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)

There has been controversy regarding the relationship between Helicobacter pylori and perforated peptic ulcer, which is known to have a high recurrence rate if only simple patch repair is performed. The aim of this study was to evaluate the association between H. pylori infection and intake of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with perforated duodenal ulcers. Of the 73 patients recruited over a 16-month period, 51 (70 per cent) had evidence of H. pylori infection by intraoperative gastroscopy and antral biopsies. The infection rate rose to 80 per cent if NSAID users were excluded. The H. pylori-infected group was significantly younger (mean 47.6 versus 62.5 years), with a male preponderance (49 of 51 versus 14 of 22 patients), and had significantly less NSAID consumption (three of 51 versus ten of 22) and more prolonged dyspepsia (40 of 51 versus ten of 22), compared with H. pylori-negative patients. H. pylori infection probably plays an important role in the causation of non-NSAID-induced duodenal ulcer perforation. Whether eradication of the bacteria can alleviate the strong ulcer diathesis in this subgroup of patients is unknown.
Br J Surg 1996 Dec
PMID:High prevalence of Helicobacter pylori infection in duodenal ulcer perforations not caused by non-steroidal anti-inflammatory drugs. 924 Jan 65

A retrospective study of 330 patients who had been endoscoped in Mulago hospital was done. It was found that of these 119 (36.1%) were normal endoscopically. Normal endoscopy was significantly associated with patients presenting with dyspepsia. Dyspepsia was commoner in the age group 13-45 years compared to the age group 46-85 years. The older age group, 46-85 years, had a significantly higher prevalence of serious disease. It is concluded that it is the younger patients with dyspepsia who should be screened to reduce the endoscopy workload. Published guidelines should be used to assist in the screening process.
East Afr Med J 1996 Dec
PMID:Who should be screened to reduce the endoscopy workload in Mulago Hospital? 910 97

Although certain factors appear to predispose the host to infection by Helicobacter pylori, clearly the bacterium possesses a well-defined battery of virulence factors that allow the organism to: (1) colonize the gastric mucosa (urease, flagella, adhesins, acid-inhibitory protein, iron acquisition proteins, and heat shock proteins); (2) evade host defense (shedding of surface proteins, catalase, superoxide dismutase, and poorly reactive lipopolysaccharide); and (3) damage host tissue (vacuolating cytotoxin, protease, CagA-related factors, inducers of cytokines, and chemotaxins). Together these factors allow H. pylori to persist in the host, establishing a chronic infection. Although many of these virulence factors are produced by all strains of H. pylori, there are also well-defined pathogenicity islands (contiguous stretches of chromosomal DNA) present in some strains that encode additional proteins including CagA that potentiate virulence. Strains possessing these "virulence cassettes" are isolated more frequently from patients with the more serious clinical manifestations associated with duodenal ulcer than from patients with gastritis alone or nonulcer dyspepsia.
Gastroenterology 1997 Dec
PMID:Helicobacter pylori factors associated with disease development. 939 56

A major role for Helicobacter pylori gastritis in nonulcer dyspepsia (NUD) is controversial. Gastroduodenal dysfunction may be associated with H. pylori infection, but there is little evidence for a causal link with dyspepsia. Population-based studies with appropriate methodology have generally failed to confirm an association between H. pylori and NUD. Furthermore, no definite association between subgroups of NUD (ulcer-like, dysmotility-like, reflux-like, and nonspecific) and H. pylori has been identified however the subgroups have been defined, and no specific symptom pattern characterizes patients with H. pylori infection. Whether H. pylori-induced alterations of gastric physiology can explain NUD remains open to debate while we await the results of more specific experiments. Although acid secretion in response to gastrin-releasing peptide may be increased in a subset of NUD patients who are infected with H. pylori, uninfected patients with NUD have not been assessed and the results require confirmation. Most studies suggest no association between H. pylori and gastroduodenal motor or sensory dysfunction in NUD. Treatment trials have been unconvincing. The trials with bismuth therapy have not been adequately blinded. Furthermore, some studies suggest that H. pylori-negative patients with NUD may respond to bismuth treatment, although the results have not been uniform. Therapies aimed at curing H. pylori infection have produced mixed results, with small positive and negative trials. The trials that have used adequate outcome measures have more often than not been negative. Based on current evidence, H. pylori is not established to be of causal importance in NUD.
Gastroenterology 1997 Dec
PMID:What role does Helicobacter pylori play in dyspepsia and nonulcer dyspepsia? Arguments for and against H. pylori being associated with dyspeptic symptoms. 939 64

