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

The prevalence of lymphocytic gastritis, a specific form of chronic gastritis characterized by infiltration of gastric superficial epithelium with T lymphocytes, has been established in nonulcer dyspepsia. Among a population sample of 586 patients at risk for gastric carcinoma, 0.83% of patients with nonulcer dyspepsia and 1.63% of patients with chronic active gastritis showed lymphocytic gastritis. Among routine gastric biopsies from 5130 patients, only five cases met histological and immunohistochemical criteria of lymphocytic gastritis.
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PMID:Lymphocytic gastritis in nonulcer dyspepsia. 186

The relationship between the histologic severity of gastritis and associated symptoms was examined in 19 adult patients infected with Helicobacter pylori. At the time of gastrointestinal endoscopy, symptoms of dyspepsia were assessed by means of a linear analog scale. Gastric inflammation was quantitated with histomorphometric techniques. Symptoms such as epigastric pain, burping/belching, and nausea correlated with the degree of inflammation. These positive correlations suggest that the severity of the histologic gastritis contributes to the severity of symptoms. Therefore, utilization of a linear analog scale to assess symptoms may be a useful technique in evaluating the outcome of therapeutic trials of patients with symptomatic H. pylori infection.
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PMID:Relationship between gastric inflammatory response and symptoms in patients infected with Helicobacter pylori. 186 92

Helicobacter pylori attracted widespread interest from gastroenterologists because of its potential aetiologic role in disorders of the upper gastrointestinal tract. Based on extensive microbiological studies, Campylobacter pylori was renamed Helicobacter pylori, and the organism represents a new genus of bacteria. It is generally accepted that H. pylori causes chronic, non-specific gastritis (type B gastritis). The inflammatory response occurs even though the bacterium does not penetrate the gastric epithelium; it is found on the surface of and adjacent to the epithelium. The clinical significance of histological gastritis is unknown. The bacterium is often found in asymptomatic subjects. In Caucasian adults, the prevalence of infection increases with increasing age. Higher rates of infection are found in blacks and Hispanics than would be expected for their age. Whether these different rates are the result of racial or socioeconomic factors is not known. It is theorized, but not proven, that high rates of infection with H. pylori at an early age may explain the high incidence of gastric carcinoma found in Hispanic populations. H. pylori is found in almost every patient with duodenal ulcer disease, although no direct evidence for a causal relationship exists. Indirect evidence is based on the findings that if H. pylori infection is eradicated, ulcer recurrence is less likely (up to one year of follow-up). A small percentage of patients have a relapse despite eradication of the organism, suggesting a role for other factors in duodenal ulcer disease. The role of H. pylori in gastric ulcer disease is unknown. Seventy to eighty per cent of patients with gastric ulcer have evidence of H. pylori infection, and preliminary data seem to support the existence of two distinct aetiologic groups: those with gastric ulcers related to H. pylori infection and those with gastric ulcers related to use of non-steroidal anti-inflammatory drugs. The role of H. pylori in non-ulcer dyspepsia is unknown. Some clinicians believe that H. pylori causes non-ulcer dyspepsia and treat these patients for H. pylori infection. However, the data supporting this practice are poor. Treatment is only recommended for patients with resistant duodenal ulcers and patients who have frequent relapses of duodenal ulcers and who are willing to take triple-drug therapy (bismuth compounds, metronidazole, tetracycline) for the infection. As 95% of patients with duodenal ulcer have evidence of H. pylori infection, there is probably little need to confirm the diagnosis of H. pylori infection.
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PMID:Helicobacter pylori: review of research findings. 188 32

After definition in the group of the non ulcer dyspepsia (NUD) can be counted all those patients at whom beside the dyspeptical complaints, the radiological and endoscopical examinations didn't show ulcerative changes. The authors made biopsy 550 times on the occasion of 1390 gastroscopical examination (39.5% of the cases). The histological examination showed chronic gastritis in 372 cases (26.7% of all the examinations, 67.6% of the histological examinations). At this group of patients the dyspeptical complaints gave the principal indication of gastroscopical examination. Also it was examined the presence of dysplasia and intestinal metaplasia beside the different severity grade of chronic gastritis. The presence of Helicobacter pylori (Hp) was examined by histological methods. Hp positivity was noticed in 16.4% in the upper group. The authors made Hydrogen-breath examinations in 34 cases between patients with NUD. The results of Hydrogen-breath examinations also raise the multifactorial nature of the NUD. On the basis of examinations chronic gastritis and CP infection can form subdivisions in the heterogenic group of patients with NUD. For exacter judgement of Hp pathogenicity are needed further and wide-spread examinations. The authors would like to call the attention to the indispensability of the biopsy during the gastroscopical examination.
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PMID:[Chronic gastritis and the presence of Helicobacter pylori in patients with non-ulcerative dyspepsia]. 173 39

