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Voltaren

Generic Voltaren is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Generic Voltaren is used to treat pain or inflammation caused by arthritis or ankylosing spondylitis. Generic Voltaren works by reducing hormones that cause inflammation and pain in the body.

Other names for this medication:

Similar Products:
Celebrex, Diclofenac Gel, Mobic, Anaprox, Naprosyn

 

Also known as:  Diclofenac.

Description

Generic Voltaren is used to treat pain or inflammation caused by arthritis or ankylosing spondylitis.

Generic Voltaren is in a group of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Generic Voltaren works by reducing hormones that cause inflammation and pain in the body.

Voltaren is also known as Diclofenac, Voveran, Voltarol, Voltarol SR, Voltarol Retard, Voltarol Rapid, Diclomax SR, Diclomax Retard, Motifene, Defenac, Diclofex, Diclozip, Dyloject, Fenactol, Flamrase, Flamatak, Econac, Rhumalgan SR, Rhumalgan XL, Volsaid SR.

Generic name of Generic Voltaren is Diclofenac.

Brand names of Generic Voltaren are Cataflam, Voltaren, Voltaren-XR.

Dosage

Take Generic Voltaren orally.

Do not crush or chew the pill. Swallow it whole.

Take Generic Voltaren with great amount of water.

Take Generic Voltaren with or without food.

If you want to achieve most effective results do not stop taking Generic Voltaren suddenly.

Overdose

If you overdose Generic Voltaren and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Voltaren overdosage: nausea, vomiting, stomach pain, black or bloody stool, shallow breathing, fainting, coma.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Voltaren are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Voltaren if you are allergic to Generic Voltaren components or to aspirin or other NSAIDs.

Do not take Generic Voltaren if you are pregnant, planning to become pregnant. Do not breast-feed while taking Generic Voltaren.

Do not take Generic Voltaren if you just before or after having heart bypass surgery (also called coronary artery bypass graft, or CABG).

Be careful with Generic Voltaren if you use any other over-the-counter cold, allergy, or pain medicataion.

Be careful with Generic Voltaren if you had a history of heart attack, stroke or blood clot, heart disease, congestive heart failure, high blood pressure, liver or kidney diseases, asthma, polyps in the nose.

Be careful with Generic Voltaren if you smoke.

Be careful with Generic Voltaren if you take antidepressants, blood thinner (Coumadin); cyclosporine, lithium, methotrexate, you take diuretics, you take steroids.

Avoid exposure to sunlight or artificial UV rays (sunlamps or tanning beds).

Avoid alcohol.

It can be dangerous to stop Generic Voltaren taking suddenly.

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Both treatment groups showed significant improvement compared with their baseline values in the four primary endpoints. Mean between-treatment differences favoured aceclofenac over paracetamol on pain (VAS, 7.64 mm [95% confidence interval (CI), 0.44-14.85 mm]), Lequesne OA index (1.41 [95% CI, 0.45-2.36]), and patient's (0.33 [95% CI, 0.06-0.61]) and physician's (0.23 [95% CI, 0.01-0.47]) global assessments. Adverse events were similar for both drugs (paracetamol, 29% patients vs aceclofenac, 32%; P=0.71). Four patients withdrew in each group due to adverse events. Patients tended to prefer aceclofenac to paracetamol (P=0.001), and more treated with paracetamol withdrew from the study due to lack of efficacy (n=8 vs n=1, P=0.035, for paracetamol and aceclofenac, respectively).

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Cytochrome P450 (CYP) and uridine diphosphate glucuronosyltransferase (UGT) isoenzymes involved in riluzole oxidation and glucuronidation were characterized in (1) kinetic studies with human hepatic microsomes and isoenzyme-selective probes and (2) metabolic studies with genetically expressed human CYP isoenzymes from transfected B-lymphoblastoid and yeast cells. In vitro incubation of [14C]riluzole (15 microM) with human hepatic microsomes and NADPH or UDPGA cofactors resulted in formation of N-hydroxyriluzole (K(m) = 30 microM) or an unidentified glucuroconjugate (K(m) = 118 microM). Human microsomal riluzole N-hydroxylation was most strongly inhibited by the CYP1A2 inhibitor alpha-naphthoflavone (IC50 = 0.42 microM). Human CYP1A2-expressing yeast microsomes generated N-hydroxyriluzole, whereas human CYP1A1-expressing yeast microsomes generated N-hydroxyriluzole, two additional hydroxylated derivatives and an O-dealkylated derivative. CYP1A2 was the only genetically expressed human P450 isoenzyme in B-lymphoblastoid microsomes to metabolize riluzole. Riluzole glucuronidation was inhibited most potently by propofol, a substrate for the human hepatic UGT HP4 (UGT1.8/9) isoenzyme. In vitro, human hepatic microsomal hydroxylation of riluzole (15 microM) was weakly inhibited by amitriptyline, diclofenac, diazepam, nicergoline, clomipramine, imipramine, quinine and enoxacin (IC50 approximately 200-500 microM) and cimetidine (IC50 = 940 microM). Riluzole (1 and 10 microM) produced a weak, concentration-dependent inhibition of CYP1A2 activity and showed competitive inhibition of methoxyresorufin O-demethylase. Thus, riluzole is predominantly metabolized by CYP1A2 in human hepatic microsomes to N-hydroxyriluzole; extrahepatic CYP1A1 can also be responsible for the formation of several other metabolites. Direct glucuronidation is a relatively minor metabolic route. In vivo, riluzole is unlikely to exhibit significant pharmacokinetic drug interaction with coadministered drugs that undergo phase I metabolism.

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The removal of 10 organic micropollutants (OMPs) was studied in two MBRs using different types of membrane (flat sheet microfiltration, MF, and hollow fiber ultrafiltration, UF) operated under aerobic conditions with direct dosing of powdered activated carbon (PAC) in the mixed liquor. In both reactors high COD degradation and nitrification were achieved (>95%), while nitrate removal was only observed after PAC addition. The adsorbent improved the operation of both systems (sludge properties and microbial diversity) which resulted in an enhancement of the quality of the final effluent. The operation with both types of membrane was feasible being the UF system slightly better in terms of the quality of the final effluent. The strategy of 250 mg/L of PAC additions every 35 days was validated according to the results obtained for the removal of the most recalcitrant OMPs, such as diclofenac and carbamazepine. Concerning the type of membrane, only significant differences were observed for diclofenac and roxithromycin, which were better removed in the UF configuration. These differences were attributed to sorption and/or further biotransformation processes occurring in the cake layer.

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In India, a number of fixed dose drug combinations of non-steroidal anti-inflammatory drugs (NSAID's) are available, often as over-the-counter products. These combinations are being prescribed too. Evidence for efficacy of NSIAD fixed dose combination is lacking.

