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)

Since the mid-seventies, it is possible to treat peptic ulcers and reflux oesophagitis with acid secretion inhibitors. The most important medicaments are H2-receptor antagonists (cimetidine was registered in 1977) and proton pump inhibitors (1988: omeprazole). Surgical treatment of these conditions is almost a thing of the past. Many Dutch researchers played an important part in clinical research of acid secretion inhibitors; the first studies of effect and safety were done in patients with severe overproduction of gastric acid (Zollinger-Ellison syndrome) and in those with severe reflux oesophagitis. At present the most important syndromes in which acid secretion inhibitors are used are gastroesophageal reflux disease, gastric or duodenal ulcers and acid-related dyspepsia.
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PMID:[25 years of gastric acid blockers]. 1062 49

Proton pump inhibitor (PPI)- based triple therapy has been a recent trend for treatment of Helicobacter pylori infection, with the PPI-amoxicillin-clarithromycin (PPI/AC) regimen being one of the most popular. We have reported the effectiveness of PPI/AC regimens in the Japanese population and have demonstrated that the effectiveness of 40 mg rabeprazole, a recently developed PPI, is similar to that of 40 mg of omeprazole and 60 mg of lansoprazole when used in combination with amoxicillin and clarithromycin. In this study, we focused on whether 20 mg of rabeprazole is effective in our patient population by comparing that dosage with 40 mg of rabeprazole and 60 mg of lansoprazole. In all, 308 H. pylori-infected patients [236 men and 72 women; age (mean +/- SEM) 49.3+/-0.6 years] with peptic ulcer disease (N = 270) or nonulcer dyspepsia (N = 38) were randomly assigned to one of three different PPI/AC regimens for seven days: LAC (N = 104), consisting of lansoprazole 30 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day; RAC (N = 104), consisting of rabeprazole 20 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day; and the R1/2AC regimen (N = 100), which included rabeprazole 10 mg twice a day, amoxicillin 500 mg three times a day, and clarithromycin 200 mg twice a day. Cure of the infection was determined by the [13C]urea breath test one month after completion of the treatment. Intention-to-treat based and per-protocol based cure rates for the LAC, RAC, and R1/2AC regimens were 82.7 (95% CI, 74-89) and 88.7% (81-94), 85.6 (77-92) and 89.8% (82-95), and 87.0 (79-93) and 89.7% (82-95), respectively. Although adverse effects were reported by 20.3% of the patients, these affected compliance in only five patients in the RAC and LAC regimens and none in the R1/2AC group. Overall complete compliance was achieved in 94.7% of interviewed patients. In conclusion, the effectiveness of the PPI/AC regimen with 20 mg of rabeprazole is comparable with and even safer than that of 40 mg of rabeprazole and 60 mg of lansoprazole in our patient population.
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PMID:Efficacy of reduced dosage of rabeprazole in PPI/AC therapy for Helicobacter pylori infection: comparison of 20 and 40 mg rabeprazole with 60 mg lansoprazole. 1069 17

In-depth meetings of the XIth International Workshop on Gastroduodenal Pathology and Helicobacter pylori led to the presentation and discussion of extensive new data on H. pylori and its diseases. The mode of transmission of H. pylori remains unclear, and it remains unknown why only a small proportion of infected individuals develop duodenal or gastric ulcer disease and even fewer develop gastric cancer. The role of H. pylori eradication in persons with uninvestigated dyspepsia remains controversial. New clinical trials of H. pylori treatment show symptom relief and improvement in the quality of life of persons with functional dyspepsia, especially in those with ulcer-like or reflux-like dyspepsia. Clearly the move is toward symptom-based management of persons with dyspepsia, with fewer endoscopies being needed in the otherwise healthy young dyspeptic patients. It remains controversial whether eradicating H. pylori in duodenal ulcer or functional dyspepsia increases the risk of subsequent development of gastroesophageal reflux disease. The one-week proton pump inhibitor-based triple regimens remain the gold standard of H. pylori therapy, but some of the ranitidine bismuth citrate plus two antibiotic regimens also achieve an 80% H. pylori eradication rate on an intention-to-treat basis. While the urea breath test remains the noninvasive test of choice, interesting new data are available on the use of stool antigen testing to diagnose H. pylori infection. The number of H pylori-associated gastroduodenal diseases grows to include possible liver, vascular, immune and skin conditions.
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PMID:From bench to bedside to bug: an update of clinically relevant advances in the care of persons with Helicobacter pylori- associated diseases. 1075 16