With the realization that Helicobacter pylori is the main etiologic factor for peptic ulcer disease, recent studies have explored a potential relationship between H. pylori and nonsteroidal anti-inflammatory drug (NSAID)-related gastroduodenal mucosal injury. Using serology and/or histology to detect H. pylori, case-control studies have shown no meaningful differences in H. pylori prevalence in both arthritis and nonarthritis NSAID users and controls. Placebo-controlled short-term trials of NSAIDs have also shown no change in the frequency of detection of H. pylori by gastric mucosal biopsy specimens after 7-30 days of NSAID ingestion. A number of studies have shown that the histological gastritis identified in NSAID users is caused by H. pylori infection, whereas the reactive (chemical) gastritis can be caused by NSAID use. Although the overall relationship between H. pylori gastritis and dyspepsia remains controversial, there is no evidence from well-controlled studies using either serology or histology that this gastritis predisposes to NSAID-related dyspepsia. The effect of H. pylori on NSAID-related gastroduodenal mucosal injury may be best established by evaluating the ulcer recurrence rate after H. pylori eradication and rechallenge with NSAIDs. To date, only one such study has examined this question, and in this small study, the ulcer recurrence rate at 6 months was not reduced by H. pylori eradication.
Gastroenterology 1997 Dec
PMID:Relationship between nonsteroidal anti-inflammatory drug use, Helicobacter pylori, and gastroduodenal mucosal injury. 939 66

The publication of the National Institutes of Health Consensus Development Conference guidelines on management of Helicobacter pylori infection in 1994 set a precedence. At present, at least eight European countries have produced national guidelines, and, more recently, the European Helicobacter pylori Study Group also outlined guidelines based on the strength of available evidence. It is generally agreed that H. pylori should be eradicated in peptic ulcer disease. In nonsteroidal anti-inflammatory drug (NSAID)-related ulcers, most countries that considered the issue suggested discontinuing NSAIDs when possible and eradicating H. pylori. The prophylactic eradication of H. pylori was not recommended. A number of panels felt that there was not enough evidence available to recommend eradication of H. pylori in functional dyspepsia, whereas other groups felt that nonulcer dyspepsia, particularly after investigation and with severe or recurrent symptoms, was an indication for eradication therapy. Other conditions (i.e., gastroesophageal reflux disease [GERD] and mucosa-associated lymphoid tissue [MALT] lymphoma) have emerged in this short time as possible indications for H. pylori eradication. There is no evidence that H. pylori infection has a role in the pathogenesis of GERD, but there is evidence suggesting that patients with H. pylori infection who require long-term acid suppression may be at risk of developing atrophic gastritis. The European Helicobacter pylori Study Group has suggested that eradication therapy should be offered to infected family members of patients with gastric cancer. It also recommended that eradication therapy was "strongly recommended" on the basis of "supportive" evidence in gastritis with severe abnormalities and after early resection of early gastric cancer. An "uncertain" recommendation with "equivocal" evidence was given for asymptomatic subjects, extra-alimentary tract disease, the prevention of gastric cancer in the absence of risk factors, and in pediatric patients with recurrent abdominal pain. Despite considerable advances, further research studies are needed to provide definite direction for the treatment of many conditions.
Gastroenterology 1997 Dec
PMID:Who should be treated for Helicobacter pylori infection? A review of consensus conferences and guidelines. 939 69

Evidence-based medicine combines clinical expertise and the best available evidence from systematic research to aid decision making in patient care. Levels of evidence can be graded from I to V, with level I, the strongest, coming from large randomized controlled trials (RCTs). When a definitive RCT has not been performed, or is impracticable or inappropriate, lesser grades of evidence are used. There is level I evidence supporting the treatment of Helicobacter pylori infection in patients with duodenal or gastric ulcers. Prospective RCTs have shown that cure of the infection is associated with ultimate cure of the ulcer diathesis. Therefore, this is a "grade A" recommendation for treatment. In nonulcer dyspepsia, numerous RCTs have yielded conflicting results regarding the benefits of treatment. Although there are methodological problems with many reported studies, there is some evidence (level II at best) to support treatment--a grade B recommendation. In early gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma, the best available evidence supporting treatment of H. pylori infection is of low quality, i.e., levels III and V. Although these carry only grade C treatment recommendations, treatment is safe and carries at least some evidence of efficacy. It is therefore indicated based on the current best available evidence. No evidence exists to support treating the infection in patients receiving long-term proton pump inhibitors for gastroesophageal reflux disease or in patients with any of the nongastrointestinal conditions that have been tentatively linked to H. pylori.
Gastroenterology 1997 Dec
PMID:For what conditions is there evidence-based justification for treatment of Helicobacter pylori infection? 939 70

