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

The advent of new diagnostic and therapeutic modalities for Helicobacter pylori allows any physician to offer curative antibiotic regimens to patients with peptic ulcer disease and gastritis. This article describes new management strategies and discusses the advantages of each. In the old strategy, endoscopy was performed on patients with dyspepsia, in the hope of detecting a treatable peptic ulcer. In the new strategy, patients with dyspepsia are investigated with serology to detect those with H. pylori and potentially curable peptic ulcers. Patients with persistent symptoms require a urea breath test and only those who are now H. pylori-negative undergo endoscopy. The cost-effectiveness of these strategies will depend on the expense of each diagnostic test, particularly endoscopy. Whether a noninvasive strategy can be implemented safely may depend also on the incidence of gastric carcinoma in a particular population and the effectiveness of antibacterial therapy at reducing cancer risk.
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PMID:Managing acid peptic disease in the Helicobacter pylori era. 877 10

Helicobacter pylori-like organisms (Hp) and polymorphonuclear leucocytes (PMNs) in 2614 gastroduodenal biopsies from 602 patients with dyspepsia, in Al Ain, United Arab Emirates, between October 1990 and October 1992, were histologically graded to determine the prevalence of Hp gastritis and their utilization in the evaluation of treatment efficacy in these patients. Symptoms of functional dyspepsia included, in order of frequency, abdominal pain or discomfort, flatulence, burning sensation, regurgitation, fullness, nausea, vomiting, bloating and belching. The biopsies were paraffin embedded, sectioned and stained with hematoxylin and eosin (H and E) to grade the inflammation. In addition to H and E, several special stains including modified Giemsa (MG), Wharthin-Starry silver and cold Ziehl-Neelsen stains were utilized to clearly identify Hp organisms. Giemsa method was found to be superior to other special stains in visualizing the Hp organisms in paraffin sections, and was utilized in every case. Two immunohistochemical markers for B cells (CD20) and T cells (CD45RO) were utilized for labeling lymphocytes infiltrating the lamina propria of the gastroduodenal biopsies in formalin-fixed paraffin-embedded sections. H and E and MG stained sections were utilized to count PMNs and Hp, and were graded 0, 1, 2, and 3, corresponding to none, mild, moderate, and severe grades of the Sydney system for classification of gastritis, respectively. Of the total initial 2318 endoscopic biopsies, 98.8% of the patients had suitable biopsies for histologic evaluation. Unsuitable biopsies were recovered from patients with gastric carcinoma. Inflammation was seen in 98.5% of 595 patients with suitable biopsies. In 74.5% of these patients the inflammation was active; 37.5, 32.5 and 4.5% had mild, moderate and severe active inflammation, respectively. In the remaining 24% of the 595 patients, the gastritis was chronic without activity or atrophic changes. As many as 73.6% of the patients with suitable biopsies were Hp positive; 39.8, 29.1 and 4.7% had grades 1, 2 and 3 Hp, respectively. Intestinal metaplasia was found in 28.9% of the 602 patients, and was seen more often in Hp positive than Hp negative patients (34.5 vs 14%, P < 0.005, for d.f. = 1; chi 2 = 10.35). Of the Hp positive patients, 172 and 46 patients attended the first and second follow-up endoscopy visits, respectively. The triple treatment was composed of one dose of tinidazole (2gm), doxycycline, 200 mg initial dose and 100 mg daily for two weeks, and bismuth subcitrate (Gist-Brocades nv, Delft, The Netherlands), 2 tablets twice daily for 4 weeks. After triple drug treatment, eradication of Hp was accomplished, histologically, in 38.4 and 45.7% of the patients on first and second follow-up visits, respectively. Thus, the Sydney system-based grading scale provides an objective histological evaluation of Hp gastritis for accurate prevalence studies, and may prove to be of value in estimating treatment efficacy.
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PMID:Grading Helicobacter pylori gastritis in dyspeptic patients. 881 77