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The bark of Rhizophora mangle, the red mangrove, has been used traditionally in folk medicine of Caribbean countries due to its antiseptic, astringent, haemostatic and antifungal properties. Aqueous extracts are rich in tannins and have been proven experimentally to possess antibacterial, wound healing and antiulcerogenic effects. This work was designed to determine the gastroprotective effect of Rhizophora mangle in a model of diclofenac-induced ulcers in rats and to study the mechanisms involved, using the proton pump inhibitor omeprazole as a comparison. The lyophilized extract was given by oral gavage (125 and 62.5mg/kg) three times at 12h intervals before administering diclofenac 100mg/kg. Pretreatment with the extract resulted in a significant decrease of the ulcerated area (P<0.01). Rhizophora mangle induced a recovery of PGE(2) levels, which had been depleted by diclofenac. No anti-inflammatory effect was observed ex vivo or in vitro. The highest dose of the extract provoked a marked increase in glutathione peroxidase and superoxide dismutase activity, which was comparable to omeprazole. Furthermore, lipid peroxidation levels were inhibited in a dose-dependent manner. These results suggest that the gastroprotective effect of Rhizophora mangle in this experimental model appears through an antioxidant and prostaglandin-dependent way.

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Ketamine is currently the N-methyl-D-aspartate receptor channel blocker in clinical use. Morphine in pain management is usually limited by adverse effect such as nausea and vomiting. Adjuvant treatment with ketamine may be value in giving better analgesia with fewer adverse effects. The purpose of this meta-analysis was to evaluate the differences when patients received morphine with adjuvant ketamine (MK) compared with higher dose of morphine (MO) for acute pain.

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Ketoprofen patches are effective and safe pain relievers for the treatment of sports injury pain with advantages compared with diclofenac gel.

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DFNa was successfully dispersed into IPM as a nanosized suspension via complex formation with sucrose erucate. The resultant SONS increased the permeability flux of DFNa across the YMP skin by up to 3.8-fold compared with the control. The size of the SONS depended on the weight ratio of the surfactant to DFNa. The optimal weight ratio for the highest DFNa permeation was 8.8, at which point the mean diameter of the SONS was 14.4 nm.

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Valdecoxib was significantly better at endpoint than standard doses of naproxen, diclofenac, and ibuprofen for pain intensity scores (p < 0.05), and provided significantly improved nonpain symptom and satisfaction scores compared with naproxen for patients with RA (p < 0.05). For RA patients, the difference between valdecoxib and naproxen pain intensity scores were clinically meaningful; at all the time points, significantly fewer patients receiving valdecoxib reported severe dyspepsia pain intensity increases (>/=10 points) than those receiving naproxen. At 12 wk, fewer patients receiving valdecoxib reported severe dyspepsia pain intensity increases versus those receiving ibuprofen and diclofenac.

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Drug-induced nephrotoxicity still hampers drug development, because current translation from in vitro or animal studies to human lacks high predictivity. Often, renal adverse effects are recognized only during clinical stages of drug development. The current study aimed to establish a robust and a more complete human cell model suitable for screening of drug-related interactions and nephrotoxicity. In addition to endogenously expressed renal organic cation transporters and efflux transporters, conditionally immortalized proximal tubule epithelial cells (ciPTEC) were completed by transduction of cells with the organic anion transporter (OAT) 1 or OAT3. Fluorescence-activated cell sorting upon exposure to the OAT substrate fluorescein successfully enriched transduced cells. A panel of organic anions was screened for drug-interactions in ciPTEC-OAT1 and ciPTEC-OAT3. The cytotoxic response to the drug-interactions with antivirals was further examined by cell viability assays. Upon subcloning, concentration-dependent fluorescein uptake was found with a higher affinity for ciPTEC-OAT1 (Km = 0.8 ± 0.1 μM) than ciPTEC-OAT3 (Km = 3.7 ± 0.5 μM). Co-exposure to known OAT1 and/or OAT3 substrates (viz. para-aminohippurate, estrone sulfate, probenecid, furosemide, diclofenac, and cimetidine) in cultures spanning 29 passage numbers revealed relevant inhibitory potencies, confirming the robustness of our model for drug-drug interactions studies. Functional OAT1 was directly responsible for cytotoxicity of adefovir, cidofovir, and tenofovir, while a drug interaction with zidovudine was not associated with decreased cell viability. Our data demonstrate that human-derived ciPTEC-OAT1 and ciPTEC-OAT3 are promising platforms for highly predictive drug screening during early phases of drug development.

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Pathologic activation of both digestive zymogens and the transcription factor nuclear factor kappaB are early events in acute pancreatitis; these pathologic processes are inhibited in experimental pancreatitis by curcumin and the pH modulator chloroquine. Primary sensory neurons may constitute a final common pathway for pancreatic inflammation. Experimental acute pancreatitis and associated lung injury are attenuated by inhibiting the prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine receptor antagonist Met-RANTES. Endoscopic retrograde cholangiopancreatography-induced acute pancreatitis can be reduced experimentally by intraductal neurokinin-1 receptor antagonist and clinically by use of diclofenac and pancreatic duct stenting. MRI in the setting of acute pancreatitis is a reliable method of staging disease severity. Distinct patterns of cytokine response are observed in acute pancreatitis.

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We compared the effect of rofecoxib and three nonselective nonsteroidal antiinflammatory drugs on platelet function, measured by CD 62 P expression. Platelet function was not altered by rofecoxib, but it was inhibited by aspirin, diclofenac, and lornoxicam. Rofecoxib may be safer than classic NSAIDs with respect to platelet function during the perioperative period.

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Recent prescription NSAID use was associated with an increased risk for initiation of antihypertensive therapy (odds ratio (OR) = 1.6, 95%CI 1.5, 1.7) as were selective COX-2 inhibitors (OR = 1.8, 95%CI 1.6, 2.1). After adjusting for age, sex, co-payment, race, and exposure to other NSAIDs/COX-2, each non-selective NSAID (diclofenac, ibuprofen, indomethacin, naproxen, oxaprozin) was associated with an increased risk of antihypertensive therapy initiation, with ORs ranging from 1.4 to 1.8. Recent users of COX-2 inhibitors had an increased risk of initiating antihypertensive therapy, regardless of specific drug (celecoxib adjusted OR = 1.7 (95%CI 1.3, 2.1); rofecoxib adjusted OR = 1.7 (95%CI 1.4, 1.9)).

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Tanezumab, a monoclonal antibody, inhibits nerve growth factor and reduces chronic pain. This randomised, double-blind, controlled multicentre study was conducted to evaluate the efficacy and safety of tanezumab added to oral diclofenac sustained release (DSR) in patients with hip or knee osteoarthritis (OA) pain.

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We searched the PubMed database for peer-reviewed articles published in any language from database inception through February 2016.

