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

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.
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PMID:Helicobacter pylori: aggressor or innocent bystander? 207 88

We assessed the prevalence of Campylobacter pylori in various forms of endoscopic gastritis, including ulcer and nonulcer dyspepsia and bile gastritis and correlated it with histological evidence of inflammation. Multiple biopsy specimens were taken from 120 patients, including four normal controls, who underwent upper gastrointestinal endoscopy for evaluation of upper abdominal pain and discomfort, nausea, bilious vomiting, weight loss, and anemia. The patients included 58 men and 62 women, with a mean age of 53 years. Of these, 16 patients had gastric ulcers, 19 had duodenal ulcers, 26 had reflux gastritis (after either gastric surgery or cholecystectomy), one had a gastric polyp, one had Barrett's esophagus, and the remaining 53 had gastritis due to unspecified causes. Campylobacter-like organisms were demonstrated by light and electron microscopy in 50 of 69 patients of the nonbile gastritis group (72%) and in seven of 15 patients of the bile gastritis group (47%) (p0.05). The presence of bacteria in both groups correlated with histologically significant inflammation (particularly chronic active gastritis); similar histologic changes were noted in both major groups of nonbile gastritis and bile gastritis. Campylobacter pylori is common in all forms of gastritis in association with histologic inflammation.
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PMID:The prevalence of Campylobacter pylori gastritis: a study of symptomatic nonulcer dyspepsia and bile gastritis. 278 19

An edited summary of an Interdepartmental Conference arranged by the Department of Medicine of the UCLA School of Medicine, Los Angeles. The Director of Conferences is William M. Pardridge, MD, Professor of Medicine. Several specialists have recently recognized that gastrointestinal reflux causes complications resulting in significant disease. It causes discomfort, indigestion, esophagitis, Barrett's esophagus, and carcinoma of the esophagus. Pediatricians attribute many early pulmonary problems, and even some sudden deaths in infants, to the reflux of gastric contents. Otolaryngologists now recognize that many cases of nonbacterial, nonspecific pharyngitis and laryngitis are due to the reflux of gastrc acid secretions. Contact granuloma and cancer of the larynx may, in some instances, be secondary to nocturnal reflux. Thoracic surgeons and pulmonologists believe chronic tracheobronchitis and some cases of pulmonary disease are attributable to recurrent bathing of the respiratory epithelium by aspirated gastric contents. An awareness of the many complications of gastrointestinal reflux should lead to a multidisciplined attack on the factors responsible for these diseases.
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PMID:Complications of gastroesophageal reflux. 304 98

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

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.
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PMID:Are there more clinically important complications of Helicobacter pylori infection than peptic ulcer disease? A review of current literature. 984 18

Gastro-oesophageal reflux disease is the most common cause of indigestion in the community, and is usually chronic. Typical symptoms are recurrent retrosternal burning (heartburn) and regurgitation of sour or bitter fluid. In patients with typical symptoms and no alarm symptoms (pain on swallowing, dysphagia, weight loss or anaemia), treatment may be instituted without investigation. Patients with alarm symptoms and those who respond poorly or relapse after initial treatment require investigation (endoscopy and possibly pH monitoring). About 60% of reflux sufferers have no evidence of mucosal injury; their management aims to relieve symptoms. About 40% of reflux sufferers have oesophagitis and/or complications such as Barrett's oesophagus or oesophageal stricture at endoscopy. Drug therapy consists of H2-receptor antagonists, cisapride or proton-pump inhibitors.
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PMID:Gastro-oesophageal reflux disease. 986 14

Contrary to earlier definition of Barrett's oesophagus which referred to the presence of metaplastic columnar epithelium of either gastric or intestinal type, the new definition lays stress on presence of specialised columnar epithelium (SEC) with goblet cells. Hence this study was carried out to determine the frequency of specialised columnar epithelium in Indian population. 150 cases of dyspepsia underwent esophagogatro duodenoscopy with esophageal biopsy. Slides were stained with routine H and E stain and alcian blue-PAS stain. Histologically, esophagitis was found in 75 (50%) and columnar epithelium-gastric type in 63 (42%) cases only 4 (2.6%) cases showed presence of specialised columnar epithelium which were labelled as Barrett's esophagus, giving an incidence of 2.6% in this study.
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PMID:Barrett's esophagus. 986 4

Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for cirrhosis, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
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PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62

A panel of international gastroenterologists and other specialists convened at a Takeda-sponsored symposium held during the XIIIth International Workshop on Gastroduodenal Pathology and Helicobacter pylori (October 2000, Rome) to discuss clinical management of H. pylori. Topics such as management strategies as alternatives to eradication, long-term outcomes, and the impact of antibiotic resistance to H. pylori were discussed in an interactive session. The panel concluded that 1) patients with ulcer-like or reflux-like dyspepsia do appear to benefit from proton pump inhibitor therapy, 2) eradication of H. pylori may reduce future morbidity and mortality from peptic ulcer disease and gastric carcinoma, outweighing the theoretical risk of developing gastro-oesophageal reflux disease, Barrett's oesophagus, and oesophageal adenocarcinoma, and 3) the epidemiology of resistance to H. pylori, and the impact of the percentage of eradication, should be considered when an eradication regimen is being planned for patients with non-ulcer dyspepsia. Susceptibility testing may be of help in areas where this investigation is cost effective.
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PMID:Key topics in Helicobacter pylori eradication in the management of the dyspeptic patient: a panel discussion. 1168 29

BACKGROUND: Elevated mortality due to cardiovascular disease has been reported for patients with Barrett's esophagus (BE). We compared the prevalence of risk factors for cardiovascular disease in patients with BE, reflux esophagitis (RE), and non-ulcer dyspepsia (NUD) with that of the general population. METHODS: Patients with upper gastrointestinal complaints and BE, RE, or NUD were compared with a matched cohort from the general population using a questionnaire and blood pressure and cholesterol measurements. RESULTS: Hypertension occurred more frequently in patients with BE (odds ratio 5.1, P<0.0001) and RE (odds ratio 3.8, P<0.001), but not in those with NUD. Serum total cholesterol was higher in BE (P=0.02) and borderline in RE (P=0.06) but not in NUD. Mean HDL cholesterol levels, body mass index, and smoking did not differ. CONCLUSIONS: This study suggests that BE and RE found at diagnostic endoscopy are associated with an increased prevalence of hypertension and a higher total cholesterol level than in the general population. If so, this would explain the increased mortality during the follow-up of BE patients, and it should be taken into account when designing or evaluating follow-up studies of BE.
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PMID:Hypertension is frequently present in patients with reflux esophagitis or Barrett's esophagus but not in those with non-ulcer dyspepsia. 1222 81


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