Recognition of Helicobacter pylori (Hp) as the major cause of peptic ulcer disease has profoundly changed treatment and prognosis of this disease. The diagnostic tests are invasive (i.e. via the endoscopy) or non-invasive. The invasive tests are: urease test, histology, culture and PCR. Non invasive tests are: breath test, serology and Hp-antigens in faeces. The performance of the tests are almost similar. Sensitivities and specificities usually are > 90%, however the sensitivities and specificities of serological tests may be lower. Choice of diagnostic test depends on the clinical situation, sensitivity and specificity of test and the prevalence of Hp. Patients who should be examined for Hp: 1. The peptic ulcer patient who has used ASA/NSAID (urease test). 2. MALT-lymphoma, (histology). 3: The young (< 45 years) dyspeptic patient with no alarm symptoms and not taking NSAID/ASA (breath test). 4. Recurrence of upper dyspepsia after former eradication of Hp in peptic ulcer patients (if malignancy is not suspected breath test is first choice). 5. Verification of Hp eradication is necessary only in patients with MALT-lymphoma (histology) or patients with complicated peptic ulcer. Breath test will be the first choice in patients with complicated peptic ulcer when endoscopy is not performed. When endoscopy is performed, the urease test is the first choice. Diagnosis of Hp status not indicated: 1. There is no documentation that Hp eradication is of benefit in patients with non organic dyspepsia. Therefore, there is no indication for diagnosis of Hp. 2. Although there is some association between Hp positivity and chronic active gastritis and carcinoma of the stomach, there is at present no indication for diagnosis of Hp, as treatment of the infection has not proved effective in reversing atrophy or dysplasia. 3. The relationship between Hp and ASA/NSAIDs in peptic ulcer disease is far from clear. There is no indication for diagnosis and treatment of the infection prior to treatment with these medications. 4. For patients treated with longterm proton pump inhibitors there is no indication for diagnosis and treatment.
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PMID:[Diagnosis of Helicobacter pylori infections--how, when and in whom?]. 1101 47

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used successfully by many patients for the treatment of the signs and symptoms of arthritis, and other painful and inflammatory disorders. However, traditional nonselective NSAIDs that inhibit COX-1 and COX-2 lead to a state of propensity for gastric and duodenal ulcer disease and ulcer complications. The point prevalence of endoscopic ulcers ranges from 14 to 44% of patients using NSAIDs. Moreover, it is estimated that 1.46-1.90% of chronic NSAID users develop serious upper gastrointestinal (UGI) toxicity annually, most notably UGI bleeding, gastric/duodenal obstruction or ulcer perforation. In the USA, it has been estimated that 107,000 hospitalisations and 16,500 deaths occur annually related to the use of nonselective NSAIDs. Because these ulcer complications are often not heralded by chronic symptoms of dyspepsia, symptoms alone are not sufficient to guide long-term management of NSAID-related toxicity. Instead, prophylactic and preventive therapies are recommended in patients at above-average and high risk. Epidemiological data have identified that patients with a past history of ulcer disease, past history of UGI bleeding, greater age, concomitant corticosteroid use, and those who use higher doses and multiple NSAIDs fall into this category. Other risk factors of lesser importance have also been identified. A controversial issue remains regarding the possible increased risk of NSAID-associated ulcers and ulcer complications in patients who are infected with Helicobacter pylori. Prophylactic therapies have been evaluated primarily in randomised clinical trials, with the rate of endoscopic ulcers as the primary endpoint. It is assumed, but not proven, that these endoscopic ulcer rates are surrogate markers for gastrointestinal toxicity and are predictive of the rate of significant UGI adverse events. In the only outcomes trial to date, it was reported that misoprostol (200 microg 4 times daily) caused an approximately 50% reduction in serious UGI adverse events in a large 6-month trial involving rheumatoid arthritis patients. In parallel, this approximates the 50% reduction of endoscopic ulcers seen in randomised controlled trials using misoprostol. While H2 receptor antagonists are ineffective agents at traditional doses, proton pump inhibitors have been clearly shown to reduce the rate of endoscopic ulcers in several trials. In fact, the efficacy approximates to the efficacy seen with misoprostol. Beyond efficacy and in practical terms, the choice of optimal prophylaxis should take into consideration patient compliance, patient satisfaction, side-effects and cost.
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PMID:Who needs prophylaxis of nonsteroidal anti-inflammatory drug-induced ulcers and what is optimal prophylaxis? 1092 93