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Non-steroidal anti-inflammatory drug, Diclofenac, targeting COX have shown promise in the treatment of Acanthamoeba keratitis, but the underlying mechanisms remain unknown. Using various NSAIDs, Diclofenac sodium, Indomethacin, and Acetaminophen, here we determined the effects of NSAIDs on the biological properties of Acanthamoeba castellanii belonging to the T4 genotype. Using amoebicidal assays, the results revealed that Diclofenac sodium, and Indomethacin affected growth of A. castellanii. In contrast, none of the compounds tested had any effect on the viability of A. castellanii. Importantly, all NSAIDs tested abolished A. castellanii encystation. This is a significant finding as the ability of amoebae to transform into the dormant cyst form presents a significant challenge in the successful treatment of infection. The NSAIDs inhibit production of cyclo-oxegenase, which regulates the synthesis of prostaglandins suggesting that cyclooxygenases (COX-1 and COX-2) and prostaglandins play significant role(s) in Acanthamoeba biology. As NSAIDs are routinely used in the clinical practice, these findings may help design improved preventative strategies and/or of therapeutic value to improve prognosis, when used in combination with other anti-amoebic drugs.

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In this research, we investigated the cytotoxic mechanisms of one of the widely used pharmaceuticals that are regularly associated with the adverse effects on the liver, sometimes leading to acute liver failure, diclofenac. Diclofenac liver cytotoxicity was associated with reactive oxygen species (ROS) formation and lipid peroxidation which were inhibited by antioxidants and ROS scavengers, ferric chelator, inhibitors of reduced CYP2E1 and CYP2C9, mitochondrial permeability transition (MPT) pore sealing agents and endocytosis inhibitors. Incubation of hepatocytes with diclofenac caused rapid hepatocyte glutathione (GSH) depletion which is another marker of cellular oxidative stress. Most of the diclofenac-induced GSH depletion could be attributed to the expulsion of GSSG. Diclofenac cytotoxicity was also associated with mitochondrial injury, lysosomal membrane rupture and release of digestive proteases which were prevented by antioxidants, MPT pore sealing agents, lysosomotropic agents and inhibitors of cytochrome P450 isoenzymes. These events could cause cytochrome C release from the mitochondrial intramembrane space to cytosol. The cytochrome C release could trigger activation of caspase-3 and apoptosis. We finally concluded that diclofenac hepatotoxicity is a result of metabolic activation by CYP2E1 and CYP2C9 and ROS formation, leading to a mitochondrial/lysosomal toxic cross-talk in the liver hepatocytes.

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Symptomatic hepatic effects attributable to most NSAIDs are extremely rare and usually mild.

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We included randomised, double-blind, placebo-controlled or active-controlled studies, or both, using self administered diclofenac to treat a migraine headache episode, with at least 10 participants per treatment arm.

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Polyspecific transporters from the organic anion transporting polypeptide (OATP/Oatp) superfamily mediate the uptake of a wide range of compounds. In zebrafish, Oatp1d1 transports conjugated steroid hormones and cortisol. It is predominantly expressed in the liver, brain and testes. In this study we have characterized the transport of xenobiotics by the zebrafish Oatp1d1 transporter. We developed a novel assay for assessing Oatp1d1 interactors using the fluorescent probe Lucifer yellow and transient transfection in HEK293 cells. Our data showed that numerous environmental contaminants interact with zebrafish Oatp1d1. Oatp1d1 mediated the transport of diclofenac with very high affinity, followed by high affinity towards perfluorooctanesulfonic acid (PFOS), nonylphenol, gemfibrozil and 17α-ethinylestradiol; moderate affinity towards carbaryl, diazinon and caffeine; and low affinity towards metolachlor. Importantly, many environmental chemicals acted as strong inhibitors of Oatp1d1. A strong inhibition of Oatp1d1 transport activity was found by perfluorooctanoic acid (PFOA), chlorpyrifos-methyl, estrone (E1) and 17β-estradiol (E2), followed by moderate to low inhibition by diethyl phthalate, bisphenol A, 7-acetyl-1,1,3,4,4,6-hexamethyl-1,2,3,4 tetrahydronapthalene and clofibrate. In this study we identified Oatp1d1 as a first Solute Carrier (SLC) transporter involved in the transport of a wide range of xenobiotics in fish. Considering that Oatps in zebrafish have not been characterized before, our work on zebrafish Oatp1d1 offers important new insights on the understanding of uptake processes of environmental contaminants, and contributes to the better characterization of zebrafish as a model species.

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Low-dose droperidol and dolasetron are equally effective to reduce the incidence of PONV after cataract surgery under general anaesthesia. The combination of both drugs revealed no additional effect.

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To report the management of cardiovascular failure refractory to standard catecholamine therapy with terlipressin in a patient with tricyclic antidepressant (TCA) intoxication.

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The study included 61 patients randomized into three different groups; group A received desmopressin (40 microg, nasal spray), group B diclofenac (75 mg) intramuscularly and group C, both desmopressin and diclofenac. Pain was assessed using a visual analogue scale (a 10-cm horizontal scale ranging from 'no pain' to 'unbearable pain') at baseline, 10, 20 and 30 min after administering the treatments.

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A five-port transperitoneal laparoscopic approach with an indigenous hand port was used to perform the radical cystectomy in a patient with muscle invasive TCC of bladder. After specimen retrieval, ileal conduit reconstruction was performed extra-corporeally through the site of hand port incision.

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Several clinical trials have demonstrated that low doses of non-steroidal anti-inflammatory drugs relieve episodic tension-type headache (ETH).

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407 subjects successfully completed the 6-month treatment. Sixteen patients (12.2%) withdrew from the diclofenac group, 16 (12.2%) from the nabumetone group, 17 (11.8%) from the meloxicam group and five (9.1%) from the celecoxib group. Most withdrawals occurred during the first 3 months of treatment. Reasons for withdrawals in the first three groups were lack of efficacy (44.9%) and adverse effects (38.8%). For the celecoxib group, high cost (80%) was the main reason for withdrawal. Adverse drug reactions to NSAIDs mostly occurred at an early stage of treatment, with an incidence rate of 31.9% for the diclofenac group, 19.9% for the nabumetone group, 25.2% for the meloxicam group, and 7.27% for the celecoxib group. Clinical efficacy rates for the four NSAIDs were positively related to the length of treatment. During the first 4 months, diclofenac, meloxicam and celecoxib showed better efficacy than nabumetone. There were no significant differences in efficacy during the fifth and sixth months. The overall 6-month effectiveness rates were 68.8% for diclofenac, 59.8% for nabumetone, 67.6% for meloxicam and 69.1% for celecoxib.

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RBXG has a quicker initiation and better treatment effects than sole anti-inflammatory and analgesic agents on the treatment of repeatedly attacking acute gouty arthritis, showing no obvious toxic or adverse reactions and therefore good for long-term administration and likely to be a safe TCM preparation to control the symptoms and reduce the onsets of repeatedly attacking of acute gouty arthritis. The animal experiment shows that both the compound preparation and part of the single ingredients in the recipe have the function of reducing blood uric acid. However, the compound recipe has better therapeutic effects, proving to be superior to single drugs.

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The aim of this study was to compare the anti-inflammatory activities of ketorolac tromethamine 0.4% and 0.1%; diclofenac sodium 0.1%; and loteprednol etabonate 0.5% suspension in an animal model of ocular inflammation.

