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)

The aim of this study is to find out the prevalence of Helicobacter pylori infection in patients with nonulcer dyspepsia (NUD) and asymptomatic controls and to see if there is an etiological association between gastritis, NUD and Helicobacter pylori. One hundred thirty six patients with NUD and 71 controls had six endoscopic biopsies from different sites of the gastric mucosa for histological diagnosis. Helicobacter pylori was looked for in all biopsy specimens utilizing half Gram, Giemsa and Gimenez staining techniques. Type B chronic gastritis was detected in 96% of the NUD cases and in 100% of the asymptomatic controls (P > 0.05). Helicobacter pylori was found in 82 (65%) patients with NUD and in 38 (56%) asymptomatic controls (P > 0.05). Type B chronic gastritis is almost universal in both NUD cases and asymptomatic controls. There is no difference in the prevalence of Helicobacter pylori infection between the two groups. The absence of Helicobacter pylori in a significant number of patients (36%) and controls (45%) with gastritis contradicts the etiological association between Helicobacter pylori and gastritis reported by others, suggesting that in Ethiopia there may be a chronic environmental gastritis which may not be helicobacter-related. There is no correlation between NUD and Type B gastritis, and between symptoms and Helicobacter pylori infection in this population.
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PMID:Helicobacter pylori, gastritis and non-ulcer dyspepsia in Ethiopian patients. 884 Jun 8

It is well known that Helicobacter pylori infection is extremely common throughout the world, but most infected persons do not develop ulceration and remain asymptomatic. This study was undertaken in order to determine the prevalence of H. pylori infection, the age distribution, and the factors that may affect the frequency of H. pylori infection. We evaluated the presence of antibody against H. pylori in children and adolescents, we also assessed the efficacy of non-invasive and invasive methods for detection of H. pylori infection in children who had undergone upper gastrointestinal endoscopy. We evaluated 43 males and 18 females whose ages ranged from 1 to 17 years (mean age: 9.4 +/- 4.2). 29 of all cases were symptomatic and 32 were asymptomatic. H. pylori infection was present in 49% of the studied cases. The data were analysed by Fisher's exact chi-square and Mantel-Haenszel tests. It was found that H. pylori infection graphically increased with age in both groups from 25% at ages 3-5 to 80% at ages 16-20. But no association was determined statistically between age and H. pylori positivity (p < 0.05). H. pylori infection was determined in 14 (48%) and 16 (50%) cases in symptomatic and asymptomatic groups respectively. There was no significant difference between H. pylori and either group (p > 0.05). According to the endoscopy findings, the symptomatic group was divided into two subgroups: children with peptic ulcer and children with non-ulcer dyspepsia (NUD). An attempt was made to compare ulcer, non ulcer dyspepsia and asymptomatic cases with H. pylori positivity, but no significant relation could be established between the groups (p > 0.05). 14 (23%) of the cases had previous gastric and/or intestinal complaints in their parents (positive family history). There was a significant, statistically positive relation between family history and symptoms (p < 0.01). Nevertheless, no association was found between H. pylori infection and family history (p > 0.05). There were no significant differences in H. pylori infection related to sex, type of housing, location of housing, socio-economic status (SES) or source of water supply. It is concluded that H. pylori infection has a high prevalence in our country. Although endoscopic evaluation is an invasive method, under our conditions, histopathological examination with 97% is shown to be much more sensitive in determination of H. pylori infection. Since no community difference was determined in the prevalence of H. pylori infection, all children should be considered to be under the threat of the same risk.
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PMID:Helicobacter pylori infection in symptomatic and asymptomatic children: a prospective clinical study. 893 28

In the present study we assessed the diagnostic accuracy of four commercial IgG enzyme-linked immunosorbent assay (ELISA) kits (Autoplate, H.pylori-EIA-Well, Enzygnost, Helori-test) and evaluated the performance of these tests in patients with fundic atrophic gastritis. Serum antibodies to Helicobacter pylori were measured in 70 out-patients attending endoscopy for dyspepsia and 43 patients with non-autoimmune fundic atrophic gastritis. Using the cut-off values recommended by the manufacturers, and comparing serological findings with gastric biopsy results of dyspeptic out-patients attending endoscopy, the four kits showed a sensitivity and specificity, respectively, of 91% and 96%, for Autoplate, 67% and 100% for H.pylori-EIA-Well, 79% and 100% for Enzygnost, and 81% and 96% for Helori-test. Evaluation in patients with atrophic gastritis revealed a high prevalence of antibodies to Helicobacter pylori (84%) and it demonstrated that patients with and those without gastric colonization by this microorganism had a similar rate of seropositivity (76-84% vs 50-78%). In conclusion, our data demonstrate that: a) this assay is a reliable and valid method to detect gastric colonization by Helicobacter pylori; b) positive serum antibody associated with a negative detection of Helicobacter pylori in the gastric mucosa suggests mucosal atrophy; c) patients with fundic atrophic gastritis should be excluded from studies investigating the value of serology in diagnosing Helicobacter pylori infection.
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PMID:Value of serology (ELISA) for the diagnosis of Helicobacter pylori infection: evaluation in patients attending endoscopy and in those with fundic atrophic gastritis. 893 37