A variety of questions regarding Helicobacter pylori need to be addressed by future research. Further investigations are needed on the relationship between H. pylori and gastric cancer. In particular, the mechanism of the interaction between H. pylori infection and host genetic factors and dietary factors that lead to the cancer need to be unraveled. Also, the reversibility of cancer-associated abnormalities (e.g., hypochlorhydria, atrophy, and intestinal metaplasia) by eradication of H. pylori needs to be determined. Noninvasive means of identifying H. pylori-positive subjects at high risk of developing gastric cancer are required for such subjects to be targeted for eradication therapy. Further studies are also required on the interactions between H. pylori and proton pump inhibitor therapy that might predispose to cancer. There is considerable interest in the possibility of noninvasive H. pylori testing replacing endoscopy in determining management of nonelderly patients with uncomplicated dyspepsia unassociated with nonsteroidal anti-inflammatory drugs (NSAIDs). Randomized studies comparing endoscopy vs. noninvasive H. pylori testing in this situation are required with comprehensive outcome measures. Improvement in eradication therapy is required and will depend on the development of more effective and specific antibiotics and therapeutic vaccines. Wide-scale elimination of the infection will depend on preventing its spread from person to person. Achieving this will require further knowledge of its mode of transmission, particularly in childhood, and the development of prophylactic vaccines. Further studies are required to define the role of H. pylori infection in other diseases, including predisposition to enteric infection in the developing world as a result of H. pylori-induced chronic hypochlorhydria, nonulcer dyspepsia, pernicious anemia, atherosclerosis, and NSAID-related ulcer disease. Finally, we need to know whether H. pylori infection may be beneficial in certain circumstances and whether eradicating the infection may be disadvantageous to some subjects.
Gastroenterology 1997 Dec
PMID:What remaining questions regarding Helicobacter pylori and associated diseases should be addressed by future research? View from Europe. 939 79

Several areas regarding Helicobacter pylori that need improvement or clarification in the United States include treatment of dyspepsia, physician education on disease associations with H. pylori, and evidence from U.S. studies that 7-day H. pylori eradication regimens are more effective than current regimens. Dyspepsia, a ubiquitous condition in the United States, is routinely managed on the basis of a positive H. pylori serology without other investigations. This approach has been fostered by cost-effectiveness studies of various approaches to duodenal ulcer and dyspeptic patients. Serology-directed therapy was the most cost-effective option vs. endoscopy-directed management. The option of not obtaining endoscopy had broad appeal to primary care physicians. In addition, a recent survey suggests that even gastroenterologists routinely attempt H. pylori eradication in infected patients with nonulcer dyspepsia, despite a number of negative efficacy studies. Finally, the option of not eradicating a World Health Organization-defined carcinogen in the litigious United States is unappealing to clinicians. Eradication of H. pylori in patients with dyspepsia despite more negative trials is likely to continue. There is evidence that U.S. physician awareness of the H. pylori-disease associations and the best therapies are improving rapidly, but further improvement is needed. Discrepancy of awareness of H. pylori between gastroenterologists and family physicians exists. In a recent survey, 94% and 72% of gastroenterologists regarded H. pylori as a causative agent in duodenal and gastric ulcer, respectively, vs. 68% and 68% of family physicians, and only 9% of family physicians believed there was a definite relationship between H. pylori infection and gastric cancer vs. 21% of gastroenterologists. One hundred three different H. pylori regimens were being used; 31% of family physicians and 11% of gastroenterologists used ineffective regimens or regimens of unknown effectiveness. Although 1-week proton pump inhibitor triple therapy is promising, there is skepticism that U.S. studies will yield the optimistic results that have characterized the European studies. Unlike in Europe, the U.S. standard is to use double diagnostics to prove eradication rather than just the urea breath test and to use intent-to-treat rather than assessable patient analyses. Both approaches reduce apparent eradication rates.
Gastroenterology 1997 Dec
PMID:What remaining questions regarding Helicobacter pylori and associated diseases should be addressed by future research? View from North America. 939 80

Beyond peptic ulcer disease, Helicobacter pylori infection is associated with intestinal-type gastric cancer and low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is also currently implicated as a possible cause of dyspepsia and extraintestinal disorders such as coronary artery disease, rosacea, chronic urticaria, and delayed growth in children. There are strong epidemiological data from large cohort studies linking H. pylori to gastric adenocarcinoma. Several cofactors, including early childhood acquisition of infection, strain-specific differences, genetic predisposition of the host, and the environment, appear to play a role in the progression of chronic gastritis to gastric cancer. H. pylori infection is seen in over 90% of MALT lymphomas, and about 70% of localized nonbulky tumors will undergo complete histological regression after eradication of the bacterium. Because follow-up data are limited to less than 2 years, those undergoing H. pylori eradication as primary therapy for MALT lymphoma require frequent histological surveillance for tumor recurrence. There are conflicting data from short-term studies regarding the effect of H. pylori eradication on dyspeptic symptoms. The decision to test or not for H. pylori in the dyspeptic patient may become easier when well-controlled studies with longer periods of follow-up become available. Because H. pylori induces a systemic inflammatory response, investigators are beginning to explore possible extraintestinal disease associations with the infection. The global prevalence of both peptic ulcer disease and gastric cancer has led to studies focusing on noninvasive screening for H. pylori in high-risk populations and prevention of primary infection by means of vaccination.
Gastroenterologist 1997 Dec
PMID:Helicobacter pylori: beyond peptic ulcer disease. 953 Nov 10


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