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There were no significant differences in age, estimated blood loss, oral intake, and hospital stay between groups. A significant difference in favor of the modified group was noted with respect to analgesia use (diclofenac sodium, 50 mg vs 100 mg; P<.05) in all 3 modified methods, as well as in cosmetic outcome in the groups undergoing the first modification (score, 8.9±2.2 VS 7.3±2.8; P<.05) and second modification (score, 8.7±2.5 VS 7.1±2.4; P<.05). In addition, the mean operative time in patients undergoing ureter operations was shorter than that in the conventional group using classical 3-port positions (55±11 minutes vs 70±15 minutes, P<.05).

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Polymerized rosin (PR) a novel film forming polymer is characterized and investigated in the present study for its application in drug delivery. Films were produced by a casting/solvent evaporation method from plasticizer free and plasticizer containing solutions. Films prepared from different formulations were studied for their mechanical (tensile strength, percent elongation and Young's modulus), water vapour transmission and moisture absorption characteristics. Neat PR films were slightly brittle and posed the problem of breaking during handling. Hydrophobic plasticizers, dibutyl sebacate and tributyl citrate, improved the mechanical properties of free films with both the plasticizers showing significant effects on film elongation. Release of diclofenac sodium (model drug) from coated pellets was sustained with high coating levels. Concentration of plasticizer was found to affect the release profile. PR films plasticized with hydrophobic plasticizers could therefore be used in coating processes for the design of oral sustained delivery dosage forms.

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The most common causes of variability in drug response include differences in drug metabolism, especially when the hepatic cytochrome P450 (CYP) enzymes are involved. The current study was conducted to assess the differences in CYP activities in human liver microsomes (HLM) of Chinese or Caucasian origin.

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To review the analgesic efficacy, duration of analgesia, and adverse effects of a single oral dose of lumiracoxib for moderate to severe postoperative pain in adults and compare it with established analgesics.

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In June of 1999, the market share of generic drugs in Spain was 1.15% in units and 0.91% in pesetas of the hole drug prescription. The most used were oral ranitidine, oral diclofenac and oral amoxicillin. Catalonia, in this period, has a greater relative utilization of generic drugs, specially in psychotherapeutic agents like alprazolam and fluoxetine. During the first semester of 1999 only in 9.9% of the occasions where generic drugs could be used, were they actually prescribed. Specifically, the drug most used in its generic form was oral diclofenac with 27.1% of the all possible prescriptions. The real savings generated by the generic drugs were 0.2% of the public pharmaceutical bill, and the theoretical capacity of savings with the current generic offer were 2.3%.

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Various diclofenac acid hydrazones and amides were synthesized and evaluated for in vitro and in vivo antimycobacterial activities against Mycobacterium tuberculosis. Preliminary results indicated that most of the compounds demonstrated better in vitro antimycobacterial activity (MIC: 0.0383-7.53 microM) than diclofenac (MIC: 21.10 microM) and ciprofloxacin (MIC: 9.41 microM). Among the synthesized compounds, 1-cyclopropyl-6-fluoro-8-methoxy-7-[[N4-(2-(2-(2,6-dichlorophenylamino)phenyl)acetyl)-3-methyl]-N1-piperazinyl]-4-oxo-1,4-dihydro-3-quinoline carboxylic acid (5d) was found to be the most active compound in vitro with MIC of 0.0383 microM and was more potent than first line antitubercular drug isoniazid (MIC: 0.1822 microM). In the in vivo animal model 5d decreased the bacterial load in lung and spleen tissues with 2.42- and 3.66-log10 protections, respectively, at 25 mg/kg body weight.

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In this prospective noncomparative case series, 10 eyes of 10 patients with clinically significant diabetic macular edema (n = 5), neovascular age-related macular degeneration (n = 2), pseudophakic cystoid macular edema (n = 1), macular edema secondary to old branch retinal vein occlusion (n = 1), and cystoid macular edema secondary to chronic intermediate uveitis (n = 1) received 500 microg/0.1 mL of intravitreal diclofenac. The primary outcome measure was change in visual acuity.

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This single-arm prospective observational study was designed to evaluate patient acceptability and feasibility of the Thermablate endometrial ablation (EA) system (TEAS), a new-generation endometrial thermal balloon ablation system, as an office procedure. It was set up in a one-stop menstrual disorder clinic with a facility for outpatient hysteroscopy in the Queen's Medical Center, Nottingham University Hospitals, Nottingham, United Kingdom. Seventy premenopausal women mainly, with menorrhagia, without earlier endometrial preparation were included in the study. The exclusion criteria were women requesting general anesthesia, presence of submucous myoma, suggestion of malignant lesions, and a desire to preserve fertility. The intervention involved the use of global thermal EA with TEAS. This is an endometrial balloon ablation system that combines a "thermablation" time of 128 seconds with automatic controls of the treatment parameters of temperature and pressure, without any earlier endometrial preparation. Patients were given diclofenac sodium (100 mg orally) 2 hours before the procedure, with intracervical 4% prilocaine and intracavitary lidocaine gel for analgesia. Main results involved measurement of overall satisfaction with TEAS as an outpatient (office) procedure, intraoperative and postoperative pain scores, need for additional analgesia, nausea and vomiting rate, total time in clinic and the need for any admission, speed of recovery, and time away from home. In conclusion, the TEAS appears to be a well-accepted and safe outpatient procedure for treating menorrhagia.

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The inhibitory actions of etodolac on prostaglandin (PG) E2 biosynthesis, active oxygen generation and bradykinin formation were compared with those of indomethacin, diclofenac Na, piroxicam, naproxen, ketoprofen and aspirin. The inhibitory action (IC50 5.35 x 10(-8) M) of etodolac on PGE2 biosynthesis in rabbit articular chondrocytes stimulated by interleukin-1 (IL-1) beta was about 1/5 that of indomethacin. The inhibitory action of etodolac on spontaneous PGE2 biosynthesis in rabbit gastric epithelial cells (RGEs) (IC50 2.27 x 10(-5) M) and Madin-Darby canine kidney cells (MDCKs) (IC50 4.54 x 10(-7) M) was much less than that in rabbit articular chondrocytes stimulated by IL-1 beta and about 1/19 and 1/9 that of indomethacin in rabbit gastric epithelial cells (RGEs) and Madin-Darby canine kidney cells (MDCKs), respectively. The inhibitory action of etodolac on active oxygen generation was similar to that of indomethacin and piroxicam, and more potent than that of naproxen, ketoprofen and aspirin. The inhibitory action of etodolac on bradykinin formation was the most potent among the seven anti-inflammatory drugs tested. Both etodolac and bromelain inhibited the inflammatory pain in concanavalin A-treated paws of rats in a dose-dependent manner, but indomethacin did not. These results indicate that etodolac is an anti-inflammatory drug which suppress IL-1 beta-stimulated PGE2 biosynthesis in rabbit articular chondrocytes, active oxygen generation and bradykinin formation. It has less suppressive action against spontaneous PGE2 biosynthesis in RGEs and MDCKs. Thus, etodolac is considered to be a safe anti-inflammatory drug for clinical use.

