Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of the nonsteroidal anti-inflammatory drug, diclofenac, on stimulated monocyte superoxide production were assessed directly in vitro and following treatment of patients with rheumatoid arthritis ex vivo. Diclofenac inhibited superoxide generation provoked by serum treated zymosan (STZ) and fluoride anion (F) but not by phorbol myristate acetate (PMA) in vitro. Following patient therapy, inhibition of superoxide production occurred when STZ and PMA, but not F were used as stimuli. No changes were seen in control subjects. The contrasting profiles of inhibition seen in vitro and ex vivo suggest an indirect effect on superoxide production during clinical use of the agent. These data are consistent with the hypothesis that anti-inflammatory drugs may act in rheumatoid arthritis by inhibiting phagocyte superoxide anion production.
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PMID:Diclofenac inhibits monocyte superoxide production ex vivo in rheumatoid arthritis. 165 Sep 59

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of diclofenac sodium are reviewed. Diclofenac, the first nonsteroidal anti-inflammatory agent (NSAID) to be approved that is a phenylacetic acid derivative, competes with arachidonic acid for binding to cyclo-oxygenase, resulting in decreased formation of prostaglandins. The drug has both analgesic and antipyretic activities. Diclofenac is efficiently absorbed from the gastrointestinal tract; peak plasma concentrations occur 1.5 to 2.0 hours after ingestion in fasting subjects. Even though diclofenac has a relatively short elimination half-life in plasma (1.5 hours), it persists in synovial fluid. The drug is metabolized in the liver and is eliminated by urinary and biliary excretion. In clinical trials, diclofenac was as effective as aspirin, diflunisal, indomethacin, sulindac, ibuprofen, ketoprofen, and naproxen in improving function and reducing pain in patients with rheumatoid arthritis. For treatment of osteoarthritis, diclofenac was equivalent in efficacy to aspirin, diflunisal, indomethacin, sulindac, ibuprofen, ketoprofen, naproxen, flurbiprofen, mefenamic acid, and piroxicam. Diclofenac was as effective as indomethacin or sulindac in treating ankylosing spondylitis. The most frequent adverse effects reported for diclofenac were gastrointestinal, but these effects were fewer and less serious than occurred with aspirin or indomethacin; in addition, diclofenac caused fewer central nervous system reactions than indomethacin. Diclofenac is administered in divided doses with meals. The recommended total daily dosage is 100 to 150 mg (osteoarthritis and ankylosing spondylitis) or 150 to 200 mg (rheumatoid arthritis). Diclofenac is effective, but no more so than other NSAIDs. It is structurally distinct and offers another choice in the treatment of rheumatological conditions.
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PMID:Diclofenac sodium. 267 Mar 97

Diclofenac is the newest NSAID to be introduced to the United States. Extensive worldwide clinical studies with diclofenac have demonstrated its efficacy in the treatment of rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Its overall safety and efficacy is comparable to other available NSAIDs. The potential advantage of diclofenac is its short serum half-life but long synovial fluid concentration which enables twice daily dosing.
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PMID:Diclofenac. 268 2

Non-steroidal anti-inflammatory drugs, essential for the treatment of rheumatic diseases, are frequently associated with significant adverse effects on the integrity of the gastrointestinal mucosa. Sulglicotide (S), a natural product, has been found to possess gastromucosal protective properties. Aim of the present study was to evaluate whether (S) 200 mg t.i.d prevented or reduced the severity of gastric and/or duodenal mucosal injury induced by Diclofenac. A total of 30 patients with either rheumatoid arthritis (RA) or osteoarthritis (OA) who required NSAID therapy for at least 8 weeks were enrolled into a double-blind randomized placebo-controlled study. The main criteria for entry into the trial was the absence of gastrointestinal symptoms, and gastric/duodenal lesions assessed by endoscopy. At the end of the treatment endoscopy and relative symptoms were assessed. Six out of 15 patients, in both groups of treatment developed mucosal injury, but only in the placebo group the gastric damage was important (ulcer and petechiae) while in the group (S) we observed only hyperemia of the gastric mucosa. These preliminary data indicate the usefulness of Sulglicotide in preventing or reducing mucosal injury from NSAID treatment.
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PMID:[Sulglicotide in the prevention of gastric disease induced by NSAID. Double-blind controlled study versus placebo]. 272 26

Diclofenac sodium is a nonsteroidal antiinflammatory drug (NSAID) that has been used in 120 countries since its introduction in Japan in 1974. It is currently the eighth largest-selling drug and the most frequently used NSAID in the world. Diclofenac, a phenylacetic acid derivative, is a potent inhibitor of cyclooxygenase enzyme activity, and may also interact with the lipoxygenase enzyme pathway, and with the release and reuptake of arachidonic acid. Diclofenac is almost completely absorbed, highly protein-bound, penetrates well into synovial fluid, and is extensively metabolized. Comparative studies have shown that diclofenac is at least equivalent in efficacy to aspirin and other NSAID when used for the treatment of rheumatic diseases such as rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Diclofenac also possesses potent analgesic properties. Clinical trials suggest that diclofenac has a favorable side-effect profile, excellent patient tolerability, and a lower patient dropout rate when compared with aspirin and other NSAID.
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PMID:Review of diclofenac and evaluation of its place in therapy as a nonsteroidal antiinflammatory agent. 306 24

