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A total of 1052 osteoarthritis patients were enrolled into the trial. The incidence of gastroduodenal ulcers over 12 weeks was 5% in patients receiving valdecoxib 10 mg q.d., 4% in patients receiving valdecoxib 20 mg q.d., 7% in patients receiving placebo, 16% in patients receiving ibuprofen 800 mg t.i.d. (P <0.05 v. placebo), and 17% in patients receiving diclofenac 75 mg b.i.d. (P <0.05 v. placebo). The incidence of gastroduodenal ulcers at week 12 seen in the ibuprofen 800 mg t.i.d. and diclofenac 75 mg b.i.d. groups was significantly higher than that in the valdecoxib 10 mg q.d. and valdecoxib 20 mg q.d. groups (P <0.05). The incidence rates of gastroduodenal ulcers were not significantly different between the valdecoxib treatment groups or between valdecoxib- and placebo-treated patients. Efficacy responses to valdecoxib 10 mg and 20 mg q.d. were significantly greater than placebo and comparable with both ibuprofen 800 mg t.i.d. and diclofenac 75 mg b.i.d.
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York District Hospital.
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Osteoarthritis was induced by two intra-articular injections of either 250 U or 500 U of collagenase into the left knee joint of adult male Wistar rats. A six weeks time-course assessment of movement- and loading-induced nociception was performed by the Knee-Bend and CatWalk tests. The effect of morphine, lidocaine and diclofenac on nociceptive behaviour was evaluated in animals injected with 500 U of collagenase. Joint histopathology was scored for both doses throughout time. The expression of transient receptor potential vanilloid 1 (TRPV1) in ipsilateral dorsal root ganglia (DRG) was evaluated.
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Strategies about how to mitigate or prevent the appearance of pain associated with orthodontic treatment are poorly defined. Herein we conduct a prospective, double-blind, randomized controlled clinical trial assessing the effects of a single dose of anti-inflammatory medication to preemptively treat pain following the placement of orthodontic separating elastics.
Patients (N=604) with moderate to severe knee or hip OA tolerating stable DSR were randomised and treated with DSR 75 mg twice daily combined with intravenous tanezumab 10, 5 or 2.5 mg or placebo at weeks 0, 8 and 16. Co-primary efficacy endpoints (Western Ontario and McMaster Universities OA Index (WOMAC) Pain and Physical Function subscales and patient's global assessment of OA) were assessed at week 16.
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Patients undergoing an elective colon or rectal resection with primary anastomosis because of malignancy and treated within our enhanced recovery program were included. Univariable and multivariable logistic regression analyses were used to study risk factors for anastomotic leakage.
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Rat pharmacokinetics and in vivo disposition of a novel bisphosphonic prodrug of diclofenac (DIC-BP), synthesized with the aim of osteotropic delivery of diclofenac, were determined at whole body, organ and cellular levels in a dose range 0.32-10mg/kg. With an increase in injected dose, total body clearance was decreased while the distribution volume at steady state (V(dss)) was reduced and plasma half-life was prolonged. Over 50% of a dose of DIC-BP was selectively transported into osseous tissues after intravenous injection into rats at doses up to 1mg/kg. As dose increased, the skeletal distribution decreased with hepatic and splenic accumulations increasing. The intrahepatic distribution at 10mg/kg revealed that liver macrophages play a significant role in hepatic uptake of DIC-BP. This is consistent with general arguments that bisphosphonates themselves cannot distribute in soft tissues, but are taken up by the reticuloendothelial system as foreign substances when they form large complexes or aggregate with endogenous metals in plasma. Therefore, to optimize the osteotropic delivery of diclofenac via a bisphosphonic prodrug, the dosage regimen should be such that plasma concentration of DIC-BP is maintained at a level lower than that required for precipitate formation of complexes, similar to the usage of other bisphosphonates.
