Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is increasing recognition that nonsteroidal anti-inflammatory drugs (NSAIDs), while quite effective in treating arthritic symptoms, are associated with gastrointestinal mucosal damage. Although therapy for patients with NSAID-induced ulcers or those at high risk of developing them is still a matter of debate, the current literature supports the use of misoprostol as the only drug effective for the prevention of both NSAID-induced gastric and duodenal ulceration. It has also been shown to treat NSAID-induced gastropathy in patients continuing their NSAID therapy. In a study of misoprostol (100 or 200 micrograms QID) plus NSAID, after three months of continuous therapy, a significantly lower frequency of gastric ulcers in the misoprostol-treated group was revealed: 100 micrograms misoprostol, 5.6%; 200 micrograms misoprostol, 1.4%; placebo, 21.7%. A recent three-month, placebo-controlled study established the efficacy of misoprostol 200 micrograms QID in the prevention of NSAID-induced duodenal ulcers in 429 patients with osteoarthritis (OA), rheumatoid arthritis (RA), or other rheumatic disease, who were receiving daily treatment with various NSAIDs. The incidence of duodenal ulcer development over three months was 1.0% in patients treated with misoprostol versus 6.3% in placebo-treated patients (P = 0.004). The same trial also evaluated the efficacy of misoprostol 200 micrograms QID versus placebo in preventing NSAID-induced gastric ulcers. The incidence of gastric ulcer over the three-month treatment period was 1.5% in patients treated with misoprostol versus 9.0% in placebo-treated patients (P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Making sense of NSAID gastropathy and considering the therapeutic options. 134 44

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can cause varying degrees of gastroduodenal mucosal damage. These agents are most frequently used for the treatment of rheumatic diseases because they are highly effective in reducing joint pain and swelling. Histamine H2-receptor antagonists, omeprazole, sucralfate, and misoprostol are drugs available for the treatment of gastric mucosal damage caused by NSAIDs. In controlled clinical studies, all these drugs effectively heal gastric and duodenal injury if NSAIDs are discontinued. However, current data suggest that if NSAIDs are continued while gastrointestinal damage is present, only misoprostol and omeprazole have demonstrated efficacy in healing gastric mucosal injury. Misoprostol also effectively heals NSAID-induced duodenal injury. At this time, no data exist on the efficacy of other antiulcer drugs in healing duodenal erosions or ulceration if NSAID administration is continued. Regarding prevention of NSAID-induced gastric ulcer, controlled clinical studies with H2 antagonists and sucralfate have failed to show any therapeutic benefit. Ranitidine, however, has shown efficacy in preventing NSAID-induced duodenal ulcers. The coadministration of misoprostol with NSAIDs to patients who have either osteoarthritis or rheumatoid arthritis prevents the development of gastric and duodenal ulcers. Based on current published information, this property distinguishes misoprostol from other antiulcer drugs.
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PMID:Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs. 139 9

One hundred sixty-two patients chronically ingesting ibuprofen, piroxicam, or naproxen for osteoarthritis, who had abdominal pain and an endoscopically proven gastric ulcer were evaluated for eight weeks in a randomized, double-blind trial comparing misoprostol (200 micrograms four times daily with meals and at bedtime) (N = 77) with placebo (N = 85). Patients discontinued their usual daily dose of antiarthritic medication throughout the study period, and an endoscopy was performed at four weeks and eight weeks (if necessary) to assess ulcer healing. Gastric ulcers were defined as circumscribed breaks in the gastric mucosa of 0.3 cm in diameter or greater. Misoprostol therapy significantly accelerated the rate of gastric ulcer healing compared to placebo (P = 0.033). The cumulative percent healed after four and eight weeks of therapy for misoprostol versus placebo were: 83% vs 61% at four weeks and 96% vs 90% at eight weeks (P = 0.0028 and P = 0.0977, respectively by lifetable analysis). Relief of abdominal pain did not differ significantly between the treatment groups. Misoprostol significantly accelerates the healing of ibuprofen-, piroxicam-, or naproxen-induced gastric ulcers.
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PMID:Treatment of nonsteroidal antiinflammatory drug-induced gastric ulcers with misoprostol. A double-blind multicenter study. 147 30

