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

Helicobacter pylori (formerly, Campylobacter pylori) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H. pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended.
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PMID:Helicobacter pylori: controversies and an approach to management. 217 47

The aim of this study was to determine the effect of colloidal bismuth subcitrate (De Nol) on symptoms and gastric histology in patients with non-ulcer dyspepsia. In a single centre trial, patients with food related upper abdominal pain not caused by ulcer disease were randomised to receive one tablet of colloidal bismuth subcitrate or matching placebo four times daily for eight weeks. Seventy three patients were entered and 51 completed the trial: 28 patients in the colloidal bismuth subcitrate group and 23 in the placebo group. Overall there was no difference between the two groups in terms of symptom relief. Among patients with histological gastritis (n = 23), however, those who took colloidal bismuth subcitrate used fewer antacid tablets (for three of four fortnightly periods) and were more likely to become asymptomatic (eight of 11 v three of 12, p less than 0.05); their gastritis was more likely to resolve (five of 10 v 0 of 12, p less than 0.025) and their gastric biopsies more likely to become negative for Helicobacter like organisms (eight of nine v 0 of 12, p less than 0.001) when compared with patients taking placebo. In contrast, patients who did not have gastritis in their index biopsies (n = 28) fared similarly whether they received colloidal bismuth subcitrate or placebo. Our results indicate that the administration of colloidal bismuth subcitrate benefited non-ulcer dyspepsia patients with gastritis but had no effect on those without.
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PMID:Effect of colloidal bismuth subcitrate on symptoms and gastric histology in non-ulcer dyspepsia. A double blind placebo controlled study. 218 82

In summary, therefore, there are interesting associations between H pylori, duodenal ulcer, and non-ulcer dyspepsia. In type B gastritis there may be enough evidence to suggest a causal role. The relation between gastritis and upper gastrointestinal symptomatology, however, remains contentious. The relation between H pylori and acid secretion may be more intimate than was previously thought. 'Pylorites' must temper their enthusiasm and provide hard data; 'Schwartzians' must broaden their horizons.
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PMID:Helicobacter pylori: bridging the credibility gap. 220 86

Epigastric pain is a common complaint throughout Africa, mostly in the form of non-ulcer dyspepsia. It has recently been suggested that Helicobacter (= Campylobacter) pylori, a bacterium that colonizes the gastric mucosa and causes type B gastritis, may be the cause of this epigastric pain. This paper reports the endoscopic, histological and bacteriological findings in 57 patients presenting with epigastric pain to the University of Maiduguri teaching hospital during one year, together with a review of the African literature. Of 57 patients, 49 had non-ulcer dyspepsia, 7 peptic ulceration and 1 carcinoma of the stomach. 93% of the patients had histological gastritis, and of these 87% were colonized with H. pylori. The bacterium was cultured from 13 patients. This high prevalence of gastritis and H. pylori has been found throughout Africa. The figures support a causative role for H. pylori in histological gastritis. At present the evidence in support of a causative role in non-ulcer dyspepsia is not strong enough to be able to recommend the routine use of anti-H. pylori therapy in patients with epigastric pain.
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PMID:Helicobacter (= Campylobacter) pylori in Africa. 220 7

We conducted a double-blind randomized treatment study on patients affects by non-ulcer dyspepsia in whom multiple biopsy specimens showed active gastritis. Patients were given either 3 g/day of sucralfate (n = 39) or 600 mg/day of sulglycotide (n = 50) for 6 wk, a glycopeptide isolated from pig duodenum constituents. Endoscopy was carried out at baseline and at the end of treatment. We took biopsies from the gastric body (twice) and antrum (six times) at each endoscopy in order to determine grade and extent of gastritis and Helicobacter pylori colonization. Both treatments induced a marked regression of active gastritis (sucralfate group: p less than 0.05 and p less than 0.0001, respectively, in body and in antrum; sulglycotide group: p less than 0.01 and p less than 0.001, respectively). Conversely, Helicobacter pylori colonization remained unchanged at the end of the treatments. At baseline, a close relationship was found between grade of active inflammation in each biopsy and Helicobacter pylori density. After therapy, the association was lost in each treatment group. These results suggest that there can be a remission of active gastritis in patients with non-ulcer dyspepsia even without changes in Helicobacter pylori colonization. This result can be achieved by enhancing the protective properties of the gastric mucosa.
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PMID:Effects of sucralfate and sulglycotide treatment on active gastritis and Helicobacter pylori colonization of the gastric mucosa in non-ulcer dyspepsia patients. 220

In an open, randomized controlled study, the effect of a combined bismuth preparation, bismuth nitrate and bismuth aluminate on the elimination of Helicobacter pylori, inflammatory activity in the gastric mucosa in chronic type B gastritis, and on the patient's symptoms was investigated. Included in the study were 36 patients with non-ulcerous dyspepsia and chronic gastritis. Twelve patients (Group A) received 4 x 1 tablet a day (800 mg total daily dose), 12 patients (Group B) 2 x 2 tablets a day (800 mg total daily dose), 12 patients (Group C) 2 x 1 tablet (400 mg total daily dose) for a period of 4 weeks. Elimination of Helicobacter pylori was observed in 73% of the patients in Group A, in 87% in Group B, but in only 16% in Group C. Inflammatory activity, measured in terms of polymorphonuclear cell infiltration, regressed noticeably in Group A und B (p less than 0.01), but not in Group C. In all patient groups symptoms regressed significantly (p less than 0.01). Bismuth and methemoglobin concentrations in the serum were within the normal range in all patients on conclusion of treatment.
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PMID:[Efficacy of a bismuth combination preparation. Efficacy in the treatment of chronic active gastritis and non-ulcerous dyspepsia]. 220 19