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In the human brain several cell types are capable of initiating and amplifying a brain specific inflammatory response involving the synthesis of cytokines, prostaglandins and oxygen free radicals. In Alzheimer's disease (AD), signs of an inflammatory activation of microglia and astroglia are present inside and outside amyloid deposits. Cell culture and animal models suggest an interactive relationship between inflammatory activation, reduced neuronal functioning and deposition of amyloid. The activation of inflammation-associated enzymes such as p38 mitogen-activated protein kinase (p38 MAPK) and cycloxygenase-2 (COX-2) is not restricted to glial cells but also found in neurons and may contribute to intraneuronal damage. Epidemiological studies have shown a reduced risk of AD among users of anti-inflammatory drugs. Therefore, anti-inflammatory drugs have become the focus of several new treatment strategies. Small clinical trials with non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin and diclofenac showed a trend for a disease modifying effect, while clinical trials with steroids did not show a beneficial effect. NSAIDs may not only act on COX-2 but also inhibit COX-1 activity or activate peroxisome proliferator-activated receptor gamma (PPAR gamma). Among promising new strategies to reduce the inflammatory activation in the CNS interfering with intracellular pro-inflammatory pathways has been shown to be effective in various cell culture and animal models. Inhibitors of p38MAPK and PPAR gamma agonists may be suitable agents to suppress inflammatory activation in AD.
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Diclocor is a promising corrector of inflammatory and destructive joint diseases. Owing to the presence of both diclofenac sodium and quercetin in its composition, Diclocor exhibits a complex mechanism of anti-inflammatory action affecting cyclooxygenase and lipoxygenase ways of arachidonic acid biotransformation.
A retrospective chart review of 175 children was carried out at a children's hospital and a paediatric unit in a large teaching hospital. The analgesics that were administered in the first 24 hours post-surgery were morphine, codeine, diclofenac, ibuprofen and paracetamol.
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Twelve domestic pigs, weighing 17.5 to 27 kg.
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The palonosetron-dexamethasone combination was more effective as compared to only palonosetron for reducing PONV after laparoscopic cholecystectomy.
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Different quality indicators were analysed for the following groups of medicines: oral diabetes drugs, anti-platelet aggregation drugs, anti-hypertension drugs, non-steroidal anti-inflammatories, tranquillisers and hypnotic drugs, antibiotics, anti-asthmatic drugs and the omeprazol efficiency indicator. Consumption was expressed in defined daily doses (DDD) and in DDD per 1000 persons and per day (DID). A prescription quality indicator was indicated on the basis of weighing up the indicators.
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To explore the suppressive effects of anti-inflammatory drugs on DC maturation and, in particular, polarization.
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Pain is a common distressing adverse effect in the early postoperative period following caesarean section. The aim of this study was to investigate the effect on postoperative pain, analgesic requirement and haemodynamic profile of placing a suprafacial bupivacaine-soaked absorbable gelatin sponge in the caesarean section wound.
The aim of this work was to study the regulation of LPS-stimulated PGE 2 synthesis by traditional NSAIDs (piroxicam and diclofenac) and a selective COX-2 inhibitor (NS-398), in cultured bovine corneal endothelial cells and retinal pigmentary epithelial cells. The IC50 values of piroxicam and diclofenac were compared with IC50 values of NS-398, diclofenac, in both types of cells, showed higher potency than piroxicam. Diclofenac seemed to be a COX-2 inhibitor because its IC50 values were similar to the IC50 values of NS-398. We suggest that this in vitro cell assay system could be useful for identifying compounds that selectively inhibit COX-2 in ocular tissues.
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A six week, double-blind, randomized, parallel group, multicentre study was conducted in 85 patients with osteoarthritis of the knee and hip to compare the efficacy, tolerability, and safety of Flurbiprofen-SR 200 mg with Diclofenac Sodium-SR 100 mg. Between group comparisons, based on change scores from baseline, we detected no significant differences between the two drugs with respect to efficacy for the majority of outcome measures. There was no significant difference between the groups in the proportion of patients experiencing at least one adverse medical event or in terminations from treatment. We conclude that Flurbiprofen-SR 200 mg is similar in efficacy, tolerability, and safety to Diclofenac Sodium-SR in this trial.
