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)

A double-blind, placebo-controlled study was carried out to see whether the synthetic E prostaglandin, misoprostol, would prevent gastric ulcer induced by non-steroidal anti-inflammatory drugs (NSAIDs). 420 patients with osteoarthritis and NSAID-associated abdominal pain were studied; they were receiving ibuprofen, piroxicam, or naproxen. Endoscopy was done at entry and after 1, 2, and 3 months of continuous treatment with 100 micrograms or 200 micrograms misoprostol or placebo, given four times daily with meals and at bedtime, concurrently with the NSAID. Abdominal pain was rated independently by patients and physicians. A treatment failure was defined as development of a gastric ulcer. Gastric ulcers (0.3 cm in diameter or greater) occurred less frequently (p less than 0.001) in both misoprostol treatment groups (5.6% 100 micrograms and 1.4% 200 micrograms) than in the placebo group (21.7%). The significant difference in ulcer formation between the placebo and the misoprostol treatment groups remained when comparisons were restricted to ulcers greater than 0.5 cm in diameter (12.3% placebo, 4.2% 100 micrograms misoprostol, and 0.7% 200 micrograms misoprostol). Mild to moderate, self-limiting diarrhoea was the most frequently reported adverse effect attributed to misoprostol. These results provide the first clear indication that NSAID-induced ulcers are preventable.
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PMID:Prevention of NSAID-induced gastric ulcer with misoprostol: multicentre, double-blind, placebo-controlled trial. 290 6

110 patients with benign gastric ulcer and concomitant joint diseases (rheumatoid arthritis, osteoarthrosis) were treated in a comparative short-term clinical trial to assess the relative efficacy of calcitonin (daily 100 MRC of salmon calcitonin intramuscularly), cimetidine (daily 1000 mg orally) and colloidal bismuth subcitrate (De-Nol-four times a day in doses of 5 ml diluted with 15 ml of water). Groups of patients were comparable according to age, sex, duration of ulcer disease, smoking habits, gastric acid secretion and mean ulcer size. The ulcer healing was controlled endoscopically after 2 and 4 weeks of the treatment. There was no significant difference in the ulcer healing rate between three groups neither after 2 weeks (calcitonin-36.7% of healed ulcers, cimetidine-37.5% and De-Nol-35.0% nor after 4 weeks respectively (76.7%, 72.5% and 77.5%). In the calcitonin group a gradual joint pain relief was observed in 84% of patients who complained arthralgia. The moderate side effects (headache, nausea, flush) were observed only in the patients treated with calcitonin (8 subjects). We suggest that calcitonin may be considered as a valid anti-ulcer drug in the peptic ulcer patients with concomitant rheumatological diseases especially with osteoporosis.
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PMID:Calcitonin versus cimetidine or De-Nol in gastric ulcer treatment. An endoscopically controlled trial. 307 78

During the long-term administration of nonsteroidal anti-inflammatory drugs (NSAIDs), approximately 3% of patients have gastric ulcers develop in each year. Although much is known about the endoscopic characteristics of NSAID-induced gastric ulcers in patients with rheumatoid arthritis (RA), it is not clear where in the stomach NSAIDs induce ulcers in patients without RA. We looked at that question. During the 1-year study period, 29 patients with gastric ulcer, who had been taking NSAIDs regularly for more than 4 weeks mainly for osteoarthritis, were identified. Seventy-five patients with gastric ulcers who had not taken NSAID also were found. The sites of gastric ulcers of these two groups were quite different. The NSAID-induced ulcers mainly were found in the gastric antrum, whereas the majority of NSAID-unrelated ulcers were in the gastric corpus. We conclude that NSAID-induced ulcers in non-RA patients mainly are formed in the gastric antrum.
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PMID:Intragastric distribution of nonsteroidal anti-inflammatory drug-related ulcers in patients without collagen diseases. 945 69

