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The methodological design of each study was scored according to a pre-determined system. The three main outcome measures of pain, physical function and patient global assessment were chosen based on the core set agreed upon by OMERACT (Outcome Measures in Rheumatology Clinical Trials). These were used to determine the power of each trial. The equivalency of NSAID doses was calculated using the percentage of the recommended maximum daily dose. Sample size estimates for the detection of clinically relevant changes in outcome measures used in the assessment of OA knee were used for power calculations. These calculations were performed to determine whether the trials were of a sufficient size to detect clinically relevant differences which were statistically significant. The calculations incorporate estimates of standard deviation, and minimum, median and maximum differences (delta) between drugs which are deemed to be clinically important. The number of "withdrawals due to lack of efficacy" was also selected as an outcome measure for this review. The Peto odds ratio and 95% confidence intervals were calculated where possible. The results of studies which compared the same trial and reference NSAIDs were combined where possible.
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Lumry described 6 patients who presented hypertrophic rhinosinusitis, positive nasal eosinophilia and intolerance to nonsteroidal antiinflammatory drugs, manifested exclusively with naso-ocular symptomatology. We present three patients with clinical manifestations of chronic rhinitis who had noticed before their first visit that several nonsteroidal antiinflammatory drugs precipitated their nasal symptomatology. None of them had ever presented with asthma symptoms. All of them had nasal polyps. The nasal smear showed eosinophilia of 20 to 45%. All three had sinusitis radiologically. The spirometric values were within normal limits (V.C., FEV1, MMEF25-75%). Skin tests with different inhalants antigens using the prick test technique as well as skin tests with pyrazolones (Phenyldimetrylpyrazolone: 25 and 250 mg./ml.; dipyrone: 4 and 44 mg./ml.; amidopyrine: 2.2 and 22 mg./ml.) using the intradermal technique were negative. Serum IgE (Phadezym IgE-Pharmacia) showed values of 23.9, 17.1 and 25.8 IU/ml. respectively. The bronchial inhalation challenge test with methacholine was positive with PD20FVE1 of 14 and 4.8 mg./ml. in two of our patients. Different nonsteroidal antiinflammatory drugs were administered to each patient in different days orally, with intervals of 7 and 25 days (aspirin 500 mg., dipyrone 575 mg., indomethacin 25 mg., naproxen 500 mg.) as well as tartrazine (50 mg.), paracetamol (500 mg.) and lactose as placebo. With 30 minutes intervals and up to three hours after drug administration, the symptoms were observed and spirometry was carried out. Steroids and antihistamines were suspended at least 48 hours before the test. Acetyl-salicylic acid, dipyrone, indomethacin and naproxen produced naso-ocular symptomatology without any objective reduction of FEV1; but paracetamol and tartrazine were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
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The tobacco-specific N-nitrosamine, NNK, is a potent carcinogen in laboratory animals. The authors have shown previously that NNK-induced lung tumorigenesis in A/J mice can be reduced significantly by certain nonsteroidal antiinflammatory drugs (NSAIDs), such as sulindac, ibuprofen, or piroxicam treatments. In this study, the authors investigated whether NSAIDs could reduce NNK-induced oxidative, DNA damage and/or inhibit endogenous lipid peroxidation, or prostaglandin E2 (PGE2) synthesis in A/J mice. In the first experiment, A/J mice were gavaged with NNK (112 mumol/kg b.w.) three times a week while being maintained on a diet to which either ibuprofen (263 mg/kg diet), naproxen (230 mg/kg), sulindac (123 mg/kg), piroxicam (25 mg/kg), indomethacin (5 mg/kg), or no NSAIDs had been added. Levels of 8-OH-dG in the DNA of lung and liver were measured by high-performance liquid chromatography with electron capture detector. Treatment with NSAIDs had no significant effects on the endogenous or NNK-induced formation of 8-OH-dG in the lung of the mice. In a second experiment, after treatment of A/J mice with NSAIDs for 2 weeks, lipid peroxidation was assayed by determining thiobarbituric acid-reactive substances (TBA-RS) in lung tissues, and prostaglandin E2 levels were measured in plasma by an enzyme immunoassay. Treatments with some NSAIDs lowered the levels of lipid peroxidation and plasma levels of PGE2 below basal levels. Taken together, these results suggest that the inhibition of NNK-induced lung tumorigenesis by NSAIDs is more likely related to an inhibition of prostaglandin synthesis than to a direct inhibition of lipid peroxidation or oxidative DNA damage induced by NNK.
