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)

In a retrospective study of 195 patients with a perforated peptic ulcer 18 per cent of the patients had taken aspirin, phenylbutazone or corticosteroids during the period before the perforation. In a controlled prospective trial, 18 of 22 patients (82 per cent) had taken drugs known to be potentially harmful to the stomach. Aspirin was the drug mainly used. Thirteen of 22 patients had taken the drugs within 12 hours of the perforation, usually because of symptoms not related to the gastro-intestinal tract. Drug consumption and perforation of pre-pyloric ulcers were most closely associated; the latter applies particularly to female patients, who either had only a short history of upper gastro-intestinal dyspepsia or were asymptomatic.
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PMID:Drug consumption before perforation of peptic ulcer. 85

Data from the early stages of the thrombosis prevention trial (TPT) have been used to establish and quantify the risk of extracranial bleeding due to low dose aspirin (75 mg) and low intensity oral anticoagulation with warfarin (international normalised ratio, INR, 1.5) singly or in combination, in men aged between 45 and 69 who are at high risk of ischaemic heart disease (IHD). The design of the trial is factorial, the four treatments being combined low dose aspirin and low intensity anticoagulation (WA), low intensity anticoagulation alone (W), low dose aspirin alone (A) and double placebo treatment (P). The trial is being carried out through the Medical Research Council's General Practice Research Framework, with participating practices throughout the United Kingdom. Results are based on the first 3,667 men entered. The risk of major gastrointestinal bleeding due to active treatment is probably about 1 in 500 man-years of treatment, there currently being no difference between the three active regimes (WA, W, A). Intermediate and minor bleeding episodes occur more frequently with WA than with W or A on their own, the excess being mainly due to minor nose bleeds and bruises. In turn, both W and A on their own cause more such minor episodes than placebo treatment, P. There is no evidence that any of the three active regimens increases the risk of peptic ulceration, nor do they increase reports of indigestion. Aspirin increases reports of constipation and reduces reports of blurred vision. Minor bleeding occurs less frequently in smokers than in non-smokers but is not influenced by age. The antithrombotic regimes used are feasible and acceptable.
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PMID:Extra-cranial bleeding and other symptoms due to low dose aspirin and low intensity oral anticoagulation. 151 66

Aspirin-induced hypersensitivity affects a substantial number of people, including 20% or more of asthmatic patients. A dramatic flare of symptoms occurs after indigestion of aspirin or a nonsteroidal anti-inflammatory drug, and symptoms can persist even after the agent is discontinued. Fortunately, aspirin desensitization, as described by the authors, now appears to be a treatment option.
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PMID:Aspirin sensitivity. A distressing reaction that is now often treatable. 192 10

Two hundred and sixty-four patients were included in an open, randomized, multicenter trial, with the aim of determining whether nicardipine can be useful in the prevention of cerebral infarction. The patients had experienced one or more transient ischemic attacks, reversible ischemic neurologic defect, or stroke with minor permanent neurological deficit in the 12 months before enrolling in the study. Each patient was randomly assigned to received 250 mg of aspirin once daily plus 20 mg of nicardipine thrice daily (n = 170) or 250 mg of aspirin once daily (n = 94) for 12 months. During the 12-month treatment period, 12% of the aspirin-plus-nicardipine group and 19% of the aspirin-only group experienced an ischemic cerebrovascular event; at six months, the cumulative incidence of events was significantly lower in the aspirin-plus-nicardipine group than in the aspirin-only group. One patient in each group died of a recurrent stroke. Aspirin-related side effects were dyspepsia (reported by four patients), heartburn (by seven), nausea and vomiting (by four), and melena (by five); nicardipine-related side effects were transient hypotension (by two), headache (by four), ankle edema (by three), and constipation (by four). Results indicate that the addition of nicardipine to antiplatelet treatment may safely prevent the recurrence of ischemic cerebrovascular events.
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PMID:Nicardipine in the prevention of cerebral infarction. 222 48

Upper gastrointestinal tract symptoms are common in the elderly and, despite a paucity of data, nonsteroidal antiinflammatory drugs (NSAIDs) are believed to be important risk factors. We aimed to evaluate the association of NSAIDs with dyspepsia and heartburn in a population-based study. An age- and gender-stratified random sample of Olmsted County, Minnesota, Caucasian residents aged 65 years and older was mailed a valid self-report questionnaire; 74% responded (N = 1375). Age- and gender-adjusted (to 1980 US Caucasian population) prevalence rates for NSAID use, dyspepsia (defined as pain located in the upper abdomen or nausea), and heartburn (defined as retrosternal burning pain) were calculated. Logistic regression analysis was used to estimate the association of dyspepsia and heartburn with potential risk factors adjusting for age and gender. The age- and gender-adjusted annual prevalences (per 100) of aspirin and nonaspirin NSAID use were 60.0 (95% CI 57.2, 62.7) and 26.1 (95% CI 23.6, 28.7), respectively. The annual prevalences of dyspepsia and heartburn were 15.0 (95% CI 12.9, 17.0) and 12.9 (95% CI 10.9, 14.8), respectively. Aspirin was associated with dyspepsia and/or heartburn (OR = 1.6, 95% CI 1.2, 2.2) as were nonaspirin NSAIDs (OR = 1.8, 95% CI 1.3, 2.6), but smoking and alcohol were not significant risk factors. Aspirin and nonaspirin NSAIDs are associated with almost a twofold risk of upper gastrointestinal tract symptoms in elderly community subjects.
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PMID:Nonsteroidal antiinflammatory drugs and dyspepsia in the elderly. 867 3

