Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is accumulating that Helicobacter pylori infection plays a major contributory role in peptic ulcer disease [Duodenal Ulcer (DU) and Gastric ulcer (GU)] and non-ulcer dyspepsia (NUD). We, therefore, studied prospectively 210 consecutive patients with upper gastrointestinal symptoms (62 DU, 38 GU and 110 NUD) to determine the prevalence of H. pylori infection and to investigate their association with histological gastritis. Using endoscopic biopsy of the gastric antrum for diagnosing H. pylori infection by Campylobacter-like Organism (CLO) test, histology or bacteriology, the overall prevalence of H. pylori was 63.3 per cent. When H. pylori infection was related to diagnosis, DU had the highest prevalence rate of H. pylori infection (66%), GU and NUD were less frequently associated with H. pylori infection (55% and 44% respectively). We found a close association between H. pylori infection and histologically antral gastritis, in that 72.7, 61.7, and 62.6 per cent of the DU, GU and NUD patients with antral gastritis (respectively) had H. pylori infection. In contrast, none of these patients seen with normal antrum had H. pylori infection. We also found that the prevalence of H. pylori in our patient series was not age related. Of the three procedures used to demonstrate H. pylori, the CLO test and histological staining method gave the highest yields of 84.9 and 79.6 per cent respectively, and bacteriology in only 44.3 per cent, we conclude that the prevalence of H. pylori infection in Thai patients with upper gastrointestinal symptoms is high. H. pylori infection commonly occurs in the patients with antral gastritis, suggesting a possible etiologic role for the bacterium in the histologic lesion.
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PMID:Helicobacter pylori and peptic ulcer diseases: prevalence and association with antral gastritis in 210 patients. 129 55

30 patients with non ulcer dyspepsia (NUD) were evaluated to find out if there was a relationship with Helicobacter pylori (HP) infection. Gastric biopsies from the antrum were taken and two of them sent to pathology to be stained with H&E and Warthin-Starry. The other three were sent to Microbiology, for urease-test, culture and frotis with Gram stain. To diagnose HP was necessary to get it at least in two of the performed test. This was possible in 20 (66.66%). Chronic active gastritis was observed in 15/20 (75%) and in the 3/10 HP negative patients none had histological alteration shown. Normal aspect of gastric mucosa did not predict Helicobacter pylori infection. The presence of the bacteria could not be correlated to any kind of symptoms and always was associated with chronic gastritis.
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PMID:[Nonulcerative dyspepsia associated with Helicobacter pylori]. 134 Aug 9

There seems to be a worldwide geographic variation in the prevalence of peptic ulcer disease, although there are few reliable population based studies. This study aimed to determine the prevalence of peptic ulcer disease in a community in southern India and to evaluate the relationship between dyspeptic symptoms, Helicobacter pylori infection, gastritis, and peptic ulcer disease. A sample population was selected randomly from a rural monastic settlement in southern India. Subjects were interviewed using a standardised symptom and demography questionnaire then underwent upper endoscopy and antral biopsy for histology and CLO rapid urease test. Altogether 197 subjects from a population of 1499 (13.1%) were studied. All were male monks and ethnically Tibetan. The median age was 28 years (range: 21-81). None smoked or took NSAIDs. The six month period prevalence of dyspeptic symptoms was 68.5%. Current symptoms were present in 58.9% of subjects. Dyspepsia was more common in subjects aged 40 years or younger (p < 0.0001). H pylori was detected in 77.2% subjects. There was no association between dyspepsia and the presence of H pylori or histological gastritis, although there was a strong correlation between symptoms and ulcer (p < 0.003). The point prevalence of active peptic ulcer was 6.6% (13/197). All ulcers detected were either prepyloric or pyloroduodenal in location. A further 6.6% of subjects had definite evidence of scarring or deformity indicative of ulceration in the past. Subjects with past or present ulcers comprised 17.8% of dyspeptic subjects. H pylori was present in all subjects with active ulcers and in 12/13 of those with scarring. Dyspepsia, H pylori infection, gastritis, and peptic ulcer are all more common in this population than in those from developed countries. Ulcer disease, however, accounts for only a small proportion of subjects with symptoms and neither H pylori infection nor gastritis are significantly associated with the presence of dyspepsia.
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PMID:Dyspepsia, Helicobacter pylori, and peptic ulcer in a randomly selected population in India. 145 68

Two urease-based tests--the urease slide test and the radiolabeled urea breath test, are commonly used for the diagnosis of Helicobacter pylori infection of the stomach. The reliability of these tests in chronic uremia was compared with serological tests for H pylori antibodies, and with direct detection of the organism by microscopy or culture of gastric antral biopsies. Twenty-seven patients with chronic renal failure and dyspepsia underwent upper gastrointestinal endoscopy. Twelve of these patients (46%) were judged to be infected with H pylori on the basis of identification of the organism on microscopy or culture of antral biopsy. Both urease-based tests were able to determine H pylori status, despite the markedly increased concentrations of urea in the gastric juice found in chronic renal failure. The urease slide test performed on antral biopsies obtained at endoscopy proved reliable in determining H pylori status with no false-positive nor false-negative results after 20 minutes and 24 hours of incubation. The 14C-urea breath test also differentiated the infected from the uninfected patients. The 20-minute 14CO2 excretion (kg %dose/mmol CO2 x 100) ranged from 50 to 834 in the H pylori-infected patients, compared with 0.3 to 27 in the H pylori-noninfected patients (P < 0.0001); the 90-minute values ranged from 88 to 398 in the former, compared with 1 to 79 in the latter (P < 0.0001). The excretion of 14CO2 (derived from bacterial hydrolysis of ingested 14C-urea) was higher in all the uremic patients compared with nonuremic controls, and in half of the H pylori-noninfected uremic patients there was a late increase in 14CO2 excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The diagnosis of Helicobacter pylori infection in uremic patients. 146 85

