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

The role of Helicobacter pylori infection in the pathogenesis of functional dyspepsia is debated. It is known that a substantial fraction of dyspeptic patients manifest a low discomfort threshold to gastric distension. This study investigated the symptomatic pattern in 27 H pylori positive and 23 H pylori negative patients with chronic functional dyspepsia, and potential relations between infection and gastric hyperalgesia. Specific symptoms (pain, nausea, vomiting, bloating/fullness, early satiety) were scored from 0 to 3 for severity and frequency (global symptom scores: 0-15). The mechanical and perceptive responses to gastric accommodation were evaluated with an electronic barostat that produced graded isobaric distensions from 0 to 20 mm Hg in 2 mm Hg steps up to 600 ml. Gastric compliance (volume/pressure relation) and perception (rating scale: 0-10) were quantified. Standard gastrointestinal manometry and recorded phasic pressure activity at eight separate sites during fasting and postprandially were also assessed. H pylori positive and H pylori negative patients manifested similar severity and frequency of specific symptoms and global symptom scores (mean (SEM)) (severity: 9.5 (2.0) v 9.0 (2.1); frequency: 10.8 (2.0) v 9.7 (2.2)). No differences were seen either in gastric compliance (53 (4) ml/mm Hg v 43 (3) ml/mm Hg) or in gastric perception of distension (slope: 0.50 (0.05) v 0.53 (0.06)). Postprandial antral motility was significantly decreased in H pylori positive patients (two hours motility index: 10.4 (0.6) v 12.6 (0.5); p < 0.05). It is concluded that H pylori infected patients with functional dyspepsia present no distinctive symptoms by comparison with H pylori negative counterparts and H pylori infection is associated with diminished postprandial antral motility but it does not increase perception of gastric distension.
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PMID:Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia? 767 80

Functional dyspepsia is defined as persistent or recurrent upper abdominal pain or discomfort not explained by structural or biochemical abnormalities. In about half of the patients who present to their practitioner with chronic dyspepsia, no underlying disease is established after clinical investigation. Many clinical trials have been performed to demonstrate a certain relationship between functional dyspepsia and several pathogenic mechanisms like dysmotility, Helicobacter pylori infection, acid output and hypersensitivity to distension. Unfortunately, the conclusions of those studies are conflicting. Short-term follow-up, lack of consensus about diagnostic criteria for functional dyspepsia and unvalidated symptom measures make it difficult to interpret their results.
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PMID:Functional dyspepsia. 776 Sep 72

Biopsy specimens from antral and duodenal mucosa were obtained from 64 patients with active duodenal ulcer and from 78 with nonulcer dyspepsia. Gastric metaplasia in the duodenal bulb was more frequent in patients with duodenal ulcer (82.5%) than in patients with dyspepsia and duodenitis (53.1%) or in patients with dyspepsia without duodenitis (34.5%). Helicobacter pylori infection in the duodenal bulb was found more often in patients with moderate to severe gastric metaplasia (62.3%) than in patients with mild gastric metaplasia (20%). Therefore, patients from a developing country, China, showed the same relationship between duodenitis, gastric metaplasia, duodenal colonization with H. pylori, and duodenal ulcer previously demonstrated in developed countries.
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PMID:Helicobacter pylori infection and gastric metaplasia in the duodenum in China. 776 88

Helicobacter pylori is present in up to 87% of patients with nonulcer dyspepsia. This study assessed the effect of eradicating Helicobacter pylori infection on the symptoms of nonulcer dyspepsia at four weeks and one year after treatment. Dyspepsia was assessed on the frequency and severity of six symptoms [epigastric pain (night and day), nausea and vomiting, upper abdominal discomfort, and regurgitation] where each symptom was scored from 0 to 4. Helicobacter pylori status was assessed before treatment and four weeks after treatment with histology and microbiology, and at one year with a carbon-13 urea breath test. Eighty-three patients (23 males, 60 females; mean age 56.3 years; mean symptom duration 3.6 months) with nonulcer dyspepsia and Helicobacter pylori infection entered the study. Seventy-five were available at one year follow-up. Four weeks after treatment, the mean symptom score improved in those with eradication (6.95-2.3, P = 0.01, N = 41) or persistent infection (6.69-3.0, P = 0.015, N = 42). At one year, those with persistent Helicobacter pylori infection (N = 38, score 5.24) had a higher score than those remaining clear of infection (N = 24, score 1.4, P < 0.0001) and those with reinfection (N = 13, score 2.2, P < 0.0001). In addition, persistent Helicobacter pylori infection was associated with more additional treatments than those with eradication (34/38 versus 4/37, P < 0.001). These results suggest that Helicobacter pylori plays an important role in the symptoms of nonulcer dyspepsia.
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PMID:Long-term prospective study of Helicobacter pylori in nonulcer dyspepsia. 856 62