Misoprostol effectively prevents nonsteroidal anti-inflammatory drugs (NSAID)-induced gastric ulcer and is the only agent currently indicated for this purpose. In addition, misoprostol is effective as prophylaxis against NSAID-induced duodenal ulcer. Because of the widespread use of NSAIDs, the cost of routine misoprostol prophylaxis would be high, and thus its pharmacoeconomic evaluation is an important factor in assessing the most appropriate role of misoprostol in this group of patients. Current cost-benefit analyses undertaken in major European centres and the US have generally indicated that, depending on initial assumptions, misoprostol prophylaxis over a 3-month period is cost-saving in patients with osteoarthritis taking NSAIDs. The net savings (costs) realised were dependent on several variables, including the acquisition cost of misoprostol, silent ulcer rate and patients' compliance. Importantly, misoprostol prophylaxis was consistently more cost-beneficial in elderly patients aged greater than 60 to 65 years than in their younger counterparts. In contrast, in one study misoprostol was found to reduce patients' quality of life and, although misoprostol therapy is potentially cost-saving to society, patients generally preferred no therapy. A single study assessing the cost-effectiveness of misoprostol prophylaxis in preventing ulcerative complications concluded that primary treatment was not an economically viable option for all NSAID users. Misoprostol was most cost-effective in the prevention of recurrent or secondary gastric ulcer complications in 'high-risk' patients, for example patients aged over 60 years and patients with rheumatoid arthritis. Thus, although there are areas of interest awaiting further pharmacoeconomic investigation, misoprostol prophylaxis appears to be cost-effective in elderly and high risk patients receiving NSAIDs. Additionally, misoprostol prophylaxis is cost-saving in elderly patients with osteoarthritis requiring NSAID therapy.
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PMID:Misoprostol: pharmacoeconomics of its use as prophylaxis against gastroduodenal damage induced by nonsteroidal anti-inflammatory drugs. 1014 62

Rheumatoid arthritis (RA) and osteoarthritis (OA) are frequently treated with nonsteroidal anti-inflammatory drugs (NSAIDs). Although NSAIDs are an effective therapy for the pain and inflammation of arthritis, they are associated with serious side effects, particularly ulceration, bleeding, and perforation of the gastrointestinal (GI) tract. In this study, 1826 OA or RA patients who either had been taking NSAIDS for > or =6 months or had been unable to tolerate continuous NSAID use because of adverse GI symptoms or suspected NSAID-related gastroduodenal lesions were examined endoscopically for gastroduodenal lesions and ulcers. At the same time, the patients were asked to rate the severity of any GI symptoms they had been experiencing. Of the total number of patients studied, 817 (44.7%) were OA patients with a mean (+/- SD) age of 55.8+/-12.9 years, and 1009 (55.3%) were RA patients with a mean age of 53.1+/-13.1 years. Clinically significant gastroduodenal lesions were found in 37.1% of patients (n = 678); of these, 24.0% (n = 439) had ulcers. Gastric ulcers were more frequent than duodenal ulcers (14.8% vs 10.2% of patients; P < 0.05), and most gastric ulcers (72.0%) were found in the antrum of the stomach. The prevalence of gastroduodenal ulcers increased with age (P < 0.001), duration of OA (P < 0.001), and duration of current NSAID use (P = 0.019). The prevalence of gastroduodenal ulcers in patients taking NSAIDs for <1 year was 13.8%, compared with a nearly twofold higher prevalence (25.9%) in patients taking NSAIDs for periods of > or =1 year and up to 15 years. The prevalence of gastric ulcers was 32.6% in patients with a history of gastric ulcer but only 13.5% in patients with no GI history (previous gastric ulcer, duodenal ulcer, or upper GI hemorrhage). No relationship was found between the prevalence of gastroduodenal ulcers and sex (men, 22.4%; women, 24.9%) or prevalence of gastroduodenal ulcers and type of arthritic disease (RA, 23.6%; OA, 24.5%). The prevalence of gastroduodenal ulcers increased with the severity of GI symptoms (P = 0.007). These results provide further endoscopic confirmation of the association between NSAID use and gastroduodenal lesions and ulcers and support the contention that safer treatment alternatives to conventional NSAIDs are required.
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PMID:An endoscopic study of gastroduodenal lesions induced by nonsteroidal anti-inflammatory drugs. 1044 Jun 23