Infection with Helicobacter pylori (H.p.) leads to mostly asymptomatic chronic gastritis. However, H.p. plays a role in peptic ulcer, giant fold gastritis (Menetrier's disease), and possibly in gastric carcinoma and low-grade MALT lymphoma. Whether functional dyspepsia also represents a Helicobacter-induced entity is questionable. H.p. should be eradicated in patients with peptic ulcer disease, Menetrier+s disease and - but in controlled studies only - in MALT lymphomas. Triple therapy with low-dose proton pump inhibitors and two antibiotics is the most favourable treatment compared to dual therapy with omeprazole and amoxicillin/clarithromycin despite the unresolved question of the development of drug resistance.
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PMID:[Therapy of Helicobacter infection]. 897 55

Helicobacter pylori has been linked with peptic ulcer disease, non-autoimmune gastritis, non peptic ulcer dyspepsia and gastric carcinoma and lymphoma. This study looked at the incidence of H. pylori infection in Ghanaian patients with dyspeptic symptoms referred for upper gastro-intestinal endoscopy and its relationship to various pathologies. Detection was by the CLO urease test. A hundred and thirty (130) patients were studied. 75.4% tested positive for H. pylori infection and the incidence peaks in the 5th decades. While 23.5% H. pylori positive patients had active duodenal or gastric ulcer, 18.8% of H. pylori negative patients also had the ulcer. Out of 43 patients with normal oesophago-gastro-duodenoscopy, 74.4% were H. pylori positive, 66.6% of gastric malignancies tested positive for H. pylori infection. It remains to be confirmed that eradication of H. pylori will relieve the peptic symptoms in affected patients with no ulcer disease.
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PMID:Incidence of Helicobacter pylori infection in Ghanaian patients with dyspeptic symptoms referred for upper gastrointestinal endoscopy. 902 Jun 1

Gastritis is a histopathologic diagnosis, which correlates poorly with both clinical symptoms of non-ulcer dyspepsia and endoscopic abnormalities. Worldwide, most cases of gastritis are due to Helicobacter pylori and are characterized by a diffuse superficial antral gastritis. Chronic inflammatory cells and lymphoid follicles are present in the lamina propria. Neutrophils are present in the surface and pit-lining epithelium. In North America and Western Europe, reactive gastropathy due to duodenal reflux or non-steroidal anti-inflammatory agents is also common. In this condition, there is no increase in inflammatory cells, but the pit-lining cells become hyperplastic, and the pits have a corkscrew appearance. Most examples of multifocal atrophic gastritis are the result of long standing Helicobacter gastritis, although there may be other causes as well. It is characterized by loss of glands in both pyloric and corpus mucosae with intestinal metaplasia of the surface epithelium. A subtype of intestinal metaplasia, in which sulphomucin (large bowel mucin) is present, has been associated with the development of distal gastric cancer. However, this association is relatively weak and is not considered useful for screening purposes. Gastric dysplasia may develop in areas of the stomach affected by intestinal metaplasia. High-grade dysplasia is a significant finding, with up to 60 percent of cases having coincident carcinoma and a further 25 percent of cases likely to develop an invasive malignancy within fifteen months.
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PMID:The morphology of gastritis. 904 89

Helicobacter pylori has been implicated in the pathogenesis of chronic gastritis, gastric and duodenal ulcer, and possibly gastric carcinoma. The organism may be detected by invasive or non-invasive methods with variable sensitivity. Paired gastric biopsy and gastric brush specimens were collected from 83 patients presenting with non-ulcer dyspepsia. One biopsy was tested for urease using the CLOtest, the other was processed to paraffin and consecutive sections were stained with haematoxylin and eosin, modified Giemsa and anti-H. pylori antisera. The brush specimens were stained with a rapid Romanowsky stain (Hema-Gurr) and anti-H. pylori. The CLOtest was positive in 31 cases, the Giemsa biopsy in 25, the anti-H. pylori biopsy in 27, the Hema-Gurr smear in 27 and the anti-H. pylori smear in 19. The sensitivities of the methods after omitting one inadequate biopsy were 96%, 93%, 100%, 96% and 78%, respectively. The specificities were 93% for the CLOtest and 100% for the other methods. While immunocytochemical staining of gastric biopsies may be the most sensitive method for H. pylori identification, the cost and turn around time of the technique may preclude its routine use. Gastric brush cytology is a highly sensitive and specific method for H. pylori detection that is quick and simple to perform. Its application is recommended for the routine diagnosis of H. pylori infection.
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PMID:Diagnosis of Helicobacter pylori in gastric brush and biopsy specimens stained by Romanowsky and immunocytochemical methods: comparison with the CLOtest. 907 60