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voltaren max buy 2017-08-23

A new UPLC-MS-MS method was developed and validated for quantification of diclofenac sodium in rabbit plasma. Acetonitrile-based protein precipitation method was used to extract the drug from plasma samples. Chromatographic separation was carried out on Acquity UPLC(®)BEH phenyl C18 1.7 µm, 2.1 × 50 mm column. Drug elution was facilitated by using mobile phase containing acetonitrile (0.1% glacial acetic) and water (pH 3.5), in a ratio of 75 : 25, flowing at 0.2 mL/min. Molecular ions were generated by using the positive electrospray ionization mode (ESI(+)) and analyzed on a triple-quadrupole mass spectrometer. The ionic transitions of diclofenac (m/z 296 > 214 and 249.9) and flufenamic acid (internal standard) (m/z 282.1 > 166.9 and 244) were measured in multiple reaction modes. Developed method is simple, quick, precise and accurate over a linearity range of 80-4, buy voltaren 000 ng/mL. The lower limit of quantification (LLOQ) for diclofenac was 80 ng/mL. The percentage recoveries of diclofenac at three quality control samples were 54 ± 6.1, 67.1 ± 5.4 and 62.3 ± 1.4%. Precision and accuracy of the assay at LLOQ, middle limit of quantitation and higher limit of quantitation were 100 ± 7.0, 100 ± 1.0 and 100 ± 2.0% and 81.8 ± 4.6, 106.6 ± 3.1 and 103.3 ± 4.0%, respectively.

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To compare the anti-inflammatory effect of topical diclofenac sodium 0.1% in a fixed combination with gentamicin 0.3% to the anti-inflammatory effect of dexamethasone phosphate 0.1% in a buy voltaren prospective randomized double-masked double-dummy study in patients undergoing cataract surgery.

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Both studies were performed in 16 healthy subjects. All treatments were given orally after an overnight fast. In study 1, which was performed to a four-period, open, crossover design, subjects received on separate occasions MDZ 5 mg, diclofenac 25 mg, a four drug cocktail (caffeine 100 mg, mephenytoin 100 mg, debrisoquine 10 mg and chlorzoxazone 250 mg) and a six drug cocktail (caffeine 100 mg, mephenytoin 100 mg, debrisoquine 10 mg, chlorzoxazone 250 mg, diclofenac 25 mg and MDZ 5 mg). In study 2, which was performed to a two-period, open, crossover design, subjects received a five drug cocktail (as the six drug cocktail in the first study, but without chlorzoxazone and with diclofenac dose increased to 50 mg) and a six drug cocktail (as five drug cocktail, with chlorzoxazone 250 mg). In both studies, blood samples were taken for measurement of plasma MDZ and 1- Brahmi Buy hydroxy MDZ (1-OH MDZ) concentrations. In study 1, blood samples were taken up to 12 h post-dose while in study 2 a single sample was taken 2 h after dosing. In study 1, the potential interaction between MDZ and the other components of the six drug cocktail was assessed by comparing AUClast ratios (1-OH MDZ/MDZ) between the two treatments. Additionally, a single sampling timepoint of 2 h post-dose for determination of concentration, rather than AUC, ratios was established. The 2 h plasma concentration ratios from studies 1 and 2 were combined and a pooled analysis performed to compare ratios within each study (to determine the change in ratio when MDZ was dosed with and without chlorzoxazone) and between studies (to determine the consistency of the ratios when MDZ was given either as part of the two six drug cocktails or when given alone and as part of the five drug cocktail).

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Sixty patients (45 male and 15 female) were included in the study. The mean age was 42 years for men and 40 years for women. They were placed in group Augmentin A Sulfa Drug A and B (30 cases each). Group A received local steroid injection (triamcinolone 20 mg mixed with lignocaine 2% 1 cc) and topical NSAID cream application (diclofenac diethylammonium) twice a day, tab. diclofenac sodium 50 mg twice a day for 3 weeks. Group B received tab diclofenac 50 mg twice a day and, topical NSAID cream application twice a day for 3 weeks. Assessment of patients was made 3 times; first at the start of the study, 2nd time after 6 weeks, and 3rd time after 12 weeks. A blinded assessor rated the elbow complaints of the patients at resisted dorsiflexion of wrist using VAS (0 = no severity, 1-3 mild, 4-6 moderate, 7-9 sever, 10 = maximum severity).

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In the context of the European Water Framework Directive (WFD) it is fully recognized that pharmaceuticals can represent a relevant issue for the achievement of the good chemical and ecological status of European surface water bodies. The recent European Directive on the review of priority substances in surface water bodies has included three pharmaceuticals of widespread use (diclofenac, 17α-ethinylestradiol (EE2), 17β-estradiol (E2)) in the European monitoring list, the so-called watch list. Endocrine active pharmaceuticals such as EE2 and E2 (also occurring as natural hormone) can cause adverse effects on aquatic ecosystems at very low levels. However, monitoring of these pharmaceuticals within the watch list Paracetamol Maximum Dose Pediatric mechanism of the WFD and national monitoring programs can be difficult because of detection problems of most routine analytical methods. With proposed annual average Environmental Quality Standards (AA-EQS) of 0.035 ng/L and 0.4 ng/L, respectively, the estrogenic pharmaceutical EE2 and the natural hormone E2 are among those substances. Sensitive in vitro bioassays could reduce the current detection problems by measuring the estrogenic activity of environmental samples. In a short review article the application of this approach to screen and assess the risks of endocrine active pharmaceuticals with a focus on estrogenic pharmaceuticals in environmental waters is discussed.

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The purpose of the case-study was to evaluate the efficiency of non-steroid antiinflammatory drugs (NAD) for postoperative analgesia in children after small-scope surgical interventions. Diclofenac, 1 mg/kg per day administered as rectal suppositories or intramuscular injections after initial narcosis, was used for postoperative analgesia in children of the main group; postoperative analgesia made by analgin and promedol in the control group was compared with the former. Forty-seven 6 Paracetamol And Alcohol children and 10 children with identical diseases like groin hernia, varicocele and dropsy of testicular membranes, were respectively in the main and control groups. Clinical examinations and registration of functional parameters were made in patients during certain time periods, i.e. before surgery (in the standing and lying postures) and after surgery (in 20 minutes, as well as in 1, 2, and 3 hours after surgical interventions). The efficiency of postoperative analgesia was evaluated by means of cardiointervalography according to Bayevsky method as well as by a state of central hemodynamics and by clinical examinations, including the visual-analogue 10-point scale and the 0-4 point verbal pain assessment scale. The postoperatively obtained data revealed a pronounced misbalance between the main and control groups, which is indicative of that the application of NAD for preventive and postoperative analgesia in children improves essentially the postoperative course and contributes to a fast rehabilitation of patients. A comparative analysis of the efficiency of postoperative analgesia by the discussed drugs showed that diclofenac possesses a sufficient analgetic activity and is free of any side-effects inherent in narcotic analgetics.