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Most non-steroidal antiinflammatory drugs (NSAIDs) are extensively metabolized by liver oxidation with broad interindividual variability, but little is known about the nature of the enzyme(s) catalysing these reactions. The role of specific cytochrome P450 isozymes in the formation of the major oxidized metabolites of phenylacetic acid (diclofenac), propionic acid (ibuprofen), fenamate (mefenamic acid) and oxicam (piroxicam and tenoxicam) derivatives was studied in human liver microsomes using mostly selective inhibition by known substrates and inhibitors of specific cytochrome P450 monooxygenases. A common isozyme (P450TB, CYP2C subfamily) controls the major elimination pathways of these NSAIDs. The authors have also determined, in two in vitro models of P450TB activity, the affinity for this isozyme of other NSAIDs (acetylsalicylic acid, indomethacin, pirprofen). The NSAIDs tested displayed a high affinity (5-500 microM): diclofenac approximately mefenamic acid > ibuprofen approximately indomethacin approximately piroxicam approximately tenoxicam > acetylsalicylic acid approximately pirprofen. Cytochrome P450TB therefore plays a key role in the oxidation by human liver of major NSAIDs from various chemical classes. Inhibition data and chemical structure similarities suggest that many other NSAIDs may be substrates of this isozyme as well. P450TB appears to be a common site both for the control of interindividual differences in the capacity to oxidize major NSAIDs and for interactions involving NSAIDs as well as other known substrates (oral anticoagulants, hypoglycaemic sulfonylureas, phenytoin) or inhibitors (antifungals, antibacterial sulfonamides, calcium channel blockers) of P450TB. Consequently this P450 isozyme is likely to be a major determinant of NSAIDs action.
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There is professional risk of tennis elbow for housewives, farmers and shopkeepers in context of Nepal. Only one treatment approach is not effective in management of tennis elbow for long term effect.
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Glycated albumin has been causally linked to the pathobiology of diabetic renal disease through its ability to stimulate the expression of transforming growth factor-beta1 (TGF-beta1), activate protein kinase C (PKC) and extracellular signal-regulated kinase (ERK), and promote production of extracellular matrix proteins in cultured glomerular cells. Whether glycated albumin modulates glomerular TGF-beta1 expression in vivo is not known. To address this issue, we assessed glomerular TGF-beta1 expression and pathology in response to reducing the burden of glycated albumin in vivo.
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Multimodal analgesia (MMA) by synergy with volatile anesthetics minimizes their use thus decreasing operation theater pollution and greenhouse gas emission.
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A fibrosarcoma (WEHI-164) cell line was used for evaluating tolerability, MMP-2 activity, and apoptosis. Dexamethasone, piroxicam, and diclofenac were used at concentrations of 10-200 microg/ml in triplicate, two-fold dilutions. MMP-2 activity was assessed using zymography. For assessment of apoptosis, terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) was used.
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Injectable formulations of diclofenac have long been available in Europe and other countries. These formulations use a default dose of 75 mg of diclofenac delivered IV over 30 to 120 minutes or as an IM injection. A novel formulation of injectable diclofenac sodium, Dyloject®, is solubilized with hydroxypropyl β-cyclodextrin (HPβCD) so that it can be given IV or IM in a small volume bolus. In this multicenter, multiple-dose, multiple-day, randomized, double-blind, parallel-group phase 3 study, we investigated whether lower doses of HPβCD diclofenac delivered as a small volume bolus would be effective for the management of acute pain after abdominal or pelvic surgery.
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Dihydroxy bile acids induce a bicarbonate-rich hypercholeresis when secreted into canalicular bile in unconjugated form; the mechanism is cholehepatic shunting. The aim of this study was to identify a xenobiotic that induces hypercholeresis by a similar mechanism.
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To compare the efficacy of the non-steroidal antiinflammatory drugs, diclofenac sodium and flunixin meglumine as adjuncts to the antibiotic treatment of bovine respiratory disease (BRD).