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)

Effects of carbenoxolone Na on acute or chronic types of gastric lesions or ulcer models produced in rats, guinea pigs, or dogs were studied. Carbenoxolone Na, given either orally or intraperitoneally, produced a significant inhibition of stress-induced gastric lesions in intact or in pylorus-ligated rats. Acetylsalicylic acid (ASA)-induced or serotonin-induced gastric lesions in rats were also inhibited significantly by pretreatment with the drug. However, carbenoxolone Na did not affect the development of Shay ulceration in rats even though the peptic activity in gastric juices was markedly reduced by the drug. Histamine-induced gastric lesions in guinea pigs were not prevented by pretreatment with carbenoxolone Na. Although carbenoxolone Na, given for 10-20 days, did not promote the healing of stress-induced gastric lesions and acetic acid gastric jlcers in rats, it significantly accelerated the healing of chronic gastric ulcer produced in dogs by 3 weeks' treatment. Carbenoxolone Na prevented the acid back-diffusion caused by ASA without any influence on Na+ efflux in pylorus-ligated rats.
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PMID:Effects of carbenoxolone Na on acute and chronic gastric ulcer models in experimental animals. 98 16

The effects of aspirin, salicylate formulations and substitutes, smoking (nicotine), indomethacin, corticosteroids, phenylbutazone, ethanol, caffeine and reserpine on the gastric mucosa are discussed. The damaging effects of the drugs are considered in terms of the gastric mucosal barrier, gastric erosions, microbleeding and haematemesis and melaena and finally whether they cause peptic ulcer. There is suggestive evidence that unbuffered aspirin is a cause of haematemesis and melaena and of gastric ulcer but the incidence rates for hospital admission are low, being 10 to 15 per 100,000 heavy users per year. Aspirin in solution as acetylsalicylate buffered to maintain a neutral pH protects against gastric damage. Newer aspirin substitutes (mefenamic acid, fenoprofen, naproxen, tolmetin and ibuprofen) appear to cause less faecal blood loss than aspirin but their long-term effects have not been fully evaluated. Smoking is definitely associated with peptic ucler but the mechanism is unknown. Corticosteroids are probably not ulcerogenic despite clinical bias that they are. Indomethacin and phenylbutazone may be ulcerogenic but there is insufficient evidence to make firm judgements. Ethanol, caffeine and reserpine, on available evidence, are probably not ulcerogenic.
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PMID:Drugs and gastric damage. 126 29

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

Salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of painful disorders. This article reviews the efficacy, side effects, and costs of these agents and proposes a practical approach to using them in a cost-effective manner. Although there may be some differences in efficacy among available drugs, these do not appear sufficient to justify using the more expensive agents in most cases. Adverse effects, especially gastrointestinal (GI), add to the cost of using these drugs. Aspirin and all nonsalicylate NSAIDs share a risk of causing gastric ulcer, upper GI bleeding, and GI perforation. Prostaglandin inhibition by these agents may lead to reduced glomerular filtration rate and renal failure. There may be modest differences in GI and renal risks with the different agents, but these are minimal. Prophylaxis against gastric ulceration with anti-ulcer drugs has been recommended, and one agent, misoprostol, is approved for use in the United States for this purpose. Whether use of prophylaxis will increase or decrease the costs associated with NSAID therapy remains to be determined. Nonacetylated salicylates may cause less GI adverse effects and may be somewhat "renal sparing." Strategies that would reduce the cost of care for painful musculoskeletal disorders without compromising quality of care include using acetaminophen instead of an NSAID for noninflammatory disorders, trying nonacetylated salicylates as less expensive and safer alternatives to NSAIDs, using one agent at a time, allowing sufficient time to evaluate the therapeutic effect before changing agents, returning to the least expensive and/or safest drug if a trial of several in succession fails to find one that is clearly better, and reserving prophylactic use of antiulcer agents for patients who are at especially high risk and for whom anti-inflammatory effects are clearly needed.
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PMID:Cost-conscious prescribing of nonsteroidal anti-inflammatory drugs for adults with arthritis. A review and suggestions. 141 72