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Patients with active rheumatoid arthritis have a decreased prolactin response to hypoglycaemia induced stress. The response recovers following treatment with antirheumatic drugs.
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We identified 18 randomised controlled trials and 11 observational studies. By the end of 2000 (52 myocardial infarctions, 20742 patients) the relative risk from randomised controlled trials was 2.30 (95% CI 1.22-4.33, p=0.010), and 1 year later (64 events, 21432 patients) it was 2.24 (1.24-4.02, p=0.007). There was little evidence that the relative risk differed depending on the control group (placebo, non-naproxen NSAID, or naproxen; p=0.41) or trial duration (p=0.82). In observational studies, the cardioprotective effect of naproxen was small (combined estimate 0.86 [95% CI 0.75-0.99]) and could not have explained the findings of the VIGOR trial.
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A detailed experimental analysis of the phase transition thermodynamics of (S)-naproxen and (RS)-naproxen is reported. Vapor pressures were determined experimentally via the transpiration method. Sublimation enthalpies were obtained from the vapor pressures and from independent TGA measurements. Thermodynamics of fusion which have been well-studied in the literature were systematically remeasured by DSC. Both sublimation and fusion enthalpies were adjusted to one reference temperature, T = 298 K, using measured heat capacities of the solid and the melt phase by DSC. Average values from the measurements and from literature data were suggested for the sublimation and fusion enthalpies. In order to prove consistency of the proposed values the vaporization enthalpies obtained by combination of both were compared to vaporization enthalpies obtained by the group-additivity method and the correlation-gas chromatography method. The importance of reliable and precise phase transition data for thermochemical calculations such as the prediction of solid/liquid phase behaviour of chiral compounds is highlighted.
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Both alendronate and naproxen can cause gastric ulcers. The combination appears synergistic. Alendronate should be used with caution in those who simultaneously require nonsteroidal anti-inflammatory drugs.
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Naproxen/esomeprazole was a dominant strategy (more effective and less costly) compared to celecoxib, etoricoxib and diclofenac+PPI. Celecoxib+PPI and etoricoxib+PPI were more effective. Considering a cost-effectiveness threshold of €30,000 per additional QALY, naproxen/esomeprazole was cost-effective compared to ibuprofen+PPI and naproxen+PPI with incremental cost-effectiveness ratios (ICER) of €15,154 and €5,202 per additional QALY, respectively.
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IL-1 beta is an important inflammatory mediator produced by monocytes and macrophages after LPS stimulation. In the absence of a secondary stimulus, however, little IL-1 beta is released into the medium. Previously, ATP was shown to promote the release and proteolytic maturation of IL-1 beta from LPS-stimulated murine peritoneal macrophages. Tenidap, a new anti-inflammatory and antiarthritic agent, inhibited the release and maturation of IL-1 beta induced in vitro by ATP treatment of murine peritoneal macrophages. Tenidap's inhibitory activity was mimicked by other agents that blocked anion transport, such as UK5099 and DIDS. In contrast, cyclooxygenase-inhibiting nonsteroidal anti-inflammatory drugs, such as piroxicam and naproxen, did not impair ATP-induced post-translational processing. Human monocytes responded to LPS to produce IL-1 beta, but externalized little of their newly synthesized cytokine. ATP at concentrations > or = 2 mM promoted IL-1 beta release from these cells. The degree to which the released cytokine was proteolytically processed to its biologically active 17-kDa species, however, depended on the pH of the medium; a greater processing efficiency was observed at slightly acidic (pH 6.9) values. Tenidap and other anion transport inhibitors effectively prevented the ATP response of cultured human monocytes. Likewise, LPS-stimulated human alveolar macrophages responded to ATP by releasing 17-kDa IL-1 beta, and tenidap inhibited this response. The ATP-induced release and maturation of IL-1 beta from human monocytes and macrophages, therefore, was suppressed by anion transport inhibitors, suggesting that anion conductance is a necessary component of the ATP-promoted externalization mechanism. In view of IL-1's importance as an inflammatory mediator, tenidap may demonstrate novel anti-inflammatory activities by virtue of its inhibition of the post-translational release and maturation of this cytokine.
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Randomized, double-blind, placebo-controlled, multiple dose, three-period crossover study. Patients > or =45 years of age (N=22) with symptomatic knee OA were randomized to naproxen 500 mg bid, tramadol/acetaminophen 37.5 mg/325 mg in forced titration, or placebo in each of three periods. Patients performed multiple 20-minute treadmill walks on Day 1 and Day 3 at a consistent self-selected pace predetermined at screening. Pain intensity (PI) during the walks was assessed on an 11-point numerical rating scale at 0, 3, 6, 9, 12, 15, 18, and 20 min. The primary endpoint was the time-weighted average (TWA) change from baseline PI on Day 3 for the two self-paced walks for the active treatments vs placebo. Time to moderate pain (TTMP) was a key secondary endpoint.