Since the identification of Helicobacter pylori in 1983, this pathogen has become the dominant focus of investigation in a variety of gastrointestinal tract disorders, including peptic ulcer disease, nonulcer dyspepsia, and gastric carcinoma. During the past 7 years, the efficacy of a variety of antimicrobial single, dual, and triple therapy regimens--including the use of acid-suppressive agents, such as proton pump inhibitors, and histamine2-receptor antagonists--in the eradication of H pylori have been investigated. Newer treatment approaches, such as dual therapy (proton pump inhibitor + 1 antimicrobial agent) and 7-day regimens have shown a high degree of success and have the potential to improve compliance. However, the optimal regimen, in terms of cost, efficacy, and tolerability, and optimal length of treatment still remains to be determined.
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PMID:Antimicrobial management of Helicobacter pylori-associated gastrointestinal tract disease. 907 54

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

Menetrier's disease (MD) or polyadenomes en nappe is a form of hypertrophic gastropathy occurring primarily in middle-aged males. Patients generally present clinically with dyspepsia and, on occasion, with hypoproteinemic edema and anemia. The latter feature, when combined with the radiographic appearance of the stomach in MD, can lend to confusion with carcinoma and malignant lymphoma. To illustrate this diagnostic problem, a case is reported of a 41-year-old female who initially presented to her family physician with symptoms of easy fatigue and dyspnea on exertion and signs of pallor and ankle edema. Pertinent laboratory findings included a hemoglobin of 2.8 g/dL, hematocrit of 10.3 percent, mean corpuscular volume of 63.4 mu 3, a serum albumin of 2.7 g/dL, and heme positive stools. Endoscopic examination revealed a circumferential polypoid mass involving the cardia and fundus of the stomach with relative sparing of the antrum. A CT scan of the abdomen and pelvis showed a large mass in the stomach which the radiologists and gastroenterologists believed probably represented a lymphoma or gastric carcinoma. A total gastrectomy specimen exhibited features of MD. Routine bright-field microscopy and immunohistochemical reactivity for transforming growth factor-alpha confirmed the diagnosis of MD. Moreover, ulceration of the tips of some of the hypertrophied gastric folds provided an explantation for the iron deficiency anemia. Awareness that MD may present with anemia will help in the differential diagnosis with lymphoma and carcinoma.
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PMID:Menetrier's disease presenting with iron deficiency anemia. 951 79

Screening and treating the community for Helicobacter pylori would have seemed inconceivable 5 years ago. This has now become a real possibility given that H. pylori is a major risk factor for gastric carcinoma. Screening should not be introduced, however, before the costs and benefits of the programme are established. It has been estimated that 1:30-1:60 of the UK population die from an H. pylori related disease. If treating H. pylori were to reduce premature mortality, then this would be a persuasive argument for a screening strategy. The financial costs of screening and treating H. pylori are significant but this would be partially offset by savings that would accrue from reducing dyspepsia in the community. Indeed, decision analysis models suggest H. pylori screening is cost-effective. The potential benefits are enormous and prospective randomised trials are urgently required to establish whether such a programme is worthwhile.
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PMID:Is there a rationale for eradication of Helicobacter pylori? Cost-benefit: the case for. 960 47


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