The relationship between endoscopically diagnosed gastroduodenitis, histologically confirmed gastritis, and symptoms of dyspepsia remains unclear. Marked histologically confirmed inflammation of gastric mucosa often occurs in a stomach that appears normal by endoscopy. Both histologically confirmed and endoscopically diagnosed gastritis are commonly blamed as causes of nonulcer dyspepsia (NUD), although neither disease has been convincingly shown to cause NUD. Helicobacter pylori infection of gastric mucosa is a common cause of histologically confirmed inflammation. It is unclear whether this infection with H. pylori and the resultant gastric mucosal inflammation cause symptoms since inflamed mucosae are also common in asymptomatic controls. The reported increased prevalence of H. pylori in patients with NUD compared with controls suggests a possible causative role in at least a subset of patients with NUD. In addition, three controlled studies of treatment with bismuth demonstrated a significant trend toward improvement of symptoms after clearance of H. pylori. However, two studies of therapy with bismuth failed to demonstrate improvement of symptoms. Further study of patients with NUD is needed to clarify this possible association.
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PMID:Helicobacter pylori in patients with nonulcer dyspepsia. 192 11

Colloidal bismuth subcitrate (CBS; DeNol) has been studied in clinical trials investigating the treatment of duodenal and gastric ulcer, non-ulcer dyspepsia, duodenitis, non-steroidal anti-inflammatory drug (NSAID)-induced disease, and Helicobacter pylori-induced gastroduodenitis. Healing rates for duodenal ulcer with CBS are significantly better than with placebo and are similar to results obtained with cimetidine or ranitidine. CBS is significantly better in the treatment of duodenal ulcer resistant to standard doses of H2 antagonists than increased doses of H2 antagonists. Duodenal ulcer relapse at 12 months after initial healing with CBS is significantly less than with H2-antagonist therapy. Ulcer healing with CBS is not influenced by smoking. H. pylori eradication with CBS appears to have little effect in ulcer healing but is of major importance in preventing ulcer relapse. CBS is effective in combination with antibiotics in eradicating H. pylori-associated gastritis. In gastric ulcer disease CBS therapy resulted in significant healing advantages over placebo and was comparable to treatment with cimetidine and sucralfate. CBS has been shown to be effective in the treatment of erosive duodenitis. The role of CBS in treatment of non-ulcer dyspepsia and NSAID-induced damage awaits further clinical studies.
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PMID:Clinical indications and efficacy of colloidal bismuth subcitrate. 195 21

To determine the relevance of gastric juice factors to gastric carcinogenesis, 56 patients with unoperated stomachs undergoing endoscopy for dyspepsia had gastric juice aspirated and analysed for pH, ascorbic acid, total bile acids, nitrite, nitrate and total nitroso compounds (NOCs). Plasma was obtained for vitamin C estimation. Antral and body biopsies were assessed for gastritis, Helicobacter pylori, atrophy and intestinal metaplasia (IM). Patients with chronic atrophic gastritis (n = 17) had lower gastric juice ascorbic acid concentrations (P less than 0.001), higher pH (P less than 0.05) and higher incidence of H. pylori infection (P less than 0.001) than normal subjects (n = 12). Patients with reflux gastritis (n = 9) had higher total bile acids (P less than 0.01). Patients with chronic gastritis and IM (n = 11) had higher gastric juice pH (P less than 0.01) and total bile acid concentrations (P less than 0.05), and lower gastric ascorbic acid concentrations (P less than 0.01) than those with chronic gastritis and no IM (n = 24). In chronic gastritis, high nitrite concentrations were associated with high pH (P less than 0.01). However, there were no significant differences in plasma vitamin C or gastric nitrite, nitrate or total NOC concentrations in relation to gastric histology. We conclude that the premalignant condition IM is associated with H. pylori infection, low gastric ascorbic acid levels and elevated total bile acids, but not to elevation in nitrite or total NOCs in fasting gastric juice.
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PMID:Levels of nitrite, nitrate, N-nitroso compounds, ascorbic acid and total bile acids in gastric juice of patients with and without precancerous conditions of the stomach. 199 84