While waiting for open heart surgery, in 153 patients (104 male, 49 female, 22-76 years of age) without gastrointestinal symptoms and/or history esophago-gastro-duodenoscopy was performed. 124 patients suffered from coronary heart disease, 29 from valvular defect, aneurysm of the sinus of Valsalva or tumor of the heart. In 47.1% endoscopy revealed serious abnormal findings: in 16.3% gastric ulcer, in 20.9% erosive gastritis, duodenal ulcer and erosive duodenitis in 5.2%, respectively, 1 case of gastric carcinoma, 2 of large polyps and 3 of reflux esophagitis of higher degree (totally 3.9%). In patients with coronary artery disease, the relation of erosive and ulcerous gastric lesions as compared with those of duodenal origin was 4:1, in patients with other cardiac diseases it was 2:1, respectively (p less than 0.001). Compared with a normal population, the incidence of pathological gastric findings was 54-fold higher in our patients, and 1.7-fold concerning duodenal lesions, respectively (p less than 0.001). 51 patients on acetylsalicylic acid (160 mg/die) showed pathologic findings in 41.2%, and 96 patients without ulcer-inducing therapy in 51%. Thus, low-dose Aspirin does not seem to have serious gastric side effects. The results of the study stress the necessity of routinely performed endoscopy of the upper gastrointestinal tract in patients awaiting open heart surgery. This will lead to a lower incidence of serious gastrointestinal complications postoperatively which are known to have a high mortality.
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PMID:[Frequency of pathological changes of the upper gastrointestinal tract in patients awaiting heart surgery]. 208 20

Aspirin is commonly accepted as a risk factor for gastric ulcer; however, there is little published evidence linking aspirin consumption to duodenal ulcer. The effect of 1 g of aspirin per day on site-specific ulcer hospitalizations was examined using data from a 3-year randomized, double-blind, placebo-controlled trial of 4,524 subjects (Aspirin Myocardial Infarction Study). There were 23 duodenal ulcer and 14 gastric ulcer hospitalizations during the follow-up period. All but two were verified by endoscopy, radiogram, or biopsy/surgery. For males, a Cox-model survival analysis showed that the age- and smoking-adjusted relative risk for duodenal ulcer hospitalization was 10.7 times higher for the aspirin group than for the placebo group (95% confidence interval, 2.5 to 45.5; p less than 0.0001). The adjusted relative risk for gastric ulcer was 9.1 (95% confidence interval, 1.2 to 71.4; p = 0.04). Due to the small number of females in the study, the relationship between site-specific ulcer and aspirin consumption for females was not analyzed. However, for males and females combined, the age-, smoking-, and sex-adjusted relative risk for peptic ulcer hospitalization was 7.7 (95% confidence interval, 2.7 to 21.7; p less than 0.0001). We conclude that chronic aspirin use is a risk factor for hospitalization for both duodenal and gastric ulcer in males, and for peptic ulcer in males and females.
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PMID:The effect of chronic aspirin use on duodenal and gastric ulcer hospitalizations. 219 80

It has been developed by us a simple new method for producing subacute gastric ulcer in rats, combined with a novel method for the quantitative evaluation of the healing process. Fasted rats with 120-150 g were used. The animals were anaesthesized by ether and than a polyethylene chateter was orally inserted into the stomach with a fine needle inside. After the cannule reached the gastric wall, the needle was pressed gently so as to punch the gastric wall. Drugs under study were administered orally 30 min and 24 h after the puncture. Food and water were given ad libitum from 2 h after the intervention until the end (96 h) of experiments. In order to follow the healing process of subacute ulcer, the so-called tensile strength of the ulcer was determined by inflating and expressed in mmHg. The healing rate was calculated. The antiulcer drugs: Cimetidine, Famotidin, Pirenzepine and sucralfate dose dependently and significantly increased the healing rate of ulcer. Non steroidal antiinflammatory drugs: naproxen, piroxicam, indomethacin and ibuprofen significantly delayed the healing of ulcer. ASA showed tendency to delay the healing. Strong HCl (0.5 molar) significantly delayed the healing of ulcer. N-EM given subcutaneously dose dependently delayed the healing of subacute ulcer.
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PMID:Effect of cytoprotective and antiulcer drugs on the healing process of subacute gastric ulcer in rat (a new model). 259 12