Although Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) both cause peptic ulcers, they do so by different mechanisms so any interaction is not necessarily harmful. H. pylori has been shown to enhance gastric mucosal prostaglandin synthesis, while NSAIDs suppress it Pragmatically, there is no compelling evidence in favour of H. pylori eradication in all patients who take NSAIDs. As a broad generalisation, in therapeutic studies of NSAID users, those who have no ulcer at trial entry are more prone to ulcer development if they are H. pylori-positive. By contrast, in those who have ulcers at baseline, H. pylori-positive individuals are less likely to develop ulcers, particularly if taking acid-suppressive therapy. Trials of H. pylori eradication therapy tend to replicate this dichotomy. In one study of patients starting NSAIDs for the first time, with no ulcer history and no baseline ulcer, use of bismuth-based eradication therapy was associated with a lower incidence of gastric ulcer at 2 months. Conversely, in a study of patients with endoscopically proven ulcers and/or troublesome dyspepsia, proton pump inhibitor based eradication treatment had no effect on outcome (of acid suppression) over 6 months. H. pylori eradication has been associated with significantly slower healing of gastric ulcers compared with patients who did not undergo eradication. However, the effect of H. pylori eradication on healing of NSAID-associated duodenal ulcers does not appear to be so dramatic, and limited evidence suggests that it may be possible to prevent H. pylori-associated duodenal ulcer by eradicating the infection. An evidence-based approach to treatment would suggest that NSAID users should undergo H. pylori eradication therapy if they have a duodenal ulcer, whether or not they continue NSAIDs. Because COX-2 inhibitors appear not to be ulcerogenic, management of H. pylori in patients taking these drugs can be based upon the same risk assessment as in patients not taking anti-arthritis drugs. H. pylori eradication should not be used universally or in high-risk gastric ulcer patients who require management with acid suppression.
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PMID:What consideration should be given to Helicobacter pylori in treating nonsteroidal anti-inflammatory drug ulcers? 1092 94

By inhibiting prostaglandin synthesis, nonsteroidal anti-inflammatory drugs (NSAIDs) compromise gastroduodenal defense mechanism including blood flow and mucus/bicarbonate secretion. This has led to NSAIDs being the most widely reported drug cause of adverse events. While NSAIDs also cause dyspepsia, inhibition of prostaglandin synthesis may reduce this from even higher levels that would otherwise prevail and mask ulcer-related dyspepsia, making anticipatory management difficult. On average, the risk of ulcer complications increases 4-fold, resulting in 1.25 additional hospitalizations per 100 patient-years according to one estimate. Older patients, those with a past history, and those taking anticoagulants or corticosteroids are at higher risk. Risk is dose dependent and is lower with ibuprofen at low doses than with other NSAIDs. It is unlikely that Helicobacter pylori increases the risk, and under some circumstances it may be protective. Selective inhibitors of the inducible cyclooxygenase 2 spare gastric mucosal prostaglandin synthesis and do not damage the gastric mucosa. Their place in therapy, compared with use of misoprostol or proton pump inhibitors, is currently emerging. Future competitors may include nitric oxide-donating, zwitterionic, or R-enantiomer NSAIDs.
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PMID:Nonsteroidal anti-inflammatory drug gastropathy. 1093 Mar 88

