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Voltaren (Diclofenac)

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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.


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.


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.


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.


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.


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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The current evidence-based guideline on self-medication in migraine and tension-type headache of the German, Austrian and Swiss headache societies and the German Society of Neurology is addressed to physicians engaged in primary care as well as pharmacists and patients. The guideline is especially concerned with the description of the methodology used, the selection process of the literature used and which evidence the recommendations are based upon. The following recommendations about self-medication in migraine attacks can be made: The efficacy of the fixed-dose combination of acetaminophen, acetylsalicylic acid and caffeine and the monotherapies with ibuprofen or naratriptan or acetaminophen or phenazone are scientifically proven and recommended as first-line therapy. None of the substances used in self-medication in migraine prophylaxis can be seen as effective. Concerning the self-medication in tension-type headache, the following therapies can be recommended as first-line therapy: the fixed-dose combination of acetaminophen, acetylsalicylic acid and caffeine as well as the fixed combination of acetaminophen and caffeine as well as the monotherapies with ibuprofen or acetylsalicylic acid or diclofenac. The four scientific societies hope that this guideline will help to improve the treatment of headaches which largely is initiated by the patients themselves without any consultation with their physicians.

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A selective solid-phase extraction was employed for the improvement of the determination of non-steroidal anti-inflammatory drugs (NSAIDs) in continental water and urine samples. Ketoprofen, naproxen, diclofenac, and ibuprofen were selected as target analytes due to they are the most frequently administered and consumed NSAIDs. These compounds were extracted using molecular imprinted polymers and determined by liquid chromatography with diode array (DAD), and tandem-mass spectrometry (MS-MS) detectors. Performance of DAD and MS-MS detectors was evaluated throughout this study. The obtained limits of quantification, after a 50-fold preconcentration solid-phase extraction, varied from 20 to 30μgL(-1) for DAD, and from 0.007 to 0.017μgL(-1) for MS-MS for both types of sample matrixes. Quantitative recoveries were found for blank-samples spiked at different NSAIDs concentration levels, ranging from 0.05 to 10mgL(-1) for urine and from 0.5 to 500μgL(-1) for water. The proposed methodology was applied for the determination of NSAID residues in urine of prescribed individuals, and continental waters.

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The callus and roots developed from the hypocotyl and cotyledon explants of the germinating seeds of Calotropis procera were grown in culture, and the proteins isolated from them (CP and RP) were evaluated for their efficacy in inhibiting edema formation induced by sub-plantar injection of carrageenan in the hind paw of rat. Intravenous administration of both CP and RP 30 min before inducing inflammation produced a dose-dependent inhibition of edema formation at 1 and 5 mg/kg doses. The extents of inhibition with these proteins ranged between 40 and 70 % at the doses included while the anti-inflammatory drug diclofenac produced 50 to 60 % inhibition at 5 mg/kg dose. The inhibitory effect with these proteins was accompanied by a dose-dependent reduction in the tissue levels of inflammatory mediators, tumor necrosis factor alpha (TNF-α) and prostaglandin E2 (PGE2), and oxidative stress markers namely glutathione and thiobarbituric acid-reactive substances and maintenance of tissue architecture. The present study shows that the proteins isolated from the differentiated and undifferentiated tissues derived from the germinating seeds have therapeutic application in the treatment of inflammatory conditions, and these tissues could be used as an alternative source to minimize variability of plant-derived formulations.

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An acute elevation of circulating non-esterified fatty acids (NEFAs) has previously been shown to impair endothelium-dependent vasodilation (EDV). In this study, we investigated if local administration of vitamin C (n=8, 18 mg/min), L-arginine (n=8, 12.5 mg/min), or the cyclooxygenase (COX) inhibitor diclophenac (n=8, 0.5 mg/min) can counteract the endothelial dysfunction seen during infusion of Intralipid plus heparin (n=10). EDV and endothelium-independent vasodilation (EIDV) were studied in the forearm after local administration of methacholine chloride (Mch; 2 and 4 microg/min) and sodium nitroprusside (SNP; 5 and 10 microg/min). Forearm blood flow (FBF) was determined with venous occlusion plethysmography. Intralipid and heparin increased circulating NEFA levels sevenfold and impaired EDV (P<0.001 vs baseline). Concomitant administration of L-arginine or diclophenac abolished the NEFA-induced impairment in EDV. Concomitant vitamin C administration actually improved EDV (P<0.05 vs baseline). NEFA elevation increased EIDV (P<0.01), but this effect was not significant after L-arginine or diclophenac infusions. In conclusion, an acute elevation of circulating NEFAs led to impaired EDV. Administration of L-arginine, vitamin C or COX inhibition abolished this effect, suggesting that NEFAs might interact with endothelial vasodilatory function through multiple mechanisms.