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Five RCTs were included (4465 participants); three of the studies also enrolled individuals with OA. The comparators were placebo, naproxen, diclofenac and ibuprofen. The evidence reviewed suggests that celecoxib controls the symptoms of RA to a similar degree to that of the active comparators examined (naproxen, diclofenac and ibuprofen). When compared to placebo, the percentage of patients showing improvement according to ACR 20 criteria at week 4 were 42/82 (51%) in the Prograf Cost 2mg twice daily celecoxib 200mg group and 43/82 (52%) in the twice daily celecoxib 400mg group; these were significantly different from the placebo group in which 25/85 (29%) improved. The six month data reviewed support a reduced rate of UGI complications with celecoxib but there is also evidence to suggest that these benefits may not be evident in the long-term and that celecoxib offers no additional benefit in patients who are also receiving cardio-prophylactic low dose aspirin.

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In this paper, results of an extensive monitoring programme for pharmaceutical residues in the river Rhine are presented. For one decade (1997 until 2006), the occurrence of widely used human pharmaceuticals like analgesics, lipid Augmentin 400 Mg regulators, antiepileptics and others has been studied at four locations along the river Rhine. The results of more than 500 analyses clearly prove that compounds such as carbamazepine or diclofenac are regularly found in the river Rhine in concentrations up to several hundred ng per litre. Combining concentration levels with data on water flow enables the calculation of transports, which e.g. for carbamazepine or diclofenac were in the range of several tons per year. The evaluation of the long-term monitoring data shows that only a slight decrease in concentration levels as well as in annual transports can be observed and thus the contamination of the river Rhine by pharmaceutical residues during the last decade has to be regarded as almost constant. Seasonal variations can be detected for bezafibrate, diclofenac and ibuprofen, for which the concentrations are much lower in the summer months. A more effective removal during wastewater treatment in the warmer periods of the year seems to be the major reason for those variations. For carbamazepine, no comparable seasonal effect can be found.

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All 4 currently Strattera 25 Mg available NSAIDs demonstrated anesthetic effects similar to brand diclofenac and brand ketorolac.

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TPSB under GA without prophylactic catheterisation is well tolerated, carrying acceptable postoperative symptom rates. Interestingly, a significant proportion of patients ejaculate within 7 days, Is Antabuse A Prescription Drug which again suggests good tolerance to the procedure. Patients should be provided with this data preoperatively when they are considering TPSB.

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Enzyme-coated magnetic bioreactor particles enable a fast, convenient approach to metabolic screening. A semi-automated metabolite-profiling technique using these particles in a 96 Accutane Cost Canada 2014 -well plate with liquid chromatography (LC)-mass spectrometry (MS)/MS detection is described. Reactions can be investigated over 1- to 2-min periods, and 96 or more reactions or reaction time points can be processed in parallel. Incorporation of DNA in the particle films facilitates determination of rates of DNA damage and metabolite-DNA adduct structures.

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Multilayer tablets are gaining importance in oral sustained drug delivery. They consist of an active matrix core and one or more layers applied Nolvadex Generic during tableting which may act as barriers and regulate drug release.

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The above results clearly indicated that AHG gum can be used for the development of oral controlled release dosage forms by using matrix systems Levaquin 500 Mg Cost .

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Effects of some drugs on different levels of phagocytic activity of polymorphonuclear leukocytes (PMNL) of human peripheral blood were studied in vitro. The drugs were found to regulate the phagocytic activity of PMNL. This effect depended on the initial level of PMNL phagocytic activity but not on the drug appurtenance to a certain pharmacological group.

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Levacobastine and lodoxamide but none of the three other drugs mentioned above were found to be effective in decreasing vascular permeability.

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A total of 8688 case patients, aged 89 years or younger, with a first-time acute myocardial infarction and 33,923 control subjects matched on age, sex, calendar time, and general practice attended.

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NSAIDs used for the treatment of osteoarthritis (OA) have dose-related risks for gastrointestinal, cardiovascular and renal adverse events (AEs), particularly in elderly patients. Topical NSAIDs reduce systemic NSAID exposure and may mitigate these risks.

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This literature review has found that NSAIDs are safe and effective for pain control in biliary colic, and reduce the likelihood of further complications.

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Drug-induced liver injury (DILI) is a leading cause of discontinuation of new drug approval or withdrawal of marketed medicine based on safety due to organ vulnerability. The aim of this research is to investigate the potential abilities of four different in vitro cell models (L-02, HepG2, HepaRG, and hiHeps cell lines) in assessing marketed drugs labeled with apparently different types of liver injury. A total of 17 drugs with versatile pharmacological profiles were chosen, of which, 14 drugs are recognized as DILI agents and 3 drugs are DILI irrelevant. Preliminary cellular screening assays indicated that the HepaRG cell line had an advantage over other cell lines in predicting drugs associated with DILI in vitro as it had the highest Youden's index (71.4%). A multi-parametric screening assay showed that oxidative stress, mitochondrial damage, and disorders of neutral lipid metabolism were changed notably in the HepaRG cell line after DILI-related drugs exposure, accounting for its high sensitivity in comparison with other three cell lines. In addition, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and malate dehydrogenase (MDH) all correlated with the cytotoxic effects of diclofenac sodium (p < 0.05), buspirone hydrochloride (p < 0.01), and danazol (p < 0.01) in the HepaRG cell line. We conclude that the HepaRG cell line is a superior in vitro cell model to other three cell lines for evaluating drugs with DILI potential.

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N-(p-amylcinnamoyl)anthranilic acid (ACA), a phospholipase A(2) (PLA(2)) inhibitor, is structurally-related to non-steroidal anti-inflammatory drugs (NSAIDs) of the fenamate group and may also modulate various ion channels. We used the whole-cell, patch-clamp technique at room temperature to investigate the effects of ACA on the Ca(2+)-activated chloride current (I(Cl(Ca))) and other chloride currents in isolated pig cardiac ventricular myocytes. ACA reversibly inhibited I(Cl(Ca)) in a concentration-dependent manner (IC(50)=4.2 μM, n(Hill)=1.1), without affecting the L-type Ca(2+) current. Unlike ACA, the non-selective PLA(2) inhibitor bromophenacyl bromide (BPB; 50 μM) had no effect on I(Cl(Ca)). In addition, the analgesic NSAID structurally-related to ACA, diclofenac (50 μM) also had no effect on I(Cl(Ca)), whereas the current in the same cells could be suppressed by chloride channel blockers flufenamic acid (FFA; 100 μM) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS;100 μM). Besides I(Cl(Ca)), ACA (50 μM) also suppressed the cAMP-activated chloride current, but to a lesser extent. It is proposed that the inhibitory effects of ACA on I(Cl(Ca)) are PLA(2)-independent and that the drug may serve as a useful tool in understanding the nature and function of cardiac anion channels.