Aspirin and non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs) almost invariably cause acute gastroduodenal injury and probably account for approximately 12,000 ulcer bleeding episodes and 1200 deaths per annum in the United Kingdom. Clinically significant intestinal toxicity is also recognized but less clearly defined. The main risk factors for NSAID-related peptic ulcer complications are age, past history, use of higher risk individual NSAIDs, drug dose, concurrent use of warfarin or corticosteroids. The underlying reason for NSAID use and Helicobacter pylori status is not clearly associated with increased risk. Whether NSAIDs cause drug-induced non-ulcer dyspepsia is also controversial. Acute injury occurs more readily with aspirin than with non-aspirin NSAIDs, and the spectrum of acute injury is of little value in predicting clinically significant end points in comparison with different NSAIDs. However, acute studies of co-prescribed protective agents are highly predictive of performance in clinical practice. Gastric mucosal integrity is maintained by the interplay of three protective networks: prostaglandin synthesis, nitric oxide synthesis and the activity of the enteric nervous system. Aspirin and NSAIDs act by inhibiting prostaglandin synthesis catalysed by two cyclooxygenase enzymes. Most existing NSAIDs are unselective and inhibit the activity of the constitutive cyclooxygenase (COX) 1 enzyme in the stomach as much as the cyclooxygenase (COX) 2 enzyme which is induced at sites of inflammation such as joint disease. There are, however, prospects for selective cyclooxygenase 2 inhibitors. Some NSAIDs, particularly aspirin, have additional topical toxicity, which may in part reflect mucosal trapping. Some data favor an effect of NSAIDs in inhibiting mitochondrial oxidative phosphorylation. The principal physiological mechanisms which are compromised by NSAID use are mucosal blood flow, secretion of mucus and bicarbonate and maintenance of a hydrophobic mucosal surface. Animal data suggest that polymorphonuclear leukocytes (PMNs) are important for acute damage though the relevance to humans has yet to be established. As well as damaging the mucosa, NSAIDs impair ulcer healing and are associated with reduced epithelial proliferation and evidence of diminished angiogenesis. An interaction between prostaglandins and growth factors, as well as the synthesis of antiproliferative products of arachidonic acid metabolism may be involved. Healing of NSAID ulcers by conventional doses of H2 antagonists is slow and H2 antagonists are poor at preventing gastric ulcer development or recurrence. These problems can be overcome by the use of more potent acid suppression. Misoprostol heals NSAID-associated ulcers, though whether healing is as fast as with non-NSAID ulcers has not been formally established. Misoprostol is effective prophylactic treatment but has a significant incidence of adverse events, particularly diarrhoea. Misoprostol has been reported to prevent ulcer complications, and in endoscopic studies has been superior as prophylaxis to standard dose ranitidine. Results of its efficacy compared to proton-pump inhibitors are awaited. For many patients appropriate management is avoidance of NSAIDs or use of less potent/toxic alternatives such as ibuprofen. Reductions in prescribing arising from a prior authorization scheme show that this can be achieved. For high-risk patients requiring continuing NSAID use co-prescription of omeprazole or misoprostol should be considered.
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PMID:Non-steroidal anti-inflammatory drug gastropathy: causes and treatment. 889 49

A six-week placebo-controlled trial of the efficacy and safety of 6 g per day of 4-aminosalicylic acid (4-ASA) was conducted in 30 subjects with mild to moderately severe ulcerative colitis. Subjects were stratified into groups having distal (< 60 cm) or more extensive (> 60 cm) disease. Diarrhea, bleeding, sigmoidoscopic and biopsy appearance, and physician global assessment were scored to judge efficacy. Safety was evaluated by monitoring untoward symptoms and laboratory values. Median percent improvement was significantly greater (P < 0.05) in the 4-ASA > 60-cm group (42.7%) than in the placebo > 60-cm group (21.2%), but 4-ASA was not better than placebo for the < 60-cm group or the total study group. Severe dyspepsia (one subject), abnormal AST (transient in five, persistent in one) and elevated lipase without pancreatitis (six subjects) were noted. Thus 6 g 4-ASA for six weeks was more effective than placebo in mild to moderate ulcerative colitis extending more than 60 cm above the anus, but not in distal disease, and the drug was generally well tolerated.
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PMID:Controlled trial of 4-ASA in ulcerative colitis. 905 19