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Nephrotic syndrome, with or without concomitant tubulointerstitial nephritis, is a rare renal adverse effect of NSAIDs. In the present report we describe a case of a 60-year-old Caucasian man who was admitted because of nephrotic syndrome following several days of use of meloxicam for hip osteoarthritis. Renal histopathology revealed minimal change disease, one of the commonest causes of nephrotic syndrome. The patient's condition resolved rapidly upon discontinuation of meloxicam. Because he had already experienced two episodes of nephrotic syndrome after administration of diclofenac several years previously, it was concluded that the patient had renal hypersensitivity to both diclofenac and meloxicam. While waiting for the hip arthroplasty, he was prescribed celecoxib for pain control. After 1 month of regular celecoxib use the patient remained in remission with respect to nephrotic syndrome and had normal renal function. We conclude that challenge with a structurally distinct NSAID (such as celecoxib in this case) may be an option, under close surveillance, in a patient with a history of nephrotic syndrome associated with use of an NSAID when continued treatment with an NSAID is indicated.

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This trial shows that rectal diclofenac given immediately after endoscopic retrograde cholangiopancreatography can reduce the incidence of acute pancreatitis.

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Osteoarthritis was induced arthroscopically in 1 middle carpal joint of all horses. Eight horses treated with DLC were given 7.3 g twice daily via topical application. Eight horses treated with phenylbutazone were given 2 g orally once daily. Eight control horses received no treatment. Evaluations included clinical, radiographic, magnetic resonance imaging, synovial fluid, gross, and histologic examinations as well as histochemical and biochemical analyses.

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In the present study, the validity of using a cocktail screening method in combination with a chemometrical data mining approach to evaluate metabolic activity and diversity of drug-metabolizing bacterial Cytochrome P450 (CYP) BM3 mutants was investigated. In addition, the concept of utilizing an in-house-developed library of CYP BM3 mutants as a unique biocatalytic synthetic tool to support medicinal chemistry was evaluated. Metabolic efficiency of the mutant library towards a selection of CYP model substrates, being amitriptyline (AMI), buspirone (BUS), coumarine (COU), dextromethorphan (DEX), diclofenac (DIC) and norethisterone (NET), was investigated. First, metabolic activity of a selection of CYP BM3 mutants was screened against AMI and BUS. Subsequently, for a single CYP BM3 mutant, the effect of co-administration of multiple drugs on the metabolic activity and diversity towards AMI and BUS was investigated. Finally, a cocktail of AMI, BUS, COU, DEX, DIC and NET was screened against the whole in-house CYP BM3 library. Different validated quantitative and qualitative (U)HPLC-MS/MS-based analytical methods were applied to screen for substrate depletion and targeted product formation, followed by a more in-depth screen for metabolic diversity. A chemometrical approach was used to mine all data to search for unique metabolic properties of the mutants and allow classification of the mutants. The latter would open the possibility of obtaining a more in-depth mechanistic understanding of the metabolites. The presented method is the first MS-based method to screen CYP BM3 mutant libraries for diversity in combination with a chemometrical approach to interpret results and visualize differences between the tested mutants.

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The aim of the work was to evaluate effectiveness and safety of diclofenac and nimesulide in patients with early RA. The open clinical study included 80 outpatients (mean age 49.0 +/- 11.1 years) within the first year after development RA (mean duration of the disease 4.9 +/- 3.1 months prior to the onset of basic therapy). The patients were divided into 2 groups of 40 persons each depending on the type of non-steroidal anti-inflammatory agents they received. Patients in group 1 were treated with 100 mg of diclofenac daily and in group 2 with 100 mg BID of generic nimesulide preparation (nais, Dr. Reddy Co.). Duration of therapy was 30 days in both cases. The two drugs were roughly identical in terms of therapeutic effect although nimesulide produced fewer side effects. Subjective complaints of gastrointestinal problems were recorded in 11 (27.5%) patients f group 1 and in 8 (20%) of group 2. It is concluded that timely prescription of proton pump inhibitors permits to avoid premature withdrawal of non-steroidal anti-inflammatory agents at patient discretion.