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Some nonsteroidal anti-inflammatory drugs (NSAIDs), including cyclooxygenase-2 selective inhibitors, have been associated with increased cardiovascular (CV) events in recent clinical trials or observational studies. To determine whether the cyclooxygenase-2 selective inhibitor celecoxib affects CV risk, the incidence of CV events was analyzed in patients treated with celecoxib, placebo, or nonselective NSAIDs in the clinical trial database for celecoxib using defined Antiplatelet Trialists' Collaboration end points of nonfatal myocardial infarction, nonfatal stroke, and CV death. Patient data were derived from studies in osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, low back pain, and Alzheimer's disease. This meta-analysis included (1) 7,462 patients exposed to celecoxib 200 to 800 mg/day for 1,268 patient-years compared with 4,057 patients treated with placebo for 585 patient-years, and (2) 19,773 patients treated with celecoxib 200 to 800 mg/day for 5,651 patient-years compared with 13,990 patients treated with nonselective NSAIDs (diclofenac, ibuprofen, naproxen, ketoprofen, and loxoprofen) for 4,386 patient-years. CV events were adjudicated by a 3-member expert end point committee (WBW, JSB, PBG) blinded to treatment group and study. The incidence rates of the combined CV events were not significantly different between patients treated with celecoxib and placebo or between those treated with celecoxib and nonselective NSAIDs. Event rates were similar for adjudicated and nonadjudicated data. Dose of celecoxib, the use of aspirin, or the presence of CV risk factors did not alter these results. In conclusion, these analyses failed to demonstrate an increased CV risk with celecoxib relative to placebo and demonstrated a comparable rate of CV events with celecoxib treatment compared with nonselective NSAIDs.

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Postoperative pain in patients with bone and soft tissue cancer is different from that of other surgical patients due to the severity of the pain generated during surgery and because many of them have already been in pain preoperatively. The search for optimal intravenous pharmacologic management for this population is an ongoing one. We conducted a 10-month prospective, randomised, double blind study to compare the effects of a standard morphine dose to a 35%-lower dose plus a subanaesthetic dose of ketamine for postoperative pain control in patients undergoing bone and soft tissue cancer surgery under standardised general anaesthesia.

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The major constituents of the essential oil were 1,8-cineol (15.96%), α-pinene (13.38%), camphor (7.87%), bornyl acetate (6.54%), verbenone (5.82%), borneol (5.23%), camphene (4.96%), and (E)-caryophyllene (3.8%). Topical diclofenac containing 0.5% essential oil showed more analgesic effect after 25, 30, and 35 min (p < 0.001) than the reference drug in the tail flick test. The analgesic effect of preparation containing 1% essential oil was more than reference gel after 15 min (p < 0.05). This difference was observed after 20, 25, 30, 35, and 40 min (p < 0.001) too. Rosemary essential oil 1% promoted analgesic effect of drug in comparison with diclofenac gel in the formalin early phase (p < 0.05). The enhancing effect of rosemary was observed in 0.5 and 1% concentration (p < 0.05 and p < 0.001, respectively) in the late phase.

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We provoked acute cholecystitis in pigs by the ligature of biliary pedicle associated to the gallbladder introduction of "Lysophosphatidylcoline". Two series of animals were used: P1 (pigs not treated with Diclofenac) with 17 pigs and P2 (pigs treated with Diclofenac) with 23. In the latter group we associated the administration of Diclofenac given before the production of acute cholecystitis and administered for 4 days. The microbiology of the bile was studied in 34 pigs. The following parameters were valorized: histological gallbladder lesions and microorganisms in bacteriological examination of the bile.

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Losartan, an angiotensin II receptor antagonist, is oxidized by hepatic cytochromes P450 to an active carboxylic acid metabolite, E-3174. The aim of the present investigation was to study the contribution of CYP2C9 and CYP3A4 in losartan oxidation in vitro and to evaluate the role of CYP2C9 polymorphism. Kinetic properties of different genetic CYP2C9 variants were compared both in a yeast expression system and in 25 different samples of human liver microsomes where all known genotypes of CYP2C9 were represented. Microsomes were incubated with losartan (0.05-50 microM), and the formation of E-3174 was analyzed by high-performance liquid chromatography to estimate V(max), K(m), and intrinsic clearance for all individual samples. Sulfaphenazole, a CYP2C9 inhibitor, blocked the formation of E-3174 at low losartan concentrations (<1 microM), whereas the inhibitory effect of triacetyloleandomycin, a CYP3A4 inhibitor, was significant only at high concentrations of losartan (>25 microM). In comparison to the CYP2C9.1 variant, oxidation of losartan was significantly reduced in yeast expressing the rare CYP2C9.2 or CYP2C9.3 variants. Moreover, the rate of losartan oxidation was lower in liver microsomes from individuals hetero- or homozygous for the CYP2C9*3 allele, or homozygous for the CYP2C9*2 allele. The difference between the common and rare CYP2C9 variants was mainly explained by a lower V(max), both in yeast and human liver microsomes. In summary, these in vitro results indicate that CYP2C9 is the major human P450 isoenzyme responsible for losartan oxidation and that the CYP2C9 genotype contributes to interindividual differences in losartan oxidation and activation.

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Both caudal anaesthesia and non-steroidal anti-inflammatory drugs have been used in the management of postoperative pain in children. The aim of the present study was to evaluate the combination of caudal analgesia and rectally administered diclofenac in the treatment of pain following minor surgery in children. Thirty-nine, ASA grade 1 or 2, children undergoing inguinal or penoscrotal surgery were randomly assigned to receive either a caudal block using 0.125% bupivacaine with adrenaline or a similar caudal block in combination with rectally administered diclofenac 1 mg.kg-1. Children given a caudal block alone were more likely to need analgesia in the first 24 h postoperatively. It would appear that the combination of a caudal block and rectal diclofenac in children undergoing minor lower abdominal surgery reduces the need for subsequent analgesia.