In a six-week, double-blind, randomized, multicenter clinical trial, the efficacy and safety of 150 mg/day of diclofenac sodium and a placebo were compared in 182 patients with active definite or classical rheumatoid arthritis. Safety and tolerability were evaluated in all patients and efficacy was determined in a subset of 158 patients who met all criteria for eligibility. A significantly greater improvement in six of eight treatment variables was seen in the diclofenac-treated patients than in the placebo group after one week of therapy. Fewer diclofenac-treated patients than placebo-treated patients discontinued the study because of lack of therapeutic response. Adverse experiences were reported by 28% of the diclofenac group and 21% of the placebo group, not a statistically significant difference. Gastrointestinal complaints were the most frequently reported side effects in both treatment groups, but there was no significant difference between the treatment groups. Diclofenac was found to be effective, safe, and well tolerated for the treatment of patients with active rheumatoid arthritis.
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PMID:Double-blind randomized trial of diclofenac sodium versus placebo in patients with rheumatoid arthritis. 352 43

A high-performance liquid chromatographic assay has been developed for the determination of a number of non-steroidal anti-inflammatory drugs in plasma. The samples were prepared by adding acetonitrile and perchloric acid to 200 microliter of plasma. Diclofenac, fenoprofen, ketoprofen, naproxen, phenylbutazone, piroxicam and sulindac were quantified in the supernatant produced using a mobile phase of phosphoric acid 0.03% (pH 2.5)-acetonitrile and a detecting wavelength of 254 nm. The reproducibility, linearity, precision and specificity of the assay were determined and found to be satisfactory. Alteration of the detection wavelength to 229 nm also permitted accurate determination of ibuprofen concentration in plasma. While reduction of the organic solvent content of the mobile phase and alteration of wavelength to 313 nm produced a system capable of quantifying salicylate and its metabolites in plasma and by further reducing the detecting wavelength to 237 nm, aspirin also was quantifiable. These methods have been applied in a cross-sectional study of medication compliance among rheumatoid arthritis patients treated with non-steroidal anti-inflammatory drugs.
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PMID:Rapid high-performance liquid chromatographic assay for the simultaneous analysis of non-steroidal anti-inflammatory drugs in plasma. 361 Dec 61

Three groups of subjects were selected for this study. Patients suffering from rheumatoid arthritis (RA) diagnosed according to the criteria of the ARA (mean: 6 criteria) and treated with gold salts. Control subjects treated with one type of non-steroidal anti-inflammatory agent (diclofenac). Healthy subjects receiving no treatment. The granulocytes and monocytes in the peripheral blood were tested separately for the ingestion of 3 types of particles and for the stimulation of the production of the superoxide anion. In the patients with rheumatoid arthritis, all of the phagocytic cells had a normal phagocytic response and a normal superoxide anion production. The serum of the patients did not inhibit the activity of these cells. Diclofenac did not act on phagocytosis or on the oxidative activity of the control cells. It is therefore logical to consider that the phagocytic cells are involved in RA via other mechanisms of action.
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PMID:[Role of phagocytic cells in rheumatoid polyarthritis]. 370 14

Diclofenac is a nonsteroidal anti-inflammatory drug approved in the United States in 1988 for the treatment of patients with osteoarthritis, rheumatoid arthritis, or ankylosing spondylitis. To characterize the clinical, biochemical, and histological features and possible mechanisms of hepatic injury associated with its use, a retrospective analysis was undertaken of 180 patients whose cases were reported to the Food and Drug Administration from November 1988 through June 1991, as having had possible adverse reactions to diclofenac. Of the reported 180 cases, 79% were female, 71% were 60 years of age or older, and 77% had osteoarthritis. Sixty-seven percent of the cases were detected by symptoms and the remainder by abnormal laboratory tests. Seventy-five percent of the symptomatic patients (90 of 120) were jaundiced. Seven of the 90 icteric patients died. The biochemical pattern of injury was hepatocellular or mixed hepatocellular in 66% of cases. Only 8% had a pattern of cholestatic injury. The remainder, with modestly increased values of both transaminases and alkaline phosphatase, were considered "indeterminate," i.e., either mild hepatocellular or anicteric "cholestatic" injury. Sections of liver from 21 cases were available for study. Hepatic injury was apparent by 1 month after starting the drug in 24%, by 3 months in 63%, and by 6 months in 85% of cases. The latent period in 12% was 6 to 12 months, whereas in 3% it was greater than 12 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diclofenac-associated hepatotoxicity: analysis of 180 cases reported to the Food and Drug Administration as adverse reactions. 765 88

This was a double-blind study designed to compare the efficacy and tolerability of diclofenac/misoprostol and diclofenac in patients with acute tendinitis/bursitis of the shoulder. Diclofenac 50mg/misoprostol 200 micrograms (n = 185) or diclofenac 50mg (n = 187) was administered twice or 3 times daily for 14 days. Various physician's and patient's assessments performed during and at the end of treatment showed similar improvements with both treatments. Abdominal pain, nausea and vomiting occurred somewhat more frequently with diclofenac/misoprostol, but patient withdrawals due to adverse events did not differ markedly between the groups. Thus, in the short term treatment of acute tendinitis/bursitis of the shoulder diclofenac/misoprostol possesses efficacy similar to that with diclofenac alone and provides the gastroprotective benefit of misoprostol. Previous studies in osteoarthritis and rheumatoid arthritis have established diclofenac/misoprostol to be as effective as diclofenac but with significantly less gastrointestinal damage (Verdickt et al. 1992).
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PMID:Diclofenac/misoprostol vs diclofenac/placebo in treating acute episodes of tendinitis/bursitis of the shoulder. 768 84


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