In order to investigate the relationship between Helicobacter pylori infection of the gastric mucosa and mucosal changes in portal hypertension, gastric fundic and antral biopsies were obtained from 66 patients with portal hypertension and 49 controls with non-ulcer dyspepsia (NUD). Gastric mucosa from portal hypertensive patients exhibited typical vascular dilatation and congestion, while mild dilatation of lamina propria blood vessels was not uncommon in NUD patients with histological evidence of gastritis. Colonization of the gastric mucosa by H. pylori infection was significantly less in portal hypertension (51.5%) compared to controls (75.5%; P < 0.01). The difference was more apparent in patients with marked vascular dilatation (18.8% colonization) compared to patients with minimal vascular dilatation (66.7%). H. pylori infection was significantly associated with active superficial gastritis (P < 0.001), and with atrophic gastritis (P < 0.001), in both study groups. H. pylori-negative superficial gastritis was significantly more common in portal hypertension (25/66 patients) than in controls (7/49; P < 0.05). H. pylori infection was not more common in patients who had undergone repeated sclerotherapy. The results suggest that the gastric mucosa of portal hypertension does not provide a hospitable environment for H. pylori colonization, particularly when mucosal congestion is marked. H. pylori infection does not add significantly to the gastropathy of portal hypertension.
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PMID:Colonization by Helicobacter pylori and its relationship to histological changes in the gastric mucosa in portal hypertension. 782 3

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

This study examines the relationship between Helicobacter pylori infection and peptic ulcer disease and gastric cancer--in particular, the presence or absence of bacteria, the grading of gastritis, and the degree of inflammation in the antral and oxyntic mucosae. The grading of gastritis and the detection of H pylori were determined by histology using the Sydney system. Of the 1006 patients examined, 34.5% had duodenal ulcer disease, 3.5% gastric ulcer disease, and 2% with coexistent ulceration. Most patients (50.2%) were classified as having non-ulcer dyspepsia. Altogether 2.4% of patients had gastric cancer and two further patients had carcinoma in the gastric stump. Of the ulcer disease patients, 87.2% had histological evidence of H pylori infection. After patients who had taken antibiotics or bismuth compounds in the preceding four weeks were excluded, 98.9% of the duodenal ulcer disease, 100% of the gastric ulcer disease, and 100% of the coexistent ulcer disease patients had evidence of H pylori infection. In patients with gastric cancer who had not taken antimicrobial agents in the four weeks before endoscopy, 83.3% had evidence of H pylori infection. Thus, there was a high rate of duodenal ulcer disease and a low rate of gastric ulcer disease in southern China, an area of low gastric cancer mortality. There was a specific topographical relationship between H pylori, the histological response, and gastroduodenal disease. Our data suggest that the status of a nation as either 'developed' or 'developing' can not be used to predict the upper gastrointestinal disease profile of its population.
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PMID:Helicobacter pylori associated with a high prevalence of duodenal ulcer disease and a low prevalence of gastric cancer in a developing nation. 788 17

Gastric Helicobacter pylori infection is common throughout the tropics yet does not always correlate with the incidence of serious upper gastrointestinal pathology. In a consecutive series of 213 patients examined by gastroscopy for dyspepsia in northern Nigeria, 176 (92%) of 193 with acceptable biopsies had gastritis. Only 16 (8%) had a histologically normal gastric mucosa. H. pylori was present in 161 of 192 patients (84%); 31/41 (75%) with chronic gastritis and 130/135 (96%) with active gastritis. Serious pathology, ulcer and gastric cancer were present in only 29 (14%).
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PMID:Low incidence of clinically significant gastroduodenal pathology despite a high incidence of Helicobacter pylori infection. 799 42

In the present study we evaluated the efficacy and tolerability of two different therapeutic schedules in eradicating Helicobacter pylori. Forty-six consecutive patients (suffering from either peptic ulcer or non-ulcer dyspepsia) with helicobacter pylori infection were randomly allocated to one of the following two groups: group 1 (n = 23) 2 weeks of treatment with bismuth subcitrate tablets (120 mgx4) + amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4); group 2 (n = 23) 2 weeks of treatment with amoxycillin capsules (500 mgx4) + metronidazole tablets (250 mgx4). Endoscopy, histology and bacterial culture were performed at entry, and 30 and 90 days after treatment. Two group 1 patients and one group 2 patient did not complete the treatment. Successful eradication was obtained in 20/21 (95%) patients treated with triple therapy (group 1) and in 17/22 (77%) patients treated with double therapy (group 2) (p = 0.2). Side-effects occurred in 9/21 (43%) patients of group 1 and in 9/22 (41%) patients of group 2 (p = 0.9). These were all self-limiting and required no specific treatment. These data suggest that combined therapy with amoxycillin and metronidazole, with or without bismuth subcitrate, represents a safe and effective therapeutic approach for the treatment of Helicobacter pylori infection. In our series, triple therapy determined a numerically higher eradication rate than double therapy.
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PMID:Evaluation of two therapeutic regimens for the treatment of Helicobacter pylori infection. 891 22

Biopsies of the stomach antrum and fundus from 20 male patients with non-ulcer dyspepsia were studied light- and electron-microscopically. Helicobacter pylori infection was found in 60% of cases. In 2 patients, the bacteria were found not only in the fovea and mucus, but in the tunica propria as well. The bacteria were observed in the dilated intercellular spaces of the epithelium, between epithelium and basal membrane as well as around the glands and capillaries in the form of colonies. In the tunica propria the bacteria were represented mainly by the coccus forms, they had the signs of involution. There were signs of the bacterial influence on immunocompetent cells.
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PMID:[Possibility of Helicobacter pylori invasion into the lamina propria of the gastric mucosa]. 809 33


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