We assessed the relative roles of alcohol and infection with Helicobacter pylori in the pathogenesis of chronic gastritis in alcoholic patients. Helicobacter pylori was found in 14 of 18 alcoholics with dyspepsia and was associated with chronic antral gastritis. Gastric biopsy specimens were normal in four H pylori-negative alcoholics. Studies were repeated 3 to 4 weeks after controlled abstinence. There was no change in histologic findings during this period, indicating that alcohol itself was not the major causative agent. We then eliminated H pylori in 10 subjects by giving triple therapy (bismuth subsalicylate, amoxicillin, and metronidazole). Treatment for H pylori was associated with almost complete normalization of histologic findings. Four control subjects who received antacids alone showed no improvement. Dyspeptic symptoms in H pylori-positive patients significantly improved after elimination of this organism, whereas there was no change with antacid treatment.
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PMID:Chronic alcoholic gastritis. Roles of alcohol and Helicobacter pylori. 201 61

A prospective multifactorial study of symptoms and disturbance of gastrointestinal function has been undertaken in 50 patients with non-ulcer dyspepsia. Objective tests including solid meal gastric emptying studies, gastric acid secretion, E-HIDA scintiscan for enterogastric bile reflux, and hydrogen breath studies were carried out in all patients and validated against control data. Gastroscopy and biopsy were carried out in non-ulcer dyspepsia patients only. Non-ulcer dyspepsia patients were categorised on the basis of predominant symptoms as: dysmotility-like dyspepsia (n = 22); essential dyspepsia (n = 14), gastro-oesophageal reflux-like dyspepsia (n = 11); and ulcer-like dyspepsia (n = 3). In the total non-ulcer dyspepsia population, solid meal gastric emptying was delayed (T50 mean (SEM) = 102 (6) minutes (patients) v 64 (6) minutes (controls), (p less than 0.01) and high incidences of gastritis (n = 26) and Helicobacter pyloridis infection (n = 18) were found. An inverse correlation was observed between solid meal gastric emptying and fasting peak acid output (r = -0.4; p less than 0.01). Indeed gastric emptying was particularly prolonged in eight patients (T50 mean (SEM) = 139 (15) minutes) with hypochlorhydria. In the non-ulcer dyspepsia population oral to caecal transit time of a solid meal was delayed (mean SEM = 302 (14) minutes (patients) v 244 (12) minutes (controls) (p less than 0.01]. Seven patients had a dual peak of breath hydrogen suggestive of small bowel bacterial overgrowth. No association was observed between symptoms and any of the objective abnormalities. This multifactorial study has shown that hypomotility, including gastroparesis and delayed small bowel transit, is common in non-ulcer dyspepsia and may be related to other disorders of gastrointestinal function. No relation between symptoms and disorders of function, however, has been shown.
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PMID:Evidence for hypomotility in non-ulcer dyspepsia: a prospective multifactorial study. 201 18

A population of non ulcer dyspepsia outpatients with a normal gastroscopy was assessed. Clinical complaints, the type of the gastritis, its activity and bacterial density were evaluated. Helicobacter pylori (HP) was sought by histology, urease test and culture, on 3 distinct locations. HP was found in 62 p. cent of the patients, always in association with gastritis. Urease test and histology had the same sensitivity in the detection of HP. A randomized double blind study with amoxicillin vs placebo was carried out in 23 patients. At the end of 4 week treatment, a gastroscopy with biopsies was performed. The amoxicillin treated patients were significantly cured or improved. HP was undetectable or the bacterial density was decreased in this group. After amoxicillin, urease test was more sensitive than histology. HP might be involved in the pathophysiology of non ulcer dyspepsia in patients where HP was found.
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PMID:[Dyspepsia and Helicobacter (Campylobacter) pylori. Results of a randomized therapeutic trial using amoxicillin versus placebos]. 202 80


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