Non-steroidal anti-inflammatory drugs (NSAIDs) are indicated for treatment of rheumatoid arthritis and osteoarthritis, but often induce gastric adverse experiences (AE), including gastric ulcers and complications. Inhibitors of proton pump and H(2) antagonists are very effective for duodenal ulcer; meanwhile, cytoprotective drugs are more effective for gastric ulcer. D-002 is a mixture of higher aliphatic alcohols obtained from beeswax, wherein triacontanol is the most abundant. D-002 induces anti-ulcer effects through a cytoprotective mechanism, being more effective in protecting against ethanol- and NSAID-induced ulcers. The present double-blind, placebo-controlled clinical study was undertaken to investigate the effects of D-002 on gastric symptoms associated to piroxicam use on patients suffering osteoarthritis. Fifty-nine patients, all taking piroxicam, 20 mg/day, were randomized to placebo or D-002 (40 or 100 mg/day) for 14 days. The primary efficacy variable was the reduction on the frequency of patients with gastric AE compared with placebo. Pain evolution was investigated to discard any influence on D-002 on the analgesic effect of piroxicam. The frequency of patients treated with D-002, 40 and 100 mg/day, reporting acidity [0 of 18 (0%) and 1 of 21 (4.8%), respectively] was lower (P < .05) than in placebo [6 of 20 (30%)]. Also, the frequency of patients treated with 100 mg/day reporting some gastric AE [5 of 21 (23.8%)] was lower (P < .05) than in placebo [13 of 20 (65.0%)]. The analgesic effect of piroxicam was unaffected with D-002. Treatment was well tolerated. Two patients discontinued from the study because of gastrointestinal AE: one in the placebo group and the other treated with D-002, 40 mg/day. Other three patients discontinued because of other AE: mildly uncontrolled hypertension (one in the placebo group, one treated with D-002, 40 mg/day) and headache (one treated with D-200, 100 mg/day). It is concluded that D-002 could be useful for controlling gastric AE of patients treated with NSAIDs, although further studies with a larger sample size and longer follow-up are needed for definitive conclusions.
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PMID:Effects of D-002, a product isolated from beeswax, on gastric symptoms of patients with osteoarthritis treated with piroxicam: a pilot study. 1585 12

Osteoarthritis (OA) is a costly disease that causes much morbidity and mortality in the world, and it was the sixth leading cause of disability in developed countries. We aim to study the utilization pattern of alternative therapies and their effects on quality of life and personal health spending in Chinese OA patients in Hong Kong. Five-hundred forty-seven patients with OA from four regional hospitals in Hong Kong were recruited, and we measured various types of alternative therapies, SF-36 scales, an overall Health Utility Index derived from a pre-scored multi-attribute classification system based upon SF-36 health surveys, health spending per person and out-of-pocket payments and side-effects. The study shows that out of the 547 OA patients, the patients have used a wide spectrum of alternative therapies and often used a multiplicity of them. Payment for alternative therapies constitutes 5% of the overall personal healthcare spending, and 29% of the out-of-pocket payments. The use of alternative therapies was significantly associated with higher personal healthcare spending (p = 0.01), after adjusting for socioeconomic variables, years of OA and severity of OA. The use of alternative therapies was not significantly associated with an improvement in the quality of life in the regression analysis (p = 0.64). The use of alternative therapies was statistically significant associated with the side effects, including gastric discomfort and gastric ulcer/bleeding (p = 0.04, 0.02, respectively). Alternative therapies were used extensively by OA patients in Hong Kong. Clinicians, health policy makers, and insurance carriers should be aware of the potential health and economic effects in practice and policy formulation.
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PMID:Effects of use of alternative therapies on quality of life and healthcare spending. 1743 59