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Thirty-two male SD rats were randomly divided into control group and model group. The rats of the model group were given 7.5 mg/kg diclofenac by gavage, bid; the rats of the control group were given the same dose of saline. Then they were further randomly divided into two subgroups (n=8) at the first day and the fifth day after making the models to observe the scores of anatomical lesion on stomach and small intestine and the scores of tissue damage of mucous membrane and to quantitatively analyze the height of villi, as well as the thickness and the section area of mucous membrane with Carl Zeiss Imaging Systems. Observation of the change of ultrastructural organization of mucous membrane was carried out with transmission electron microscope.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause apoptosis in several cell lines including transformed chicken embryo fibroblasts and human colon cancer cells. We herein report the apoptotic effect of NSAIDs in a non-transformed cell line derived from the rat gastric mucosa, RGMI (rat gastric mucosa cell first). 1-[p-Chlorobenzoyl]-5-methoxy-2-methylindole-3-acetic acid (indomethacin) and sodium 2-(2,6-dichloroanilino)phenylacetate (sodium diclofenac), potent and non-selective inhibitors of cyclooxygenase, were found to induce DNA fragmentation in RGM1 cells in a time- and concentration-dependent manner. The expression of mRNA for cyclooxygenase-2 was hardly detected in the intact cells but was clearly enhanced when the cells were incubated with the two NSAIDs. In contrast, the expression of mRNA for cyclooxygenase-1 was constitutive and was never affected by NSAIDs. The effect of [3,4-di(4-methoxyphenyl)-5-isoxazolyl] acetic acid (mofezolac), a potent and highly preferential inhibitor of cyclooxygenase-1, and N-[2-(cyclohexyloxy)-4-nitrophenyl]methanesulphonamide (NS-398), a selective inhibitor of cyclooxygenase-2, on DNA fragmentation and cyclooxygenase-2 mRNA expression was weak compared to the effect of indomethacin or sodium diclofenac. The DNA fragmentation induced by sodium diclofenac was hardly affected by the exogenous addition of 16,16-dimethyl prostaglandin E2 but was inhibited by caspase inhibitors such as Ac-YVAD-CHO and Ac-DEVD-CHO. The present data provide the first evidence that NSAIDs, such as indomethacin and sodium diclofenac, cause apoptotic DNA fragmentation in cultured gastric mucosal cells, and also indicate the involvement of caspases rather than the inhibition of cellular prostaglandin synthesis in the apoptotic process.

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This is a randomised, controlled, single-centre, two-arm superiority trial with 1:1 allocation ratio; with assessor and statistician blinded. Participants are blinded to the trial's hypothesis and to the interventions received by the opposite group. A total of 204 participants will be recruited from the community and randomised using a computer-generated schedule. The intervention group will receive education for joint protection and OA, a splint for the base of the thumb, hand exercises and topical diclofenac sodium 1% gel over 6 weeks. The control group will receive education for joint protection and OA alone. Main inclusion criteria are pain ≥40 mm (Visual Analogue Scale, 0-100) at the base of the thumb, impairment in hand function ≥6 (Functional Index for Hand Osteoarthritis, 0-30) and radiographic thumb base OA (Kellgren Lawrence grade ≥2). Participants currently receiving any of the intervention components will be excluded. Outcomes will be measured at 2, 6 and 12 weeks. The primary outcome is change in pain and hand function from baseline to 6 weeks. Other outcomes include changes in grip and pinch strength, quality of life, presence of joint swelling and tenderness, duration of joint stiffness, patient's global assessment and use of rescue medication. Analysis will be performed according to the intention-to-treat principle. Adverse events will be monitored throughout the study.

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In this study, diclofenac-loaded Eudragit S100-based nanosuspension was prepared by nanoprecipitation method and characterised for particle size, morphology, in vitro release, and for its in vivo ocular anti-inflammatory activity. The diclofenac-loaded Eudragit S100 nanosuspension was found to have a particle size of 172 nm, polydispersibility index of 0.14 and zeta potential of -23.7 +/- 6.07 mV, indicating that the nanosuspension is fairly stable. The nanosuspended particles were found to be spherical in shape. The nanosuspension was found to provide a sustained in vitro release, following the Higuchi square-root release kinetics. The results indicated that the nanosuspension released the drug by combination of dissolution and diffusion. The in vivo evaluation of nanosuspension in PGE(2)-induced ocular inflammation in rabbit model revealed a significantly (p  <  0.05) higher inhibition of PGE(2)-induced polymorphonuclear leukocytes migration and lid-closure scores as compared with the aqueous solution of diclofenac.

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We enrolled 152 patients with a history of hypersensitivity to NSAIDs and 136 control participants in 11 different centers between spring 2003 and spring 2006. Flowcytometric BAT was performed.

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No significant difference was observed in the IOPs before additional administration of ophthalmic solution between the dicloptin group and the control group (P=0.47). Additional administration of diclofenac sodium increased mean IOP from 15.73±1.75 to 17.32±2.23 mm Hg (P=0.01). This increase was reversed 2 weeks after discontinuing additional solutions (P=0.80); however, no significant difference in mean IOP was observed in the control group after administration and after discontinuing the additional medication (P=0.94 and 0.84, respectively).

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Despite aggressive treatment with radiation and combination chemotherapy following tumor resection, the 5-year survival rate for patients with head and neck cancer is at best only 50%. In this study, we examined the therapeutic potential of localized release of diclofenac from electrospun nanofibers generated from poly(D,L-lactide-co-glycolide) polymer. Diclofenac was chosen since anti-inflammatory agents that inhibit cyclooxygenase have shown great potential in their ability to directly inhibit tumor growth as well as suppress inflammation-mediated tumor growth. A mouse resection model of oral carcinoma was developed by establishing tumor growth in the oral cavity by ultrasound-guided injection of 1 million SCC-9 cells in the floor of the mouth. Following resection, mice were allocated into four groups with the following treatment: 1) no treatment, 2) implanted scaffolds without diclofenac, 3) implanted scaffolds loaded with diclofenac, and 4) diclofenac given orally. Small animal ultrasound and magnetic resonance imaging were utilized for longitudinal determination of tumor recurrence. At the end of 7 weeks following tumor resection, 33% of mice with diclofenac-loaded scaffolds had a recurrent tumor, in comparison to 90%-100% of the mice in the other three groups. At this time point, mice with diclofenac-releasing scaffolds showed 89% survival rate, while the other groups showed survival rates of 10%-25%. Immunohistochemical staining of recurrent tumors revealed a near 10-fold decrease in the proliferation marker Ki-67 in the tumors derived from mice with diclofenac-releasing scaffolds. In summary, the local application of diclofenac in an orthotopic mouse tumor resection model of oral cancer reduced tumor recurrence with significant improvement in survival over a 7-week study period following tumor resection. Local drug release of anti-inflammatory agents should be investigated as a therapeutic option in the prevention of tumor recurrence in oral squamous carcinoma.

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Tranilast suppressed proliferation in cultured keratocytes from the corneal haze region at doses of 30 and 300 micromol/L and collagen synthesis at doses of 3, 30, and 300 micromol/L. Normal corneal cultures showed suppression of keratocyte proliferation and collagen synthesis only at a high dose of tranilast (300 micromol/L). Betamethasone suppressed proliferation of keratocytes in both haze and normal cornea at a dose of 10 micromol/L, as well as collagen synthesis at respective doses of 1 and 10 micromol/L. Diclofenac sodium suppressed collagen synthesis of keratocytes in haze cornea at a high dose of 100 micromol/L, and in keratocytes in normal cornea, at doses of 10 and 100 micromol/L. In an in vivo study, either 0.5% tranilast, 0.1% betamethasone phosphate eye drops, or a tranilast base solution (control) was instilled four times daily to rabbits that had undergone PRK. Weekly evaluation of the inhibitory effect of these drugs on the development of haze was performed 2 weeks after surgery. Tranilast suppressed haze 6-13 weeks after PRK, but betamethasone phosphate showed no effect.

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To determine whether antipyretic treatment for influenza infection influences the risk of mortality in animal models and humans.