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Significantly more subjects treated with diclofenac potassium for oral solution (N=343) achieved a two-hour pain-free response (25% vs. 10%, p<.001), no nausea (65% vs. 53%; p=.002), no photophobia (41% vs. 27%; p<.001) and no phonophobia (44% vs. 27%; p<.001) compared to placebo. Pain intensity differences between treatments were significantly lower in the diclofenac potassium oral solution group, starting at 30 minutes post-treatment (p=.013) with significant differences at all time points thereafter (p<.001). Twenty-four-hour sustained pain-free response favored diclofenac potassium oral solution treatment versus placebo (19% vs. 7%, p<.0001). The most common adverse event considered to be treatment related was nausea (diclofenac potassium for oral solution [4.6%]; placebo [4.3%]).

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Induction of a freeze lesion in human skin is an experimental model of hyperalgesia that allows assessing the antihyperalgesic effects of traditional non-steroidal anti-inflammatory drugs (NSAIDs). We have investigated whether this model is also sensitive to selective cyclooxygenase (COX)-2 inhibitors and have characterized morphological substrates of the generated hyperalgesia in the skin. In eight healthy subjects, a freeze lesion was induced and mechanical pain thresholds (MPT) were tested for 5h following administration of the non-selective COX inhibitor diclofenac (75mg), the COX-2-selective inhibitor parecoxib (40mg) or placebo in a randomized, double-blind cross-over study. In five additional healthy subjects, biopsies were taken from normal skin and the area of freezing injury. Induction of the freeze lesion resulted in hyperalgesia expressed by a decrease of MPT after 24h. Diclofenac and parecoxib, but not placebo, statistically significantly elevated MPT. Histochemical and Western blot analyses of skin biopsies revealed a strong upregulation of COX-2, a slight decrease of COX-1 and activation of nuclear factor kappa B (NF-kappaB) in the area of the freezing injury. These findings indicate that the freeze lesion model is sensitive to NSAIDs including selective COX-2 inhibitors, and that NF-kappaB-dependent COX-2 upregulation contributes to the hyperalgesia in this model.

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The SADRAC received 151 reports of suspected ADRs with fatal outcome from liver injury; 48 cases were either unlikely or excluded. Of the remaining 103 cases, 13 (13%) were highly probable, 48 (47%) probable and 42 (41%) possible. The median age of the 103 patients was 64 years (47-77 interquartile range (IQR)) and 59 (57%) were males. The majority of cases were classified as hepatocellular (75%), with only 15% cholestatic and 10% mixed. Halothane, paracetamol, flucloxacillin, sulfamethoxazole/trimethoprim and diclofenac were the most common drugs associated with fatal outcome. Seventeen patients underwent liver transplantation, most commonly because of paracetamol and disulfiram toxicity.

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This contribution is the second part of the project on strategies used in the selection of electrolyte systems for anionic ITP with ESI-mass spectrometric detection. It presents ITP as a powerful tool for selective stacking of anionic analytes, performed in a nonconventional way in moving-boundary systems where two co-anions are present in both the leading and terminating zones. The theoretical background is given to substantiate the conditions for the existence and migration of ITP boundaries in moving-boundary systems and stacking of analytes at these boundaries. The practical aspects of the theory are shown in form of stacking-window diagrams that bring immediate information about which analytes are stacked in a given system. The presented theory and strategy are illustrated and verified on the example of analysis of a model mixture of salicylic acid, ibuprofen and diclofenac, and comparison of regular and free-acid ITP with moving-boundary ITP systems formed by formic and propionic acids and ammonium as counterion.

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The IER microcapsules were suspended in 0.1% methylcellulose and stored at 23 and 37 degrees C and the dissolution study conducted over a 6-month period. The surface morphology of the microcapsules was examined using scanning electron microscopy (SEM).

