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

The variation in the healing and the relapse rates of peptic ulcer disease has led to the search for other factors in the pathogensis of peptic ulcer disease. Helicobacter pylori is believed to be responsible for these different patterns of healing. The results of a study to detect Helicobacter pylori in Sri Lankan patients having duodenal ulcer, gastric ulcer, gastritis and non-ulcer dyspepsia are presented in this paper. The method employed was the urease test which detects the urease enzyme of H. pylori in gastric mucosal biopsies taken during upper gastrointestinal endoscopy. There is a high incidence in those with gastritis and duodenitis.
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PMID:Helicobacter pylori and peptic ulcer disease in Sri Lanka. 158 90

To evaluate the association of Helicobacter pylori infection with gastroduodenal ulceration and symptoms in rheumatoid arthritis patients chronically ingesting nonsteroidal anti-inflammatory drugs (NSAIDs), a population-based study was performed. Residents of Olmsted County, Minnesota, and surrounding counties, 40 years of age and over with active rheumatoid arthritis taking therapeutic dose of NSAIDs daily for 6 months or more were evaluated (n = 50). An endoscopic score from 0 to 5 was assigned and independently confirmed. Biopsies were obtained from the antrum and gastric body for the presence of H. pylori. A symptom score based on the frequency and severity of dyspeptic symptoms was calculated. Substantial mucosal injury (greater than or equal to grade 2) was observed at endoscopy in 33 patients (66%); 14 (28%) had chronic ulcers. Eleven of the community patients with rheumatoid arthritis (22%) were H. pylori positive; adjusting for age, the prevalence of H. pylori was not significantly different to that in 67 health controls (25%). One or more upper gastrointestinal symptoms were reported by 19 of the community patients (38%). Adjusting for age, community rheumatoid arthritis patients with H. pylori were not more likely to have visible mucosal damage or dyspepsia, but were significantly more likely to have histological gastritis (P less than 0.01). The results suggest that, in primarily asymptomatic persons from the community with rheumatoid arthritis taking daily NSAIDs for 6 months or more, H. pylori infection is not related to the severity of visible mucosal injury.
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PMID:Long-term nonsteroidal anti-inflammatory drug use and gastroduodenal injury: the role of Helicobacter pylori. 158 9

Helicobacter pylori is both virulent and pathogenic, yet it is not clear what is the best way to treat the infection. This study compares the ability of 4 regimens of colloidal bismuth subcitrate (CBS) 120 mg q.i.d. for 4 weeks, combined with one or two antibiotics, to eradicate helicobacter pylori and assesses the outcome of eradication on antral gastritis and on symptoms of non-ulcer dyspepsia in 140 consecutive subjects (44 duodenal ulcers and 96 non ulcer dyspepsia). Endoscopy with antral biopsies was repeated in all patients before (T0) and one month after stopping treatments (T2) while duodenal ulcers were endoscoped also at the completion of treatments (T1). The four regimens showed similar eradication and ulcer healing rates (p = ns). After treatments (T1), about 60% of dyspeptic patients achieved a subjective improvement, not significant despite therapeutic regimen, and persisting at T2. Antral gastritis significantly improved after treatments (p less than 0.0001), even with the persistence of the infection (p less than 0.001). The 4 regimens are relatively safe, as no abnormality in laboratory assessment was found, albeit the frequency of side effects (most of whom tinidazole related) and the difficulty of the schedules (6-10 tablets/day) may limit patient compliance.
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PMID:Helicobacter pylori infection: comparison among four different therapeutic regimens. 158 52

A layer of water-insoluble mucus gel is secreted by the gastric epithelium, and is believed to form an important barrier to acid injury. It is postulated that Helicobacter pylori can alter pH gradients by damaging the mucus layer, but no data on pH gradients in vivo in patients with H. pylori gastritis have been published. We aimed to construct a map of mucus-bicarbonate layer pH gradients in health and disease. Fourteen healthy asymptomatic volunteers (mean age, 46 yr) and 14 symptomatic patients with non-ulcer dyspepsia (NUD) (mean age, 46 yr) were studied. A flexible pH microelectrode was passed through the biopsy channel of an endoscope; luminal readings and three mucosal surface pH readings were obtained from each of five specific gastric sites (fundus greater curve, body greater curve, antrum greater curve, antrum lesser curve, and antrum anterior wall) using standardized methodology. Gradients at each site were calculated (mean juxta mucosal pH minus luminal pH); pH electrode accuracy was tested in standard buffer solutions. Biopsies were obtained from each site to assess for H. pylori status. Among asymptomatic volunteers, 21% had H. pylori; in NUD, 50% were infected. There was a significant association between H. pylori and histological gastritis at each site. The overall mean (+/- SE) pH gradients in H. pylori-positive and -negative cases were similar, being 5.35 (+/- 0.06) and 5.26 (+/- 0.07), respectively. There was also no significant correlation between the histological gastritis score and the pH gradient at each gastric site. The pH gradients in healthy subjects (mean 5.31) and NUD (mean 5.29) were not significantly different. We conclude that pH gradients appear to remain stable throughout the stomach in healthy subjects and NUD, independent of H. pylori gastritis.
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PMID:Stability of pH gradients in vivo across the stomach in Helicobacter pylori gastritis, dyspepsia, and health. 159 45

The discovery of Helicobacter pylori has stimulated great interest in its role in gastritis, non-ulcer dyspepsia and peptic ulceration. Treatment regimens to eradicate this organism from gastric mucosa have also received considerable attention. Current recommendations limit the use of triple drug combinations only to specific patient groups.
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PMID:Review article: the treatment of Helicobacter pylori infection. 160 47