The IARC convened a Working Group of experts in Lyon, France, on April 2-8, 1997 to evaluate the cancer-preventive activity of four nonsteroidal anti-inflammatory drugs (aspirin, sulindac, piroxicam, and indomethacin). Epidemiological observational studies of aspirin that differed in design, location, population, and motivating hypothesis have consistently shown that regular use lowers the risk for colorectal cancer by up to 50%; however, the one randomized trial did not show protection by aspirin. Definite evidence of chemopreventive activity normally requires data from appropriately designed randomized trials. The strength of the scientific evidence that aspirin prevents colorectal cancer in humans was thus considered to be limited. In animal models, there was sufficient evidence that aspirin prevented against cancer. Aspirin and aspirin-like drugs may have an important adverse side effects, the most frequent of which are gastrointestinal disturbances ranging in severity from dyspepsia to peptic ulcer. Given the remaining uncertainties in the preventive effect and the risk of adverse side effects, detailed consideration of the total benefits and of toxicity will be required before widespread use of aspirin for the prevention of colorectal cancer can be recommended. Sulindac shows promise in reducing the number and size of adenomatous polyps in patients with familial adenomatous polyposis. Further research is required, however, to determine whether and to what extent the risk for colorectal cancer in such patients is reduced. In people without familial adenomatous polyposis, there is inadequate evidence that sulindac has cancer-preventive activity. Fewer data were available on piroxicam and indomethacin than on aspirin and sulindac. Although these drugs consistently prevent colorectal cancers in experimental animal models, the evidence that they prevent colorectal cancer in humans was considered to be inadequate. The results of the meeting, including recommendations for future research, will be published as Volume 1 of the IARC Handbooks of Cancer Prevention.
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PMID:An international evaluation of the cancer-preventive potential of nonsteroidal anti-inflammatory drugs. 929 84

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

Despite limited understanding of therapeutic aetiopathogenesis of ulcerative colitis and Crohn's disease, there is a strong evidence base for the efficacy of pharmacological and biological therapies. It is equally important to recognise toxicity of the medical armamentarium for inflammatory bowel disease (IBD). Sulfasalazine consists of sulfapyridine linked to 5-aminosalicylic acid (5-ASA) via an azo bond. Common adverse effects related to sulfapyridine 'intolerance' include headache, nausea, anorexia, and malaise. Other allergic or toxic adverse effects include fever, rash, haemolytic anaemia, hepatitis, pancreatitis, paradoxical worsening of colitis, and reversible sperm abnormalities. The newer 5-ASA agents were developed to deliver the active ingredient of sulfasalazine while minimising adverse effects. Adverse effects are infrequent but may include nausea, dyspepsia and headache. Olsalazine may cause a secretory diarrhoea. Uncommon hypersensitivity reactions, including worsening of colitis, pancreatitis, pericarditis and nephritis, have also been reported. Corticosteroids are commonly prescribed for treatment of moderate to severe IBD. Despite short term efficacy, corticosteroids have numerous adverse effects that preclude their long term use. Adverse effects include acne, fluid retention, fat redistribution, hypertension, hyperglycaemia, psycho-neurological disturbances, cataracts, adrenal suppression, growth failure in children, and osteonecrosis. Newer corticosteroid preparations offer potential for targeted therapy and less corticosteroid-related adverse effects. Azathioprine and mercaptopurine are associated with pancreatitis in 3 to 15% of patients that resolves upon drug cessation. Bone marrow suppression is dose related and may be delayed. The adverse effects of methotrexate include nausea, leucopenia and, rarely, hypersensitivity pneumonia or hepatic fibrosis. Common adverse effects of cyclosporin include nephrotoxicity, hypertension, headache, gingival hyperplasia, hyperkalaemia, paresthesias, and tremors. These adverse effects usually abate with dose reduction or cessation of therapy. Seizures and opportunistic infections have also been reported. Antibacterials are commonly employed as primary therapy for Crohn's disease. Common adverse effects of metronidazole include nausea and a metallic taste. Peripheral neuropathy can occur with prolonged administration. Ciprofloxacin and other antibacterials may be beneficial in those intolerant to metronidazole. Newer immunosuppressive agents previously reserved for transplant recipients are under investigation for IBD. Tacrolimus has an adverse effect profile similar to cyclosporin, and may cause renal insufficiency. Mycophenolate mofetil, a purine synthesis inhibitor, has primarily gastrointestinal adverse effects. Biological agents targeting specific sites in the immunoinflammatory cascade are now available to treat IBD. Infliximab, a chimeric antibody targeting tumour necrosis factor-or has been well tolerated in clinical trials and early postmarketing experience. Additional trials are needed to assess long term adverse effects.
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PMID:Comparative tolerability of treatments for inflammatory bowel disease. 1108 48


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