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Significant improvement is demonstrated for transdermal delivery of steroidal and nonsteroidal antiinflammatory drugs (NSAID), including betamethasone valerate and dipropionate, indomethacin, diclofenac, piroxicam, and naproxen, when formulated in a submicron Emulsion (SME) vehicle rather than in standard creams. SMEs comprise oil droplets, with mean size of approximately 100 nm (0.1 micron), dispersed in a continuous water phase. Hydrophobic drugs are incorporated into the oil phase of the SME, resulting in improved penetration and increased efficacy of the incorporated antiinflammatory drug. The voltaren buy performance of medicated topical SME was compared with that of regular topical cream formulations, as measured by the carrageenan-induced paw edema rat model. Indomethacin in SME topical vehicle was 50% more active than in regular cream base, Diclofenac in SME proved to be 40% more active than Voltaren Emulgel. Improvement of steroidal antiinflammatory drugs action in topical SME cream was even more pronounced; that is, up to 3-4-fold. Antiinflammatory drugs in SME also demonstrate noticeable systemic activity, but for regional edema treatment, local delivery is advantageous. The new SME delivery system was tested for primary irritation in humans in a 48-h trial. Low irritancy and excellent human acceptance for SME placebo or diclofenac-loaded SME cream make this novel transdermal/topical DDS attractive for further development.

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Male Sprague-Dawley rats were pretreated either Prograf Drug Class with saline (0.3 ml subcutaneously) or octreotide (0.001-1 ng/kg subcutaneously). After 30 minutes gastric ulcers were induced by the intragastric application of NSAIDs (20 mg/kg indomethacin, 200 mg/kg aspirin, 200 mg/kg ibuprofen, or 50 mg/kg diclofenac). Four hours later the rats were killed and gastric mucosal lesions were assessed by computed planimetry. To determine whether octreotide could prevent indomethacin induced injury in humans, 20 healthy volunteers were evaluated in a double blind, placebo controlled study.

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This study aims to Zanaflex 6 Mg compare the effects of tramadol and gabapentin, as premedication, in decreasing the pain after hysterectomy.

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This double-blind, multicentre, placebo-controlled, parallel-group study compared the incidence of gastroduodenal ulcers associated with valdecoxib 10 mg daily (q.d.) and 20 mg q.d. with that of ibuprofen 800 mg three times daily (t.i.d.) or diclofenac 75 mg twice daily (b.i.d.) when administered over a 12-week period. Desyrel Cough Syrup The incidence of gastroduodenal ulcers was assessed by upper-gastrointestinal endoscopy, performed at baseline and again at the end of week 12 (or at early study termination). Efficacy assessments were performed at baseline and at weeks 2, 6 and 12 using Patient's and Physician's Global Assessments of Arthritis.

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Both groups (M1 and M2) showed a reduction of pain during treatment using the visual analogue scale (VAS). However, no statistical difference was found between both groups concerning pain reduction at any time. A significant Mestinon And Alcohol pain relief was monitored in the patients of the M1 group towards the end of treatment. Concerning the daily impairment because of pain measured by the Griss scale an improvement was seen in 70 % of the patients receiving fluvoxamine versus 44 % in patients receiving placebo. Additionally, an improvement in the M1 group was seen in the WOMAC scale and in factors such as pain, stiffness and mobility compared to the M2 group. Using the CGI scale, 56.6 % of the M1 group compared to 37.9 % of the M2 group were stating that their overall status had improved "much" or "very much" at the end of the treatment (V9). A depression had been excluded in all patients. No statistical differences were seen in the Bf scale (von Zerssen) during all evaluations (V1 to V9). During the whole study 127 side effects were registered in 49 patients. None of the 5 severe events were related to the investigated drug.

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Although CYP2C8/9 activity plays an essential role in the metabolism of and clinical response to many NSAIDs, the use of pharmacogenomic techniques is not equally useful for Cymbalta Canada Cost all these drugs.