General practitioners must prescribe cost effectively to control drug expenditure and provide optimal treatment for patients requiring long-term management. An audit was implemented in general practices to review the management of dyspepsia, improve care, rationalise therapy and reduce costs. Policy included identifying patients receiving proton pump inhibitor (PPI) therapy and changing to low-dose cost-effective therapy. If PPI therapy was not required, patients were changed to antacids, H2 receptor antagonists or no treatment. This was an audit in general practice, not a clinical trial, therefore findings reflect outcomes in normal clinical practice. This paper describes the implementation and findings of the audit between January 1997 and July 1999 in 91 general practices involving 7121 patients. Extrapolation of the results concluded that savings of up to 50,000 Pounds could be made in a practice of 10,000 patients, allowing reinvestment in health improvement plans and optimal care.
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PMID:Cost-effective prescribing of proton pump inhibitor therapy: an audit in general practice. 1095 54

The Working Party Report on the Management of Helicobacter pylori serves as a clinical practice guideline for Malaysian doctors. H. pylori is not uncommon in the Malaysian population. Marked racial differences and the consistently low prevalence rates amongst Malays are noted. The working party recommends that if endoscopy is to be performed, a rapid urease test should be used for diagnosis. Where suspicion of the infection is strong and the urease test is negative, histology should be performed on gastric biopsies. Culture should be used to monitor resistance patterns to antibiotics and regional laboratories should assume this responsibility. The urea breath tests are highly accurate tests for diagnosis of H. pylori but is as yet not widely available in Malaysia. The working party strongly recommends that all peptic ulcer patients infected with H. pylori whether active, in remission and complicated ulcers should be treated for the infection. Patients with low-grade gastric mucosal lymphoid tissue lymphoma should also be treated for H. pylori infection. It is considered advisable that patients on long term nonsteroidal antinflammatory drug (NSAID) treatment with a history of peptic ulcers or dyspepsia and patients following resection of early gastric cancer or those with a family history of gastric cancer should also be tested and treated for H. pylori. The working party recommends, as first line treatment a 7-day combination therapy of a proton pump inhibitor, clarithromycin and metronidazole or amoxicillin. High metronidazole resistance rates locally may adversely affect regimens containing the antibiotic. It should also be noted that regimens that yield lower eradication rates may result in higher long term expenditure.
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PMID:Management of Helicobacter pylori infection--a Working Party Report of the Malaysian Society of Gastroenterology and Hepatology. 1096 73

The treatment of Helicobacter pylori (H.p.) infection is based on the recommendations of the Maastricht consensus conference 1996. The main indications for eradication of H.p. are peptic ulcer disease, gastritis with severe histological abnormalities, low grade gastric MALT lymphoma and a history of resection for gastric cancer. The results of recent studies demonstrate that the symptoms of non-ulcer dyspepsia are not improved by H.p. eradication. A family history of gastric cancer and an earlier operation for peptic ulcer are considered advisable indications for the treatment of H.p. infection. Triple therapies consisting of a proton pump inhibitor (PPI) or ranitidine bismuth citrate plus 2 antibiotics are established as effective and well-tolerated first line regimens. The most important antibiotics are clarithromycin and amoxicillin. The efficacy of metronidazole is impaired by an increasing rate of resistant strains. Only few new antibiotics are currently tested in clinical trials. After the failure of a first anti-H.p. treatment it is advisable to change antibiotics according to the probability of resistance, to increase dosage and duration of treatment and to include bismuth compounds in the second line regimen. An alternative option after failed triple therapies may be a high dosage and prolonged dual regimen with a PPI and amoxicillin or quadruple therapy consisting of a PPI, bismuth subcitrate, tetracycline and metronidazole.
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PMID:[Treatment of Helicobacter pylori infections]. 1098 77


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