Based on an American multicenter study, an economic evaluation of prophylactic misoprostol was undertaken in Sweden. The study included 420 patients with osteoarthritis and nonsteroidal anti-inflammatory drug (NSAID)-associated abdominal pain, but no gastric ulcer at inclusion. The frequency of ulcer development with and without prophylactic misoprostol was assessed at 21.7% and 5.6%, respectively, for a 3-month period. All costs for drugs, ambulatory care, hospital care, loss of production, as well as other factors such as dosage and compliance, were transferred to Swedish conditions. It was concluded that in patients with osteoarthritis and NSAID-induced abdominal pain, prophylaxis with misoprostol is cost-effective in Sweden, which is similar to what is found for other countries. A prerequisite for this result is a frequency of ulcer development of 15%. A patient compliance to prophylactic treatment of more than 60% is also presupposed (79% was observed in the above study). Due to the high age of the osteoarthritis patient population, the cost-effectiveness is influenced to only a minor extent by whether indirect costs are included in the calculation.
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PMID:Cost-effectiveness of misoprostol in Sweden. 162 6

Prostaglandins (PGs) and aluminum-containing antacids (Al.AAs) are effective in preventing gastric and duodenal lesions induced by neutralizing agents. The efficacy of Al.AAs is thought to be due to neutralizing properties and to stimulation of endogenous PGs synthesis. Liquid Maalox has the same effect as cimetidine 400 mg on postprandial duodenal acid load. In numerous prospective studies, Al.AAs have been shown to be as effective as cimetidine in the short-term treatment of duodenal ulcer (DU). Maalox TC at a dosage of 3 tablets b.i.d. provides an effective method for preventing DU relapse. Its effect is similar to that of nighttime cimetidine. Meta-analysis of prospective trials suggests that Al.AAs prevent stress ulcers more effectively than does cimetidine. It has been suggested that Al.AA acts by inducing surface epithelial cell disruption. Al-induced mucosal protection could be caused by a stimulated release of endogenous PGs, induced by Al microcrystal penetration of cells. In a recent study, we showed that small amounts of Al were absorbed by human gastric mucosa and accumulated in lysosomes; however, we did not observe any histological or ultrastructural lesions of the gastric mucosa. Prostaglandins (enprostil, misoprostol, and rioprostil) are as effective as cimetidine, but less effective than ranitidine, in healing DU. Enprostil and rioprostil have been shown to be as effective as ranitidine in treating gastric ulcer (GU). Moreover, enprostil inhibits postprandial gastrin release, whereas H2-blockers increase gastrin levels. Coadministration of misoprostol with aspirin is highly effective in healing aspirin-induced gastroduodenal lesions. Moreover, cotreatment with misoprostol was associated with a marked decrease in GU in patients with osteoarthritis receiving NSAIDs chronically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphologic and ultrastructural effects of Maalox TC on human gastric and duodenal mucosa. 194 Jan 88

A multicenter, double-blind, placebo-controlled trial was undertaken to evaluate the efficacy of the synthetic prostaglandin E1 analog misoprostol in preventing and healing gastric ulcer induced by nonsteroidal antiinflammatory drugs (NSAID) in patients receiving chronic NSAID therapy for osteoarthritis (OA). A total of 420 patients with OA and NSAID-associated abdominal pain who were receiving ibuprofen, piroxicam or naproxen were enrolled in the study. Endoscopy was performed at study entry and after 1, 2 and 3 months of continuous therapy with misoprostol 100 micrograms, misoprostol 200 micrograms or placebo given q.i.d. while NSAID therapy was continued. Treatment failure was defined as development of gastric ulcer (greater than 0.3 cm in diameter). The occurrence of ulcer in each misoprostol group (5.6% and 1.4% for 100 micrograms and 200 micrograms, respectively) was significantly lower (p less than 0.001) than that in the placebo group (21.7%). The statistically significant difference persisted when comparisons were restricted to development of ulcer greater than 0.5 cm in diameter (12.3, 4.2 and 0.7% for placebo, misoprostol 100 micrograms q.i.d. and misoprostol 200 micrograms q.i.d., respectively). Mild-to-moderate, self-limiting diarrhea was the most frequently reported adverse event attributed to misoprostol use.
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PMID:Misoprostol in the prevention of NSAID-induced gastric ulcer: a multicenter, double-blind, placebo-controlled trial. 210 73

