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

Considerable knowledge has recently accumulated on the mechanism by which Helicobacter pylori (H. pylori) induces chronic gastritis. Although H. pylori is not an invasive bacterium, soluble surface constituents can provoke pepsinogen release from gastric chief cells or trigger local inflammation in the underlying tissue. Urease appears to be one of the prime chemoattractants for recruitment and activation of inflammatory cells. Release of cytokines, such as tumor necrosis factor alpha, interleukin 1 and 6, and oxygen radicals, leads to a further tissue inflammation accompanied by a potent systemic IgA and IgG type of immune response. Chronic inflammation and antigens on glandular epithelial cells lead to a progressive destruction with loss of the epithelial barrier function. Within the gastric mucosa, patches of intestinal metaplasia develop, which may be a risk factor for subsequent development of gastric carcinoma. Hyperacidity in duodenal ulcer patients induces gastric metaplasia in the duodenal bulb, which represents a target for H. pylori colonization and ulcer formation. H. pylori can be detected in the majority of patients with peptic ulcers and, compared to age-matched healthy people, it is also found more often in patients with dyspepsia and gastric carcinoma. Although H. pylori can be detected in healthy people, the marked reduction of the ulcer recurrence rate by eradication of H. pylori (80 percent versus 20 percent relapse within one year) suggests that H. pylori is a major risk factor for duodenal ulcer formation. The potential role of H. pylori in non-ulcer dyspepsia and carcinogenesis is under investigation. Current regimens aimed at eradicating H. pylori use a combination of several drugs that are potentially toxic. Since the risk of complications may exceed the potential benefit in most patients, eradication treatment should be limited to clinical trials and to patients with aggressive ulcer disease. New drug regimens, e.g., the combination of proton pump inhibitors with one antibiotic, may provide less toxic alternatives. Beyond ulcer treatment, effective and well-tolerated eradication regimens may have a place in prophylaxis of gastric carcinoma.
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PMID:Pathophysiology and clinical relevance of Helicobacter pylori. 134 Oct 68

Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.
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PMID:Antacids. Indications and limitations. 751 3

The majority of patients with dyspepsia are managed in general practice. However, most of the literature on Helicobacter pylori and its association with gastrointestinal disease has originated from secondary care. This review summarizes the role of H pylori in dyspepsia from the perspective of primary care and suggests a new strategy for the management of dyspeptic patients in this setting. Recent meta-analyses and consensus statements have supported the use of eradication therapy as first-line treatment of peptic ulceration. Studies from primary care have supported the use of eradication therapy in patients who have H pylori related peptic ulcer disease and require long-term H2-antagonist medication, on both clinical benefit and cost-effectiveness grounds. Of the many regimens proposed for the eradication of H pylori, the best evidence supports a triple combination of bismuth, metronidazole and tetracycline. Regimens using proton pump inhibitors may be more acceptable to patients but lack good evidence from trials. Use of a positive serum enzyme-linked immunoabsorbent assay for H pylori antibodies as a criterion for endoscopic investigation has been shown to result in a 23% reduction in endoscopic workload. Further research should answer questions of importance to general practitioners, such as the role of eradication therapy in patients with nonulcer dyspepsia and the effectiveness of eradication of H pylori in the prevention of gastric cancer.
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PMID:Role of Helicobacter pylori in gastrointestinal disease: implications for primary care of a revolution in management of dyspepsia. 874 55

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

Helicobacter pylori has been identified as a major factor in duodenal ulcerogenesis. After H pylori eradication, the recurrence rate of duodenal ulcers falls dramatically and cure of this chronic relapsing disease has been claimed by several authors. H pylori eradication was first attempted with bismuth salts alone or with antibiotics. H2-receptor antagonists are not effective against H pylori, although proton pump inhibitors such as omeprazole and lansoprazole are active in vitro against H pylori. Their minimum inhibitory concentration is close to that of the imidazoles (metronidazole, tinidazole): proton pump inhibitors and imidazoles have common structural features. Consequently, lansoprazole has been tested in monotherapy and triple therapy. In monotherapy, the H pylori clearance rate with lansoprazole 30 mg during 4 weeks was 40% in our study and 19% in a study by Jhala et al. No eradication was achieved. These results were in agreement with those of another proton pump inhibitor. In triple therapy, two studies used the same regimen in nonulcer dyspepsia patients: lansoprazole 30 mg/day for 2 weeks, amoxicillin 2 g/day for 2 weeks, and tinidazole 1 g/day for 2 weeks. Pooled data from these two French trials show that H pylori eradication was achieved in 14/17 patients (82.4%). Lansoprazole administered concomitantly with two antibiotics is effective in the eradication of H pylori and is as effective as other triple therapy regimens with bismuth salts, or with other proton pump inhibitors. One of the most important problems is metronidazole resistance of H pylori strains. Antibiotics such as new macrolides (clarithromycin or roxithromycin) should be tested in a triple therapy regimen against H pylori strains with lower primary resistance.
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PMID:Effect of lansoprazole on Helicobacter pylori. 820 93