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The novel anti-tumor agent 5,6-dimethylxanthenone-4-acetic acid (DMXAA) was developed in the Auckland Cancer Society Research Center. Its pharmacokinetic properties have been investigated using both in vitro and in vivo models, and the resulting data extrapolated to patients. The metabolism of DMXAA has been extensively studied mainly using hepatic microsomes, which indicated that UGT1A9 and UGT2B7-catalyzed glucuronidation on its acetic acid side chain and to a lesser extent CYP1A2-catalyzed hydroxylation of the 6-methyl group are the major metabolic pathways, resulting in DMXAA acyl glucuronide (DMXAA-G) and 6-hydroxymethyl-5-methylxanthenone-4-acetic acid. The predominant metabolite in human urine (up to 60% of total dose) was identified as DMXAA-G, which was chemically reactive, undergoing hydrolysis, intramolecular rearrangement, and covalent binding to plasma proteins. In vivo formation of DMXAA-protein adducts were also observed in cancer patients receiving DMXAA treatment. The comparison of the in vitro human hepatic microsomal metabolism and inhibition of DMXA by UGT and/or CYP substrates with animal species indicated species differences. Renal microsomes from all animal species examined had glucuronidation activity for DMXAA, but lower than the liver. In vitro-in vivo extrapolations based on human microsomal data indicated a 7-fold underestimation of plasma clearance in patients. In contrast, allometric scaling using in vivo data from the mouse, rat, and rabbit predicted a plasma clearance of 3.5 mL/min/kg, similar to that observed in patients (3.7 mL/min/kg). Based on in vitro metabolic inhibition studies, it appears Paracetamol Recommended Dosage possible to predict the effects on the plasma kinetic profile of DMXAA of drugs such as diclofenac, which are mainly metabolized by UGT2B7. However, it did not appear possible to predict the effect of thalidomide on the pharmacokinetics of DMXAA in patients based on in vitro inhibition and animal studies. These data indicate that preclincial pharmacokinetic studies using both in vitro and in vivo models play an important but different role in predicting pharmacokinetics and drug interactions in patients.

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Degradation kinetics and mineralization of an urban wastewater treatment plant effluent contaminated with a mixture of pharmaceutical compounds composed of amoxicillin (10 mg L(-1)), carbamazepine (5 mg L(-1)) and diclofenac (2.5 mg L(-1)) by TiO(2) photocatalysis were investigated. The photocatalytic effect was investigated using both spiked distilled water and actual wastewater solutions. The process efficiency was evaluated through UV absorbance and TOC measurements. A set of bioassays (Daphnia magna, Pseudokirchneriella subcapitata and Lepidium sativum) was performed to evaluate the potential toxicity of the oxidation intermediates. A pseudo-first order kinetic model was found to fit well the experimental data. The mineralization rate (TOC) of the wastewater contaminated with the pharmaceuticals was found to be really slow (t(1/2)=86.6 min) compared to that of the same pharmaceuticals spiked in distilled water (t(1/2)=46.5 min). The results from the toxicity tests of single pharmaceuticals, their mixture and the wastewater matrix spiked with the pharmaceuticals displayed a general accordance between the responses of the freshwater aquatic species (P. subscapitata>D. magna). In general the photocatalytic treatment did not completely reduce the toxicity under the investigated conditions (maximum catalyst loading and irradiation time 0.8 g Hytrin Dosage Forms TiO(2) L(-1) and 120 min respectively).

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Topical treatment with dexamethasone was particularly effective during Azulfidine And Alcohol the first week after surgery; the second week after surgery, a similar result was observed in the corneas treated with diclofenac. Low doses of steroidal and nonsteroidal antiinflammatory drugs would seem to have the potential to improve biomechanical properties only during the early stage of the healing process of the cornea.

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Platelet count, closure time as measured by platelet function analyzer (PFA-100), prothrombin time (PT), activated partial thromboplastin time (aPTT), and plasma concentrations of the study drugs were obtained over 24 hours after each treatment. The primary endpoint was the area under the curve for PFA collagen-epinephrine (CEPI) closure time difference from 0-6 hours post-drug administration (AUC(0-6h)). Secondary endpoints included the maximum change from baseline in PFA CEPI closure time.