Acute Helicobacter pylori infection is associated with dyspeptic symptoms but chronic infection has not clearly been shown to cause symptoms. To define further the role of H. pylori infection and gastritis in dyspepsia, we interviewed all patients about to undergo upper endoscopy, recorded the primary indication for endoscopy, noted the endoscopic findings, and obtained antral biopsies. Among non-ulcer patients there was a strong correlation of acute gastritis with H. pylori. Gastritis and H. pylori increased with age, and non-steroidal anti-inflammatory drug use correlated with normal histology. Neither H. pylori concentration nor gastritis grade correlated with gender, use of alcohol and tobacco, indication for endoscopy, or symptoms (epigastric pain, nausea, vomiting, bloating, belching, heartburn, halitosis, and flatulence).
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PMID:Symptoms, gastritis, and Helicobacter pylori in patients referred for endoscopy. 851 92

Helicobacter pylori colonization and the incidence, severity, activity and topography of gastritis were investigated systematically in antrum and corpus mucosal biopsies of 1177 subjects undergoing endoscopy in the absence of gastric complaints (asymptomatic, 49) or for non-ulcer dyspepsia (NUD; 631 patients, 72 of whom had gastric and/or duodenal erosions), active gastric ulcer (GU, 76 patients), active duodenal ulcer (DU, 138 patients), and healed gastric (HGU, 39 cases) or duodenal ulcer (HDU, 230 cases). In the antrum, H. pylori colonization and the incidence, severity and activity of gastritis increased progressively in the sequence asymptomatic, erosion-free NUD, erosive NUD, healed ulcer and active ulcer. The same trend was observed in the corpus as regards H. pylori and gastritis incidence, whereas the severity and activity of gastritis were lower in active DU and erosive NUD and higher in active, proximal GU than in the remaining patients. Active DU and erosive NUD showed the highest incidence of non-atrophic gastritis and lowest type-A or AB atrophic gastritis, while active GU had lowest normal mucosa or type-A gastritis and highest type-B atrophic gastritis. In conclusion, H. pylori colonization and gastritis incidence, severity and, especially, activity of the antrum might all contribute to mucosal erosion and ulceration, whereas the same factors, at least in part and with the exception of proximal GU, seem to have a preventive role when affecting corpus mucosa.
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PMID:Helicobacter colonization and histopathological profile of chronic gastritis in patients with or without dyspepsia, mucosal erosion and peptic ulcer: a morphological approach to the study of ulcerogenesis in man. 160 9

Helicobacter pylori (HP) are Gram-negative spiral bacteria which occur in the human stomach. The bacteria were cultured in vitro for the first time in 1983. It is suspected that the bacteria may cause chronic gastritis of type B and may also be a contributory cause of chronic ulceration and cancer of the stomach. The bacteria are accompanied by characteristic inflammatory changes in the gastric mucosa. The significance for gastritis, chronic ulceration, non-ulcer dyspepsia and carcinoma of the stomach is discussed. HP occurs in a great proportion of the population of the world and the frequency increases with age. The route of infection is unknown but faecal-oral infection is probable. Correlation between the presence of HP and the occurrence of symptoms is poor in the individual patient. The bacteria can be demonstrated histologically, cytologically, by culture, by the urease test, by the urease expiration test or serologically. The bacteria are sensitive for a series of antibiotics and bismuth but no effective treatment is known as the recurrence rate is high.
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PMID:[Helicobacter pylori]. 163 4

Although Helicobacter pylori is both a frequent cause of gastritis and an important factor in duodenal ulcer recurrence, no treatment regimen exists that is completely safe and effective. We have studied a short eradication regimen of tripotassium dicitrato bismuthate 120 mg four times daily and amoxycillin 500 mg four times daily for seven days with metronidazole 400 mg five times daily for three days (days 5-7). 106 patients with peptic ulceration and non-ulcer dyspepsia, who were also infected with H pylori, were entered into the study. H pylori was successfully eradicated in 76/106 (72%) patients (median follow-up 9.3 months). The rate of eradication was higher among patients with metronidazole-sensitive H pylori (40/43, 93%). In 17/30 patients in whom eradication failed, pretreatment metronidazole-resistant strains were subsequently isolated. Side-effects were mild, the commonest (24/106, 24%) being taste disturbance with metronidazole. A one-week eradication regimen is a safe, effective, cheap, and well-tolerated treatment for metronidazole-sensitive H pylori.
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PMID:One week eradication regimen for Helicobacter pylori. 134 68

We present the results of ultrastructural studies of gastric mucosa obtained through upper digestive endoscopy of eight patients with suspicious symptoms of non ulcer dyspepsia or peptic ulcer. Two were male and six female with a median age of 54 years. The urease test to determine the presence of HP and Hematoxylin-Eosin and Warthin-Starry staining techniques were practiced with the purpose of a better detection of bacteria and gastritis. We did not find any correlation between the endoscopic results and the presence of gastritis or HP. Of the 8 patients only one had negative results for HP and for Electron microscopy studies. Chronic active gastritis was seen with light microscopy in all of the cases. Three in this group presented mild focal dysplasia and one case intestinal metaplasia type IIa. The main ultrastructural findings were: a) diminished or absent microvilli underneath the bacteria; b) HP inside phagolysosomes in the cytoplasm of the epithelial cells; c) in some cases, the bacteria was attached to the cell membrane; d) the cellular wall of HP contains mucopolysaccharides and up to four polar flagella; e) there are polymorphonuclear leucocytes in the epithelium. We conclude that Electron Microscopy is not a routine method for studying HP, but it constitutes a good method to study pathogenicity of the bacteria.
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PMID:[Ultrastructural study of the antral mucosa to determine the presence of Helicobacter pylori and its association with chronic active gastritis]. 172 15


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