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)

Indomethacin, 100 mg orally, was compared with prednisolone, 5 mg, as addititional therapy at night, in a two-week, double-blind, between-patient study in twenty-four in-patients with rheumatoid arthritis. Both therapies proved equally effective, and significantly lessened morning stiffness and increased grip strenght. Two patients with dyspepsia were discontinued from the indomethacin group. Using indomethacin at night avoided the central nervous system side-effects frequently seen with this compound.
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PMID:Indomethacin or prednisolone at night in rheumatoid arthritis? 73 14

46 patients with rheumatic diseases suffering from dyspepsia and endoscopically proven gastroduodenal lesions entered a double-blind placebo-controlled study with ranitidine 150 mg b.i.d. over 4-8 weeks. The patients had to be treated for at least 3 months with the non-steroidal antiinflammatory drugs (NSAID) Diclofenac, Indomethacin, and Piroxicam before entering the study. During the trial all patients had to continue on NSAID. At entry patients in the placebo group (n = 23) had a total number of 33 gastrointestinal lesions of grade 1-3. In the ranitidine group (n = 23) a total number of 28 gastrointestinal lesions had been counted. After 4 weeks of treatment the number of lesions had been reduced in the placebo group to 20 and in the ranitidine group to 6 (p less than 0.05). The total damaging score at entry averaging 2.0 under placebo and 1.0 under ranitidine had been reduced to 1.3 (placebo) and 0.3 (ranitidine). (p less than 0.05). Our results underline the efficacy of ranitidine in the treatment of NSAID-induced gastroduodenal mucosal lesions.
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PMID:[Ranitidine in the treatment of non-steroidal anti-inflammatory agent-induced damage of the stomach and duodenal mucosa. Results of a randomized, placebo-controlled double-blind study in patients with rheumatic diseases]. 306 Nov 83

Nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori (H. pylori) are major factors in gastritis and peptic ulcer However, the role of NSAIDs and H. pylori infection in dyspepsia remains unclear. Gastric adaptive relaxation may be related to the pathogenesis of functional dyspepsia because the response is often disturbed in dyspeptic patients. In this study, we investigated the effects of indomethacin or H. pylori water extracts on gastric adaptive relaxation. This experiment was performed using the modified method of Desai et al. Isolated guinea-pig stomach in an organ bath was monitored for intragastric pressure and volume. Adaptive relaxation was induced by gastric luminal distention. The effects of indomethacin and H. pylori on gastric relaxation were tested in this system. Indomethacin (> 1 x 10(-5) M) significantly inhibited adaptive relaxation. Indomethacin (> 3 x 10(-6) M) induced gastric relaxation in a dose-dependent fashion. However, aspirin at a concentration sufficient for cyclooxygenase (COX)-1 inhibition did not induce gastric relaxation. Preincubation with N-nitro-L-arginine methyl ester, a nitric oxide (NO)-synthase inhibitor, inhibited indomethacin-induced gastric relaxation. Adaptive relaxation was not affected by H. pylori water extracts. In conclusion, indomethacin inhibited adaptive relaxation via prior gastric relaxation. NO production, but not COX-1 inhibition, may be involved in this effect of indomethacin. H. pylori water extracts may not have direct effects on adaptive relaxation. Inhibition of adaptive relaxation may be one of the major mechanisms underlying NSAID-induced dyspepsia.
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PMID:Indomethacin, but not Helicobacter pylori, inhibits adaptive relaxation in isolated guinea-pig stomach. 1570 Jul 51