We modified a novel topical therapeutic method for the treatment of Helicobacter pylori infection to increase its effectiveness and tolerability. Sixty-six patients (with nonulcer dyspepsia, inactive ulcer, or active ulcer) were given lansoprazole (30 mg, h.s.) and pronase (18,000 tyrosine units, b.i.d.) orally for 2 days before the topical therapy. One hundred milliliters of 7% sodium bicarbonate solution containing bismuth subnitrate, amoxicillin, metronidazole (at two different regimens), and pronase was instilled into the stomach through an endoscope. A double-lumen tube with a balloon at the tip was inserted into the duodenum along with the endoscope. The balloon was inflated with 25 ml of air and was lodged postbulbarly. The solution was kept in the stomach for 2 h, and the patient's position was changed every 15 min from the sitting to the supine, prone, and right lateral position, each position being maintained twice, to expose the entire gastric mucosa. The solution was aspirated at the end of the procedure. H. pylori infection was cured in 16/22 (72.7%) of patients with nonulcer dyspepsia, in 21/26 (80.7%) of patients with inactive ulcer, and in 1/18 (5.6%) patients with active ulcer. H. pylori eradication was confirmed 4 weeks after the therapeutic procedure by smear, culture, and histology of antral and corpus biopsy specimens. Side effects (loose stools) were observed in two patients only, and one patient had loss of appetite. These effects were transient. This endoscopic topical therapy for H. pylori infection is a safe, effective, and well tolerated procedure. With further modifications of the drug regimens and the method itself, this procedure could be of interest as anti-H. pylori therapy.
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PMID:Endoscopic topical therapy for the treatment of Helicobacter pylori infection. 895 24

The aim of this article is to determine, by reviewing the literature, whether treatment of Helicobacter pylori infection in patients with non-ulcer dyspepsia affects symptoms. Ten publications were identified through a computerized and manual literature search, and the percentage of patients with symptom improvement after successful or unsuccessful eradication therapy for H. pylori infection was calculated. In the 10 studies, symptom improvement after treatment was found in 73% of the patients that became H. pylori-negative and 45% of the patients that remained H. pylori-positive. Symptom improvement was modified by various clinical features and methodological aspects. If eradication of H. pylori failed, symptoms only improved over a short period. Symptom improvement was more pronounced in dyspeptic patients in whom H. pylori was eradicated than in those in whom H. pylori infection persisted.
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PMID:Review article: symptom improvement through eradication of Helicobacter pylori in patients with non-ulcer dyspepsia. 897 Dec 79

The aim of our study is to evaluate the efficacy and tolerability of four different therapeutic regimens for Helicobacter pylori eradication. One-hundred and thirty-two consecutive patients suffering from either peptic ulcer or non-ulcer dyspepsia, with Helicobacter pylori infection, were allocated to one of the following 4 groups with different therapeutic regimens: A) omeprazole 20 mg bid for 14 days/amoxycillin 1000 mg bid for 14 days/tinidazole 500 mg bid for 14 days (30 patients, 13 with peptic ulcer); B) omeprazole 20 mg bid for 14 days/amoxycillin 1000 mg bid for 14 days (41 patients, 23 with peptic ulcer); C) omeprazole 20 mg bid for 14 days/azithromycin 500 mg/day for 3 days for 2 consecutive weeks (25 patients, 12 with peptic ulcer); D) omeprazole 20 mg/day for 7 days/clarithromycin 250 mg bid for 7 days/tinidazole 500 mg bid for 7 days/ (36 patients, 14 with peptic ulcer). The Helicobacter pylori status was evaluated by means of histology, culture and urease test, at entry and 8 weeks after treatment. 2 group A, B and D patients, 1 D patient didn't complete the treatment. In evaluable patients, the Helicobacter pylori eradication was obtained in 24 patients of group A (85.71%), in 24 of group B (58.98%), in 11 of group C (45.83%) and in 24 of group D (70.58%). On intention-to-treat analysis, Helicobacter pylori eradication was 80% in group A, 56.09% in group B, 44% in group D and 66.67% in group D. Sideeffects occurred in 6 patients of group A (20.68%), in 5 of group B (12.5%), in 3 group D (8.82%) and none of group C. In conclusion, triple therapy with omeprazole/clarithro-mycin/tinidazole is better for cost/benefit ratio; omeprazole/amoxycillin/tinidazole is more effective than others regimens in the Helicobacter pylori eradication, but causes more side effects; double therapy with omeprazole/azithromycin is the most tolerable and the least efficacy for Helicobacter pylori eradication.
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PMID:Evaluation of the efficacy and tolerability of four different therapeutic regimens for the Helicobacter pylori eradication. 900 77