Aspirin often causes acute gastric mucosal damage that can be seen endoscopically or assessed indirectly (for example, by measuring increased gastrointestinal blood loss). The occurrence of most adverse effects is apparently related to the dose administered. This dose-response effect, evident in both endoscopic and microbleeding studies done after acute or short-term aspirin administration, is also associated with the risk of developing chronic gastric ulcer. The occurrence of gastric adaptation, or lessening injury with continued treatment, obscures the interpretation of results from studies of acute administration. Moreover, evidence of dose-response effects has frequently been ignored when lists of complications and side effects are compiled. The absence of symptoms does not correlate with acute or chronic mucosal damage and appears to have no predictive value. Endoscopic studies linking the extent and degree of acute mucosal injury to various nonsteroidal anti-inflammatory drugs have little or no value in predicting the frequency or severity of chronic gastric ulcer or gastrointestinal bleeding.
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PMID:Aspirin and the stomach. 351 24

Aspirin and paracetamol (acetaminophen) are the most commonly used minor analgesics, but their effects on the gastrointestinal tract differ widely. The effects of other nonsteroidal anti-inflammatory drugs (NSAIDs), including phenylbutazone, are intermediate. Aspirin is significantly associated with major upper gastrointestinal haemorrhage, whereas paracetamol is not. Short term use of aspirin produces erythema, erosions and occasionally ulcers; paracetamol does not, while other NSAIDs do so to varying degrees. Chronic gastric ulcer is linked to aspirin intake in patients with rheumatic disease, and epidemiologically in all heavy aspirin users. In only one epidemiological study was a paradoxical significant association reported between paracetamol intake and chronic gastric ulcer. Faecal occult blood loss is increased in most regular aspirin users but not in those taking paracetamol. Although formal studies in children have apparently not been made, in isolated small clinical series it has been reported that gastrointestinal bleeding and anaemia do occur in the paediatric age group after the use of aspirin. Pathophysiologically, aspirin alters the gastric mucosal barrier to hydrogen ions and lowers gastric potential difference; paracetamol has no effect on these parameters. Such changes correlate ultrastructurally with damage in surface epithelial cells and microerosions after the use of aspirin, but not after the use of paracetamol. Aspirin and other NSAIDs cause a dramatic reduction in the ability of gastric mucosa to generate protective prostaglandins; however, paracetamol also reduces prostaglandins. Other postulated mechanisms of aspirin damage include reduction in gastric mucosal secretion, reduction in bicarbonate output, and alteration of cell turnover. Because damage to gastric mucosa by aspirin and NSAIDs is often 'silent', the clinician needs a high level of suspicion and awareness regarding this problem. In patients prone to gastric damage, or in those with a past history of aspirin-induced gastric damage, paracetamol is the drug of choice when a minor, non-inflammatory problem requires an analgesic.
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PMID:Gastrointestinal intolerance and bleeding with non-narcotic analgesics. 355 87

Aspirin is generally regarded as a cause of gastric ulcer but the role of non-steroidal anti-inflammatory agents and paracetamol in the aetiology of peptic ulcer is unclear. To investigate this we conducted a case control study of 180 matched pairs of peptic ulcer patients and controls obtained from surgical and dermatology outpatient clinics. There were 95 gastric ulcer and 85 duodenal ulcer patients. A statistically and clinically association (relative risk = 5) was found between the regular use of non-steroidal anti-inflammatory agents and gastric ulcer. There was also evidence of positive associations between gastric ulcer and aspirin containing preparations with or without non-steroidal anti-inflammatory agents. By contrast, duodenal ulcer was unrelated to these drugs. Too few patients used paracetamol for any conclusion to be drawn on its role.
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PMID:Peptic ulcer and non-steroidal anti-inflammatory agents. 373


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