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Tepoxalin, a dual inhibitor of cyclooxygenase (CO) and 5-lipoxygenase (5LO) with cytokine modifying activity, is also a potent inhibitor of the transcription factor, nuclear factor kappa B (NF kappa B). NF kappa B is a pleiotropic activator that is involved in the regulation of many genes whose products participate in immune or inflammatory responses. Tepoxalin inhibited in a dose related manner NF kappa B activation by PMA + ionomycin or H2O2 in Jurkat and HeLa cells. TNF-alpha-induced NF kappa B was also inhibited by tepoxalin in HeLa cells, while relatively less marked inhibition was observed in Jurkat cells. Activation of NF kappa B in several monocytic cell lines was also suppressed by tepoxalin. However AP-1 stimulation under the same conditions was not affected by tepoxalin. Other CO, LO inhibitors such as naproxen or zileuton did not inhibit NF kappa B activities. This inhibitory activity of tepoxalin was further illustrated by its suppression of NF kappa B regulated genes such as IL-6 in PMA stimulated human PBL and c-myc in IL-2 dependent T cell lines. Tepoxalin also blocked PMA + ionomycin-induced I kappa B degradation in a time-dependent fashion. The possible mechanism of tepoxalin in NF kappa B activation and its potential clinical application are discussed.
Treatment with LLLT caused a significant improvement in mouth opening and pain intensity in patients with MPDS. Similar improvement was not observed in naproxen group.
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Acute ethanol intoxication increased triacylglycerides (TAG) and thiobarbituric acid reactive substances (TBARS) in liver and promoted the liberation of epinephrine. Four non-steroidal anti-inflammatory drugs (NSAIDs)--aspirin, naproxen, nimesulide and piroxicam--prevented this increase in TAG and TBARS. Because fatty acids provided by adipose tissue contribute substantially to elevated hepatic TAG in ethanol-intoxicated rats, it was thought that the NSAIDs might reduce epinephrine-stimulated lipolysis in these rats. Isolated rat adipocytes were activated with epinephrine in the presence or absence of the NSAIDs. The NSAIDs inhibited epinephrine-stimulated lipolysis. These drugs did not modify the binding of dihydroalprenolol (beta-adrenergic agonist) to their receptors in isolated guinea-pig liver membranes. The NSAIDs, at concentrations 3,000-fold lower than that of cAMP, inhibited stimulated lipolysis by this messenger. In conclusion, aspirin, naproxen, nimesulide and piroxicam reduce the release of fatty acids from adipose tissue to the liver by inhibiting the epinephrine-stimulated lipolysis, and this, in part, explains the protective action of these NSAIDs against hepatic signs of acute ethanol intoxication.
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Aqueous (POR) and alcoholic (PE) fractions were successfully isolated from P. vietnamenis. Further biological investigations were performed using a classic test of paw edema induced by carrageenan, writhing induced by acetic acid, hot plate method and naproxen induced gastro-duodenal ulcer.
The significance of endogenously formed prostaglandins in the vasodilation induced by nicotinic acid (NIC) was investigated. The forearm venous plasma level of radioimmunoassayed PGE (R-PGE) and the forearm blood flow (FBF) were measured in 13 healthy male volunteers at rest and during infusion of NIC. Each subject was subsequently re-studied after pretreatment with the PG synthesis inhibitor, naproxen. In the absence of naproxen, NIC infusion resulted in an almost four-fold rise in the release of R-PGE and a 60% increase in FBF. Pretreatment with naproxen did not affect the basal release of R-PGE or the basal FBF but inhibited both the release of R-PGE and the increase in FBF following NIC. The data support the hypothesis that the vasodilating effect of NIC is largely dependent upon an increased vascular formation of PG.