Celecoxib is a frequently used nonsteroidal anti-inflammatory drug (NSAID) in the treatment of rheumatoid arthritis and osteoarthritis. It selectively inhibits cyclooxygenase II (COX-2) enzyme which is responsible for the production of proinflammatory prostanoids. It has been proposed that since it does not significantly inhibit COX-1, an isoenzyme responsible for the production of cytoprotective prostanoids, celecoxib has fewer side effects in the stomach. Dipyrone which is a drug with potent analgesic activity has no significant inhibitory effect on COX. In this study, the effects of celecoxib and dipyrone on experimentally induced gastric ulcers in rats were compared with respect to different parameters. In the first experiment, in an attempt to identify the best dose for both drugs, a histamine-induced gastric ulcer model was used and each drug was administered at 5, 25 and 100 mg/kg doses, and ulcer index, acidity and mucus secretion were measured in the stomach. The best dose was determined to be 5 mg/kg for both drugs. Celecoxib was found to delay ulcer healing when compared to dipyrone especially when ulcer index was used as measure. In the second experiment, ulcer index, acidity, mucus secretion, and the levels of myeloperoxidase (MPO), lipid peroxide (MDA), non-protein sulfhydryl groups (NP-SH), and prostaglandin E2 (PGE2) were investigated in the stomach of rats with gastric ulcers induced by histamine, stress and diethyldithiocarbamate (DDC). While celecoxib increased the ulcer index in stress-induced ulcer, dipyrone decreased the index in DDC-induced ulcer. Celecoxib also caused a significant increase of gastric mucus secretion in histamine-induced ulcer model. Gastric lipid peroxidation was significantly increased by dipyrone in the control group without gastric ulcer induction, whereas it was significantly increased by celecoxib in the histamine-induced and stress-induced ulcer groups. Dipyrone promoted a decrease in gastric NP-SH levels in the control group with stress-induced ulcer. With respect to gastric MPO activity, dipyrone caused a decrease in the histamine-induced ulcer group but it caused an increase in the stress-induced and DDC-induced ulcer groups. Gastric PGE2 levels in the control group without gastric ulcer induction were not affected by celecoxib while they were increased by dipyrone. In conclusion, celecoxib prompted the formation of experimentally induced gastric ulcers more than did dipyrone. The study was supported by Osmangazi University Research Funds.
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PMID:The effects of some nonsteroidal anti-inflammatory drugs on experimental induced gastric ulcers in rats. 1823 17

Ibuprofen is the first line of treatment for osteoarthritis and arthritis. The main side effects of ibuprofen especially in long-term treatment include gastric ulcer, duodenal ulcer and indigestion etc. Therefore, screening drugs with effective gastric protective effects and low toxicity for combination therapy with ibuprofen is necessary. The mechanism of gastric damage induced by ibuprofen is still unclear, however, cell damage caused by reactive oxygen species (ROS) is considered as the main reason. Preliminary screening of literature with the criteria of low toxicity led to four histamine-2 receptor antagonists (H2RAs): nizatidine, famotidine, lafutidine, and roxatidine acetate, which were selected for further investigation. These drugs were evaluated systemically by examining the gastric ulcer index, lipid peroxidation (LPO), membrane permeability, toxicity to main organs, and the influence on the activity of antioxidant enzymes, and myeloperoxidase (MPO). Nizatidine was found to be the best gastric protective agent. It exhibited excellent protective effect by increasing antioxidant enzyme activity, decreasing MPO activity, reducing LPO, and membrane permeability. Combination treatment with nizatidine and ibuprofen did not show any significant toxicity. Nizatidine was considered as a good option for combination therapy with ibuprofen especially for diseases that require long-term treatment such as arthritis and osteoarthritis.
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PMID:Gastroprotective effects of several H2RAs on ibuprofen-induced gastric ulcer in rats. 2688 79

Objective. This study examined whether duration of treatment effect should be considered in a benefit-risk assessment using a case study of osteoarthritis medications. Study Design and Setting. A discrete choice experiment was completed by 300 residents of the United Kingdom with hip and/or knee osteoarthritis. In 16 choice tasks, participants selected their preferred option from 2 medications. Medications were described in terms of effect on pain, stiffness, and function; duration of treatment effect; and risk of heart attack and stomach ulcer bleeding. The analysis used mixed-effects logistic regression. Results. Pain, disease severity, and duration of treatment effect had the greatest influence on medication preferences, whereas stiffness did not significantly affect medication choice. Participants were willing to accept an increase in the risk of heart attack of 2.6% (95% confidence interval: 2.0% to 3.2%) to increase the duration of treatment effect from 1 month to 12 months. Reducing pain from moderate to mild was valued the same as increasing duration of effect from 1 month to 3 months; both were seen as equivalent to an absolute reduction of 1.2% in the risk of heart attack in the next year. Subgroup analysis suggested disease severity influenced patient preferences. Conclusions. Along with treatment benefits and risks, the results suggest that duration of treatment effect is an important factor in the medication choices of people with osteoarthritis. This could have implications for the design and interpretation of clinical trials, for example, incorporating longer-term surveillance of trial participants and accounting for duration of treatment effect in risk-benefit assessments. Future research is needed to assess whether these findings are generalizable to other samples, disease areas, and levels of duration of effect.
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PMID:Duration of Treatment Effect Should Be Considered in the Design and Interpretation of Clinical Trials: Results of a Discrete Choice Experiment. 3095 59


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