Antacids have for long been regarded as the mainstay of pharmacologic therapy in patients with dyspepsia. The advent of the histamine H2-antagonist and of proton pump inhibitors has provided simpler and overall more efficient therapeutic modalities for severe forms of dyspepsia. This relates especially to aggressive forms of peptic ulcer disease and severe reflux oesophagitis, where even high dose histamine H2-antagonist therapy has its clear limitations. Antacids nevertheless continue to be widely used in less severe forms of dyspepsia, especially in patients suffering from heartburn. In such patients self medication of antacids as first therapeutic measure is still very common. This is well exemplified by an American nd British survey. Out of 6760 randomly selected British general practice patients 875 suffered from reflux-like symptomatology without having consulted their physician for the symptomatology for minimum one year. Antacids were taken by 61% of them. The advent of controlled endoscopic trials and the emergence of the H2-receptor blockers as a yardstick of ulcer therapy, however, facilitated reappraisal of the value of antacids in various conditions. This has given a clear-cut answer in well defined entities such as peptic ulcer disease and stress ulcer prophylaxis but has left many open questions in heterogeneous conditions especially in and around gastroesophageal reflux disease.
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PMID:Clinical use of antacids. 826 Jul 36

Although dyspeptic symptoms are very common, the vast majority of patients have modest symptoms and rarely seek medical advice. The major organic causes of dyspepsia are chronic peptic ulcer disease, gastro-oesophageal reflux disease and malignancy. Functional dyspepsia is very common. In the fit elderly patient, prompt investigation may be more appropriate than empirical treatment in view of the higher proportion of patients with organic disease and the likelihood of malignancy. The symptoms of peptic ulceration and gastro-oesophageal reflux disease are often atypical in the elderly population. Frail patients, especially those with multiple pathology, should be treated empirically in the first instance. Empirical treatment should be with histamine H2-receptor antagonists or prokinetic agents. Drug treatment is not always required in dyspepsia and should be avoided where possible, especially given the increased risk of drug interactions and poor compliance in the elderly. For those patients with documented non-malignant organic disease, the advent of the H2-receptor antagonists, proton pump inhibitors, prokinetic drugs and regimens which eradicate Helicobacter pylori means that treatment is almost always successful.
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PMID:Diagnosis and treatment of dyspepsia in the elderly. 857 90

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

Gastrointestinal involvement occurs in most patients with systemic sclerosis and is subclinical in about one third. Early pathology is characterized by vasculopathy, resulting in tissue ischemia and progressive dysfunction. Noninvasive esophageal studies using semisolid bolus scintigraphy are sensitive but lack specificity. Long-term treatment of reflux with high-dose proton pump inhibitors appears safe and effective for symptom relief and may prevent recurrence of esophagitis and stricture. Dyspepsia may result from gastroparesis and antral distension. Gastric antral vascular ectasia is a vascular manifestation, and bleeding may be controlled endoscopically. Prokinetic agents effective in pseudoobstruction include metoclopramide, domperidone, cisapride, octreotide, and erythromycin. Patients with intestinal neuropathy or response to bolus octreotide are more probable long-term responders. The combination of octreotide and erythromycin may be particularly effective in systemic sclerosis. The combination of cisapride and erythromycin may cause serious cardiac arrhythmia and is contraindicated. Omeprazole may predispose to small intestinal bacterial overgrowth. Malabsorption not responding to antibiotic therapy should be investigated with small-bowel biopsy to rule out more unusual causes. Pneumatosis cystoides intestinalis may be due to excessive hydrogen production by intestinal bacteria altering the partial pressure of nitrogen in the intestinal wall. In selected cases, surgery for intestinal failure is an option with resection or bypass of affected segments or placement of enterostomy tubes for feeding or decompression. Careful preoperative characterization of intestinal segments is required.
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PMID:Gastrointestinal features of scleroderma. 901 61

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


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