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The efficacy and safety of ademetionine (A) vs naproxen (N) were tested in a double-blind trial carried out in 20 patients, each with activated gonarthrosis. The trial lasted 6 weeks. During the first week, A was administered at a daily dose of 3 x 400 mg and afterwards at a dose of 2 x 400 mg, whereas the daily dose of N during the first week was 3 x 250 mg and subsequently 2 x 250 mg. During the first two weeks, the patients were allowed to take paracetamol as an additional analgesic. The patients were examined at the beginning of the study and after 2, 4 and 6 weeks. The parameters tested were: pain (under different conditions), crepitation, joint swelling, circumference of joint, extent of motility and walking time over 10 meters. In addition to the usual laboratory tests, the serum keratane-sulphate concentrations (with monoclonal antibodies according to the ELISA technique of Eugene et al. ) were also determined. At the end of the 6th week no statistically significant difference between the two patient groups treated was found; both groups exhibited a marked improvement on all parameters. At the end of medication, the keratane-sulphate concentrations were not significantly changed. Five patients under A and 3 under N reported gastrointestinal side effects which were possibly drug-related. This study, performed in a small number of patients, showed a good efficacy and safety of ademetionine. Only further studies on a larger scale will show the importance of ademetionine in the therapy of rheumatic diseases.
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One hundred twenty patients with moderate to severe menstrual cramping were randomized. Eighty-seven patients completed all treatment cycles.
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Nimesulide was significantly more effective than placebo for the treatment of postoperative pain, as measured by the primary efficacy variable of summed pain intensity difference within 6 hours after first treatment (10.91 vs. 6.29). Furthermore, nimesulide also provided significantly better pain relief than naproxen on this parameter. Overall, nimesulide demonstrated superior analgesic activity compared with naproxen and placebo for the majority of secondary efficacy variables. All 3 treatments were well tolerated, with a lower number of patients reporting adverse events in the nimesulide group. Nimesulide recipients reported no gastrointestinal disorders.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may interfere with the anti-platelet activity of aspirin at the level of the platelet cyclooxygenase-1 (COX-1) enzyme. In order to examine the interference of common NSAIDs with the anti-platelet activity of aspirin the human platelet rich plasma from voluntary donors was used for arachidonic acid-induced aggregation and determination of thromboxane synthesis. Further, docking studies were used to explain the molecular basis of the NSAID/aspirin interaction. The experimental results showed that celecoxib, dipyrone (active metabolite), ibuprofen, flufenamic acid, naproxen, nimesulide, oxaprozin, and piroxicam significantly interfere with the anti-platelet activity of aspirin, while diclofenac, ketorolac and acetaminophen do not. Docking studies suggested that NSAIDs forming hydrogen bonds with Ser530, Arg120, Tyr385 and other amino acids of the COX-1 hydrophobic channel interfere with antiplatelet activity of aspirin while non interfering NSAIDs do not form relevant hydrogen bond interactions within the aspirin binding site. In conclusion, docking analysis of NSAID interactions at the COX-1 active site appears useful to predict their interference with the anti-platelet activity of aspirin. The results, demonstrate that some NSAIDs do not interfere with the antiplatelet action of aspirin while many others do and provide a basis for understanding the observed differences among individual non-aspirin NSAIDs.
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Neither traditional NSAIDs, nor COX-2 inhibitors, nor muscle relaxants dominated prescriptions for back pain. However, a small number of individual drugs were attributable to most of the prescriptions for traditional NSAIDs or muscle relaxants. The prescription of some of the medications demonstrated wide variations across different regions or different racial and educational groups. More studies are needed to understand the source of the variations and what constitutes optimal prescribing.
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Over the 17-year period 1969-1985, 2,721 reports of 3,521 suspected adverse drug reactions (ADRs) associated with non-steroidal anti-inflammatory drugs (NSAIDs) were submitted to the Danish Committee on ADRs. The results are presented together with the consumption of each drug during the same period. The total sale of NSAIDs showed a four-fold increase during the 17 years, the average corresponding to a permanent intake by 2.2% of the population. The number of reported ADRs per defined daily dose (DDD) sold was markedly lower for "older" drugs like the butazones, indomethacin, ibuprofen, naproxen, ketoprofen, and fenoprofen than for the drugs marketed during the last decade. These differences could not be accounted for by the well-known biases attached to spontaneous ADR reporting. Of 67 fatal reactions, 25 were due to bleeding or perforation of a gastric ulcer, mostly during treatment with indomethacin and naproxen, and in elderly people, and 27 were caused by bone marrow depression or leukaemia, begun mostly during treatment with butazones, but some with indomethacin and naproxen as well. It is pointed out that all reports on fatal bone marrow depression associated with butazones were submitted before 1976 and that the fact that none have been received since that time could be a result of better understanding of the proper dosage of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
To inform physicians who utilise over-the-counter (OTC) analgesics to treat osteoarthritis (OA) pain on differences among agents and to guide decisions in therapy selection.