Helicobacter pylori infection, histological features of the gastric mucosa, and gastric motor and secretory functions were evaluated in 45 consecutive patients with chronic idiopathic dyspepsia. H. pylori infection was found in 60% of dyspeptic patients, compared with 33% of 15 healthy controls (P = 0.1). No difference was detected in basal or stimulated gastric acid secretion between dyspeptic patients and healthy controls. Gastric emptying was significantly (P less than 0.01) delayed in dyspeptic patients compared with healthy controls when standardized for age and sex. Delayed gastric emptying was associated with a low frequency of H. pylori infection, female gender, and young age. Epigastric pain or burning and postprandial fullness were, respectively, more severe in patients with H. pylori infection (P less than 0.02) and in those with delayed gastric emptying (P less than 0.01). These findings support the existence of separate subsets of patients with chronic idiopathic dyspepsia. Despite the presence of overlaps, there appear to be partially different functional derangements and clinical features in different subgroups of dyspeptic patients.
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PMID:Helicobacter pylori infection and gastric function in patients with chronic idiopathic dyspepsia. 149 26

The association and causative role of Helicobacter pylori infection of the stomach with gastric ulcer, duodenal ulcer, non-ulcer dyspepsia, and gastritis has remained controversial. The authors studied the effects of daily intragastric administration of H. pylori suspension in saline (10(8) CFU/ml) and bacteria-free filtrates of saline H. pylori suspensions in 85 Sprague-Dawley rats (weight, 150 to 200 g) with normal mucosa and with surgically produced experimental gastric ulcers. Group I rats (n = 30) with pre-existent experimental gastric ulcers received H. pylori suspension (ATCC 43504, 10(8) CFU/ml); Group II rats (n = 20) with experimental gastric ulcers received bacteria-free H. pylori filtrates; Group III rats with ulcers (n = 20) received saline alone; and Group IV control rats (n = 15) without ulcers received intact H. pylori organisms in suspension (ATCC 43504, 10(8) CFU/ml). At death, ulcer surface areas were measured with a dissecting microscope. Full-thickness sections were obtained for quantitative and qualitative histologic parameters, including the area of remaining mucosal necrosis; characteristics and cellular composition of restored mucosal architectures; and presence or absence of inflammation including counts of neutrophils and lymphocytes. H. pylori organisms were identified within the surface mucus and crypts using routine, special, and immunohistochemical stains. Our results indicate that the continued presence of either intact H. pylori organisms or bacteria-free H. pylori filtrates in the stomachs of rats with pre-existent gastric ulcers resulted in delayed healing of the ulcers and persistence of chronic active inflammation. Daily administration of suspensions of H. pylori organisms to sham-operated rats with intact gastric mucosa, however, resulted in no ulceration or inflammation despite identification of surface H. pylori organisms at death. The authors conclude that H. pylori alone causes little or no effect on an intact gastric mucosa in the rat, that either intact organisms or bacteria-free filtrates cause similar prolongation and delayed healing of pre-existing ulcers with active chronic inflammation, and that the presence of predisposing factors leading to disruption of gastric mucosal integrity may be required for the H. pylori enhancement of inflammation and tissue damage in the stomach.
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PMID:Helicobacter pylori. Its role in the pathogenesis of peptic ulcer disease in a new animal model. 151 73

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

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

The relationships between gastric pH and Helicobacter pylori infection were studied in 37 consecutive subjects affected with nonulcer dyspepsia. Each underwent esophagogastroduodenoscopy with multiple gastric biopsies for both H. pylori and histologic assessment, and 24-hr antral pH monitoring. H. pylori was harbored by 59.5% of the subjects with whole gastric spread of infection in all but one patient. Histologic gastritis was shown in 70.3% of the subjects. H. pylori was strongly associated with gastritis, both antral nonatrophic and multifocal atrophic. The ranges of 24-hr pH values were 1.3-6.9 in the H. pylori-positive and 1.2-6.8 in the H. pylori-negative group. Differences in pH values between the two groups were not significant. Moreover, the mean percent time duration of pH above 2, 4, and 6 did not significantly differ between the two groups. Therefore, this study has shown that chronic H. pylori infection is not related to luminal gastric pH.
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PMID:Helicobacter pylori and luminal gastric pH. Relationships in nonulcer dyspepsia. 173 61

The aim of this study was to evaluate the long-term prognosis for patients suffering from gastritis associated with Helicobacter pylori infection, and in particular the proportion of cases progressing to peptic ulcer. The study was carried out in one urban general practice. One hundred and three patients who had presented with dyspepsia over the 1973-80 period and who were found to have a macroscopically normal endoscopy were reassessed between seven and 14 years later. Gastric antral biopsies had been taken routinely at endoscopy and were subsequently re-examined for the presence of H pylori. The patients' medical records were examined to establish their consulting rates over the follow-up period and whether they suffered from any other medical conditions. Patients were interviewed to assess the course of their dyspeptic symptoms. Comparison of patients who were unequivocally H pylori positive with those who were negative revealed no significant differences in the consultation rate for gastroenterological symptoms, in the proportion of patients referred to a hospital consultant or for further gastroenterological investigations or in the proportion reporting that their symptoms had improved. However, a statistically highly significant relationship was found between H pylori infection and hypertension. The results of this study have shown that there is a good prognosis for non-ulcer dyspepsia whether or not H pylori infection is present. The association between H pylori gastritis and hypertension clearly merits further investigation.
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PMID:Long-term follow up of patients with gastritis associated with Helicobacter pylori infection. 174 67


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