed tissue but is also present in normal healthy mucosa in low numbers. The hypothesis is proposed of an equilibrium between virulence of H. pylori on the one hand and mucosal defence mechanism on the other hand. Distortion could lead to an attack of gastritis. The present view is that the bacterium is neither commensal nor pathogen, but is able to change its role depending on the local and momentary situation. Given the presence of H. pylori infection in patients with non-ulcer dyspepsia, with or without gastritis, the significance of the infection is probably greater than thought.
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PMID:The role of Helicobacter pylori in non-ulcer dyspepsia and gastritis. 844 30

The hypothesis that non-secretors of ABO blood group antigens, a group shown to be more susceptible to certain bacterial infections, may be at greater risk of gastroduodenal disease because of increased susceptibility to Helicobacter pylori infection was investigated. Of 101 patients with symptoms of dyspepsia who were undergoing endoscopy, 32% were non-secretors (determined from Lewis blood group phenotype), 36% had endoscopically visible gastroduodenal disease (antral gastritis, gastric ulcer, erosive duodenitis, duodenal ulcer or some combination), and 58% had H pylori detected in antral biopsy specimens. Non-secretors and patients with H pylori infection were significantly more likely to have gastroduodenal disease (p = 0.02 and p = 0.002 respectively). There was, however, no significant association between secretor status and H pylori infection, logistic regression analysis confirming that these were independently associated with gastroduodenal disease. Overall, the relative risk of gastroduodenal disease for non-secretors compared with secretors was 1.9 (95% confidence intervals 1.2, 3.2). Non-secretion of ABO blood group antigens is not related to H pylori infection but is independently and significantly associated with endoscopic gastroduodenal disease. The mechanism of this remains to be explained.
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PMID:Secretor status and Helicobacter pylori infection are independent risk factors for gastroduodenal disease. 847 82


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