This study assesses the economic benefits of misoprostol in the prophylaxis of gastric ulcers larger than 0.3 cm in patients with osteoarthritis receiving non-steroidal anti-inflammatory drugs. Independent epidemiological data were obtained for patients in Scotland and the West Midlands. Co-diagnosis of arthritis with gastric ulcer recorded in the routine data was substantially less (4% Scotland, 10% West Midlands) than the 21% found at case review. These data were combined with cost and patient management data in a decision analysis model to explore whether prophylactic use of misoprostol altered substantially the average cost of managing gastric ulcer. Using conservative assumptions and a daily dose of 400 micrograms, cost savings per patient to the National Health Service of 5-8 pounds over a 3-month period are expected in the groups of patients studied, while at the 800 micrograms dose there would be a net cost of 23-25 pounds. Sensitivity analysis showed that under many assumptions misoprostol is expected to be cost saving or cost neutral.
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PMID:Economic evaluation of gastric ulcer prophylaxis in patients with arthritis receiving non-steroidal anti-inflammatory drugs. 212 Jun 90

Rheumatic complaints, particularly associated with osteoarthritis, are responsible for about one third of all General Practice consultations in people over the age of 65 and non-steroidal anti-inflammatory drugs (NSAIDs) are used on a vast scale for pain relief. Although the individual risk to life is small NSAIDs are the major cause of serious adverse reactions (ADRs) reported to drug regulatory authorities and ADRs are more common and more serious in the elderly. Gastric ulceration, haemorrhage and perforation are the major concern but fluid retention, renal and hepatic failure, asthma, skin reactions, bone marrow suppression and a host of drug interactions can occur. NSAIDs are responsible for a fifth of all admissions to hospital with bleeding or perforated peptic ulcer and thousands of deaths worldwide. Strategies for minimising the risks of ADRs are discussed and emphasis is placed on using minimal analgesic, rather than anti-inflammatory, doses of short-acting NSAIDs and where possible avoiding their use in high risk patients. For the future cytoprotection with prostaglandin analogues may have a role to play.
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PMID:Pain control and the use of non-steroidal analgesic anti-inflammatory drugs. 240 46

Prophylactic use of misoprostol has been found to cause a 15-fold reduction in the rate of gastric ulcer among symptomatic nonsteroidal anti-inflammatory drug users with osteoarthritis. Using data from a variety of sources, we performed a decision analytic-based evaluation of direct medical costs in these patients to determine whether routine prophylactic use of this medication is a preferred strategy over no prophylaxis. The base-case analysis revealed that misoprostol is cost-reducing for the initial 3 months of prophylaxis when the compliance rate is 60%, the silent ulcer rate is 40%, and the medication is priced below $1.74/d (expected costs per patient of approximately $300). The model is highly sensitive to changes in these parameters. Changing the rates of hospitalization and operation have less effect. Reliable estimates of misoprostol's economic impact after the initial 3 months of treatment are impossible to develop with current data. Nonmedical direct costs, patients' out-of-pocket costs, and indirect economic effects, such as work loss, were not considered in the model. All would enhance the economic benefit of the medication. Health care policy makers and payers must consider trade-offs between the clinical and economic implications of preventive medical interventions, such as misoprostol, especially as the call intensifies for more efficient allocation of health care resources.
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PMID:Economic effects of prophylactic use of misoprostol to prevent gastric ulcer in patients taking nonsteroidal anti-inflammatory drugs. 250 6

The fact that nonsteroidal antiinflammatory drugs (NSAIDs) damage the gastroduodenal mucosa is now accepted as NSAID use has been associated with a disproportionately high frequency of upper gastrointestinal bleeding and perforation of gastric and duodenal ulcers. More than 10% of patients receiving NSAIDs chronically will have a gastric ulcer on any given day, a point prevalence of ulcer disease 5-10 times higher than in patients who are not taking NSAIDs. Endoscopic studies comparing the effect of acute administration of NSAIDs on the gastroduodenal mucosa in normal volunteers have failed to predict which NSAIDs would be safest when administered chronically. All of the newer NSAIDs appear to be similar in their propensity to cause chronic mucosal damage, including peptic ulceration. Recent studies have suggested that in those starting NSAID therapy, prophylactic cotreatment with H2-receptor antagonists or sucralfate has minimal or no effect on preventing the development of NSAID-induced gastric ulcers, although duodenal ulcers may be reduced. Nonsteroidal antiinflammatory drug-induced gastric ulcers are also not prevented by drug formulations that prevent or markedly reduce the amount of active NSAID in the stomach. Cotreatment with the synthetic prostaglandin misoprostol was associated with a marked reduction in gastric ulcer development in patients with osteoarthritis receiving NSAIDs chronically, suggesting that prevention of prostaglandin generation in the gastric mucosa may play a pivotal role in NSAID-induced gastric ulcers.
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PMID:Prevention of gastroduodenal injury induced by chronic nonsteroidal antiinflammatory drug therapy. 264 52


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