The present study tests the efficacy of the multi-scaled urease test (MUT) in detecting Helicobacter pylori infection and determines whether the MUT can predict the bacterial density on histology. A total of 111 sets of gastric specimens were obtained from patients with dyspepsia but without recent bleeding. Two biopsies were taken as closely as possible in each set. One sample was used for the MUT (Hp fast; GI Supply, Camp Hill, PA, USA), while the other was used to determine the histological density of H. pylori by modified Giemsa stain (grade 0-5). The results of MUT were interpreted as negative if the colour was yellow or bright green (reaction score 0) and positive if the colour was green, light blue, or blue (reaction score 1, 2 and 3, respectively). The reaction scores of MUT were recorded sequentially at 15 and 30 min and 1, 4 and 24 h. On the basis of histological confirmation, MUT had a sensitivity of 89.6%, a specificity of 88.2%, a positive predictive value of 94.5% and a negative predictive value of 78.9%. Focusing on specimens with the presence of bacteria under histology, 77 specimens were divided into five subgroups by grades of density of H. pylori (HPD1-5). The reaction scores had become sequentially elevated from 30 min through to 24 h in each subgroup. For subgroups HPD4 and 5, the positive rates of MUT were 70.6 and 66.6%, respectively, as early as 30 min and progressed to 100% within 4 h. In contrast, the positive rate for the HPD1 subgroup was 16.6% at 4 h and increased to only 62.5% at 24 h. In subgroups HPD 2 and 3, the positive rates were less than 30% at 30 min, but became more than 66.6% at 4 h and were 100% at 24 h. The early (i.e. mean value of reaction scores before 4 h) and late (24 h) mean reaction scores disclosed two elevated trends as the density of H. pylori increased (early: 0.2, 0.7, 0.8, 1.5, 1.2; late: 1.4, 2.3, 2.6, 3.0, 3.0; P < 0.05). In conclusion, MUT is a reliable method for the diagnosis of H. pylori infection. It can also indirectly predict the density of H. pylori on histology.
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PMID:Clinical assessment of the bacterial load of Helicobacter pylori on gastric mucosa by a new multi-scaled rapid urease test. 907 14

Helicobacter pylori infection has been associated with chronic atrophic gastritis, a precursor of gastric cancer. We conducted a prospective, case-controlled study to investigate whether H. pylori infection increases the risk of gastric cancer in Korean people with a high risk of gastric cancer. We enrolled 160 gastric cancer patients who were confirmed by endoscopic biopsy during 1994 and 160 age-matched control subjects with non-ulcer dyspepsia were compared to document the relationship between H. pylori infection and gastric cancer. The presence of H. pylori infection was determined by the rapid urease test and/or histology by Wright-Giemsa staining. The overall presence of H. pylori infection was 60% in gastric cancer patients and 51.9% in age-matched control subjects (odds ratio 1.39; 95% confidence interval 0.894-2.17; P = 0.143). Carcinomas of cardia, body and antrum were not associated with H. pylori infection (odds ratio 1.43, 1.69 and 1.29, respectively; 95% confidence interval, 0.271-7.52, 0.787-3.62 and 0.689-2.43, respectively; P = 0.178, 0.177 and 0.642, respectively) nor was the intestinal or diffuse type of cancer (odds ratio 1.39 and 1.40, respectively; 95% confidence interval 0.791-2.45 and 0.681-2.87, respectively; P = 0.250 and 0.835, respectively). Gender was not a risk for gastric cancer. In contrast to previous studies, these results do not provide evidence of H. pylori infection for gastric carcinogenesis in Korea.
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PMID:Helicobacter pylori infection and the risk of gastric cancer among the Korean population. 908 9

Although the discovery of Helicobacter pylori infection in peptic ulcer disease is revolutionizing ulcer diagnosis and treatment, the role of universal empiric therapy for infected patients with dyspepsia or peptic ulcers is not fully elucidated. This article reviews current thinking on the diagnosis of H pylori infection in 1997.
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PMID:H pylori 1997: testing and treatment options. 910 14

Indications for eradication of Helicobacter pylori infection have widened since the National Institutes of Health consensus conference in 1994. It is argued that they should now include infected patients with non-ulcer dyspepsia, those concerned about the risk of gastric cancer, patients with gastric lymphoma, and those requiring long-term treatment with a proton pump inhibitor. Problems with existing clinical trials are discussed, and the results of different treatment regimens are discussed. It is proposed that future eradication trials should investigate H. pylori-infected subjects identified by serology, rather than ulcer patients, and that eradication is proved only by a pair of 13C-urea breath tests.
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PMID:The treatment of Helicobacter pylori infection. 914 89


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