Biopsy samples were taken endoscopically from the antral-mucosa of 693 patients with peptic ulcer and chronic gastritis presenting dyspepsia symptoms. Campylobacter pyloridis cultures were positive in 59 of 98 (60.2%) cases and histopathologically the organisms were found in 411 of 693 cases (59.3%). Pathologically, Campylobacter pyloridis was positive in 273 out of 300 patients with chronic superficial gastritis (91.0%), in 102 of 249 patients with chronic atrophic gastritis (40.9%), in 36 out of 144 patients with chronic atrophic gastritis with intestinalization or dysplasia (25.0%). We found that there was a significant association between the presence of Campylobacter pyloridis and chronic superficial gastritis, also the degree of lymphocyte infiltration showed a strong inverse association with the presence of Campylobacter pyloridis, suggesting that a local immune response might exert an important action in the eradication of this organism. These findings support the view that Campylobacter pyloridis, may be etiologically related to chronic gastritis and peptic ulceration, even though its role still remains to be determined.
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PMID:Preliminary study on the microbiology of Campylobacter pyloridis and gastric histopathology. 221

Based on clinical and histopathological features, three different types of chronic gastritis can be distinguished: gastritis A is confined to the proximal stomach and is the result of an autoimmunological process with antibodies against parietal cells and intrinsic factor. It is a rare disorder and may lead to pernicious anaemia. Distal, antral gastritis B is caused by an infection of the gastric mucosa with Helicobacter pylori (HP). Its incidence increases with age (greater than 50% above age 50). Gastritis C may be caused by drugs and alcohol but is mainly found in gastric remnants after partial resection as a consequence of biliary reflux. Gastritis A rarely causes symptoms. A relationship between gastritis B and C and non-ulcer dyspepsia (NUD) is highly controversial. Gastritis B is very closely associated with peptic ulcer disease. HP-positive antral gastritis seems to be the prerequisite for ulcer formation. All 3 types of gastritis carry an increased risk of malignancy, which seems to be positively correlated with hypoacidity, the chronicity of the inflammation and the histopathological feature of intestinal metaplasia. Noninvasive diagnostic tests (serology, breath tests, scintigraphy) are available, but the diagnosis of gastritis is still mainly based on endoscopy and biopsy. Treatment of gastritis A is not possible. Gastritis B can be healed by eradication of HP using bismuth salts and antibiotics but only combinations of 2-3 compounds seem to afford long-term positive results. Further clinical trials are needed to determine whether such treatment is justified in patients with gastritis and NUD. In patients with chronic recurrent peptic ulcers eradication of HP prevents relapses and heals ulcer disease. Gastritis C complicated by severe symptoms or ulcer can only be successfully treated by a biliary diversion, i.e. Roux-Y-gastrojejunostomy. The discovery that gastritis B is caused by HP improves our understanding of peptic ulcer disease and will change therapeutic concepts.
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PMID:[Chronic gastritis. Pathogenesis, clinical aspects and therapy]. 221 59

Helicobacter pylori (formerly Campylobacter pylori) is causally related to active antral gastritis and is highly associated with duodenal and gastric ulcers. However, the relationship of H pylori to nonulcer dyspepsia is less clear. We determined the presence of H pylori in unselected patients who were undergoing upper gastrointestinal tract endoscopy, and we found a prevalence of 37% in 110 patients with nonulcer dyspepsia that was similar to previous data. Patients with nonulcer dyspepsia who had H pylori were found to be significantly older than patients with nonulcer dyspepsia who did not have H pylori. In addition, when stratified according to age, we detected an increased prevalence of H pylori in patients with nonulcer dyspepsia with increasing age, similar to that reported for asymptomatic control populations. This finding casts doubt as to the causal role of H pylori for most patients with nonulcer dyspepsia and stresses the importance of considering epidemiologic factors, such as age, when evaluating the role of H pylori in specific disease states.
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PMID:The prevalence of Helicobacter pylori in nonulcer dyspepsia. Importance of stratification according to age. 206 5

Nonulcer dyspepsia remains to this date a clinical disease entity that is diagnosed and treated empirically by considering such patients potential ulcer carriers and treating them accordingly with H2 antagonists. The purpose of this study was to assess the therapeutic effectiveness of sulglycotide in patients with nonulcer dyspepsia in a random double-blind trial vs sucralfate. One hundred and eighty-seven consecutive patients with nonulcer dyspepsia were treated with sulglycotide (oral, 200 mg t.i.d. for 6 weeks, n = 93) or with sucralfate (oral, 1 g t.i.d. for the same length of time, n = 94). Drug effectiveness was evaluated in terms of apparent clinical symptom modifications, fiberoptic endoscopy findings and histological aspects of biopsy specimens. Both treatments resulted in prompt abatement of the clinical complaints of nonulcer dyspepsia and the improvement of macroscopic gastritis at endoscopy. These results confirm the usefulness of cytoprotective drugs in nonulcer dyspepsia characterized by gastroduodenal inflammation.
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PMID:A multicenter double-blind study of sulglycotide versus sucralfate in nonulcer dyspepsia. 222 22


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