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In mammals, procedures such as handling, restraint, or exposure to open spaces induces an increase in body temperature (T(b)). The increase in temperature shares some characteristics with pyrogen-induced fever and so is often called "stress fever." Birds also respond to acute handling with a stress fever, which may confound thermoregulatory studies that involve animal restraint. We have measured the T(b) responses of Pekin ducks on days when they were restrained and compared them to days when the birds remained unrestrained. Restraint induced a 0.5 degrees C increase in T(b) that was sustained for the entire 8 h of restraint. To determine whether the restraint-induced increase in T(b) is mediated by prostaglandins (PGs) we compared the T(b) responses during restraint after intraperitoneal injection with saline to the responses during restraint after injection with diclofenac sodium (15 mg/kg). There was no difference in response, suggesting that restraint affects T(b) by a PG-independent mechanism. We also compared the T(b) response to intramuscular injection of lipopolysaccharide (LPS; 100 microg/kg), a bacterial pyrogen, when the ducks were restrained or unrestrained. Despite T(b) being higher at the time of LPS injection when the ducks were restrained, the maximum temperature reached after LPS injection was higher, and the period that T(b) remained elevated was longer when the ducks were unrestrained. We conclude that restraint should be considered as a potential confounder in thermoregulatory studies in birds and presumably other species too.

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We conducted a single-center, prospective, open-labeled, randomized trial for evaluating the use of rectal diclofenac in prevention of post-ERCP pancreatitis in high-risk patients. We assessed 526 patients coming for ERCP for different indications. Four hundred patients were eligible for the study. Those not fitting the high-risk criteria and with acute pancreatitis were excluded. These patients were randomized in two groups: 200 patients received rectal diclofenac prior to or during the procedure, while 200 patients received placebos. Serum amylase was measured at 2 and 36 hours. Post-ERCP pancreatitis was defined as serum amylase > 3 times upper limit of normal with associated severe abdominal pain. Severity was graded according to days of hospitalization and complications.

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In these patients undergoing abdominal surgery, the BUP-i + BUP-b regimen controlled postoperative pain as well as did MO-i + MO-b or the combinations of BUP and MO. BUP neither inhibited the analgesia provided by MO nor induced undesired sedation or hemodynamic or respiratory effects.

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LNCaP-COX-2 and LNCaP-Neo cell lines experienced cytotoxic effects of diclofenac in a dose related manner. Clonogenic assays demonstrated that LNCaP-COX-2 cells were significantly more resistant to RT than LNCaP-Neo cells. Furthermore, the addition of diclofenac sensitized LNCaP-COX-2 not but LNCaP-Neo cells to the cytocidal effects of radiation. In LNCaP-COX-2 cells, diclofenac enhanced radiation-induced apoptosis compared with RT alone. This phenomenon might be attributed to enhancement of RT-induced TRAIL expression as demonstrated by real-time PCR analysis. Lastly, tumor volumes of LNCaP-COX-2 cells xenograft treated with diclofenac or RT alone was >4-fold higher than in mice treated with combined diclofenac and radiation (p<0.05).

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Non-melanoma skin cancer (NMSC) is the most common form of skin cancer. Owing to the significant adverse effects of existing treatments, alternatives are needed. The aim of this study was to evaluate the use of topically administered combination therapy and 5-flurouracil (5-FU) for the treatment of UVB induced NMSC in a mouse model. Ninety-six SKH-1 mice were randomized to one placebo group and two treatment groups (diclofenac+calcitriol+difluoromethylornithine (DFMO) and 5-FU). After UVB radiation for 20 weeks, the mice with tumours were treated topically for the following 17 weeks. Both treatments significantly reduced the number of tumours, number of mice with tumours as well as tumour area size compared with placebo. As the clinical use of 5-FU may induce more adverse effects, a combination of diclofenac+calcitriol+DFMO could be a promising alternative. Human studies are warranted to determine the beneficial effects and possible adverse effects of this new treatment.

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The average stone size for groups 1, 2, and 3 was comparable (6.17, 6.70, and 6.35 mm, respectively). Stone expulsion was observed in 28 of 34 patients (82.3%) in group 1, 24 of 34 patients (70.5%) in group 2, and 12 of 34 patients (35.2%) in group 3. The average expulsion time for groups 1, 2, and 3 was 12.3, 14.5, and 24.5 days, respectively. The results of both study groups (groups 1 and 2) were superior to those in the placebo group (P = .003 and P = .001, respectively), but the study failed to show any statistically significant differences between tamsulosin and alfuzosin (P = .25). Alfuzosin was associated with fewer side effects than tamsulosin, especially in terms of retrograde ejaculation.