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Arcoxia (Etoricoxib)
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Arcoxia

Generic Arcoxia is a high-powered medication in battle against arthritis (rheumatoid arthritis, osteoarthritis) and chronic musculoskeletal pain, acute gout, and ankylosing spondylitis. Generic Arcoxia can be helpful for patients with injury, joint pain, fever and inflammation. Generic Arcoxia acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation.

Other names for this medication:

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Prednisone, Indocin, Mobic, Zyloprim, Allopurinol, Feldene, Anaprox, Naprosyn, Motrin, Relafen

 

Also known as:  Etoricoxib.

Description

Generic Arcoxia is produced with efficacious pharmacy formula making Generic Arcoxia wonderful weapon against arthritis (rheumatoid arthritis, osteoarthritis), chronic musculoskeletal pain, acute gout, ankylosing spondylitis, inflammation, fever, joint pain and injury. Target of Generic Arcoxia is to prevent pain and inflammation. Generic Arcoxia acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation. Generic Arcoxia acts blocking hormones of pain and inflammation.

Generic Arcoxia is NSAID (nonsteroidal anti-inflammatory drug).

Arcoxia is also known as Etoricoxib, Algix, Tauxib.

Generic name of Generic Arcoxia is Etoricoxib.

Brand names of Generic Arcoxia are Algix, Tauxib, Arcoxia.

Dosage

Generic Arcoxia can be taken in form of pills which should be taken by mouth with water.

It is better to take Generic Arcoxia every day at the same time with meal or without it.

Take Generic Arcoxia and remember that its dosage depends on patient's health state.

Generic Arcoxia can't be used by patients under 16 years.

For treatment of osteoarthritis and chronic musculoskeletal pain

Usual Generic Arcoxia dosage is 60 mg. Take it once a day.

For treatment of rheumatoid arthritis and ankylosing spondylitis

Usual Generic Arcoxia dosage is 90 mg. Take it once a day.

For treatment of gout attacks

Usual Generic Arcoxia dosage is 120 mg. Take it once a day.

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

Overdose

If you overdose Generic Arcoxia and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Do not store it in the bathroom or near a sink. Do not leave it in the car or on window sills. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Arcoxia 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 Arcoxia if you are allergic to Generic Arcoxia components or to aspirin.

Do not take Generic Arcoxia if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not use Generic Arcoxia in combination with other non-steroidal anti-inflammatory drugs (NSAIDs).

Do not use Generic Arcoxia in case of suffering from peptic ulcer or bleeding from the gut, inflammatory bowel disease or peripheral arterial disease.

Generic Arcoxia can't be used by patients under 16 years.

Try to be careful with Generic Arcoxia in case of using such medication as Ciclosporin; Tacrolimus; ACE inhibitors (Captopril, Enalapril); Angiotensin II antagonists (Losartan); Digoxin; Warfarin; Oestrogens; Lithium; Diuretics; Methotrexate.

Try to be careful with Generic Arcoxia in case of having heart, liver or kidney disease, high cholesterol, diabetes, intestines disorders, stomach disorders.

If you want to achieve most effective results without any side effects it is better to avoid smoking.

It can be dangerous to stop Generic Arcoxia taking suddenly.

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An intensive surveillance program from November 2000 to October 2004, adopting the World Health Organization Collaborating Centre for Drug Monitoring causality assessment criteria and algorithm.

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We identified 8973 manuscripts from our search, of which 74 randomised trials with a total of 58,556 patients were included in this analysis. 23 nodes concerning seven different NSAIDs or paracetamol with specific daily dose of administration or placebo were considered. All preparations, irrespective of dose, improved point estimates of pain symptoms when compared with placebo. For six interventions (diclofenac 150 mg/day, etoricoxib 30 mg/day, 60 mg/day, and 90 mg/day, and rofecoxib 25 mg/day and 50 mg/day), the probability that the difference to placebo is at or below a prespecified minimum clinically important effect for pain reduction (effect size [ES] -0·37) was at least 95%. Among maximally approved daily doses, diclofenac 150 mg/day (ES -0·57, 95% credibility interval [CrI] -0·69 to -0·46) and etoricoxib 60 mg/day (ES -0·58, -0·73 to -0·43) had the highest probability to be the best intervention, both with 100% probability to reach the minimum clinically important difference. Treatment effects increased as drug dose increased, but corresponding tests for a linear dose effect were significant only for celecoxib (p=0·030), diclofenac (p=0·031), and naproxen (p=0·026). We found no evidence that treatment effects varied over the duration of treatment. Model fit was good, and between-trial heterogeneity and inconsistency were low in all analyses. All trials were deemed to have a low risk of bias for blinding of patients. Effect estimates did not change in sensitivity analyses with two additional statistical models and accounting for methodological quality criteria in meta-regression analysis.

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Rheumatoid arthritis (RA) is an autoimmune disease affecting about 1% of people, with the highest incidence between 40 and 70 years. Methotrexate is an anti-folate analogue that has good efficacy and safety in the treatment of RA. Methotrexate (MTX) and non-steroidal anti inflammatory drugs are often concomitantly administered in clinical practice for the treatment of RA. In this case report, a 57-year-old female was treated with oral methotrexate 7.5 mg per week for a diagnosed case of RA. Since her pain persisted after completing six weeks of treatment with methotrexate, oral etoricoxib 60 mg once daily was added to the treatment regimen. Six weeks later, the patient complained of oral ulcerations and blisters on all fours limbs and trunk. The patient was re-evaluated and was diagnosed with Stevens-Johnson syndrome-Toxic epidermal necrolysis (SJS-TEN) overlap. This case highlights the possible pharmacokinetic interaction between methotrexate and etoricoxib that has a significant clinical implication.

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NSAIDs appear to be a very effective treatment for dysmenorrhoea, though women using them need to be aware of the substantial risk of adverse effects. There is insufficient evidence to determine which (if any) individual NSAID is the safest and most effective for the treatment of dysmenorrhoea. We rated the quality of the evidence as low for most comparisons, mainly due to poor reporting of study methods.

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Our results revealed that moderately intense pain is associated with routine orthodontic treatment, and that the amount of pain individuals perceive varies widely. We observed statistically significant differences in the pain control among the three groups, and that etoricoxib 60 mg proved most efficient.

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The present study was designed to evaluate the effects of three non-steroidal anti-inflammatory drugs (NSAIDs) with varying cycloxygenase selectivities on the small intestinal biochemical composition, function and histology during 1, 2-dimethylhydrazine (DMH) administration. Sprague Dawley male rats were divided into five different groups viz: Group 1 (control, vehicle treated), Group 2 (DMH-treated, 30 mg/kg body weight/week in 1 mM EDTA-saline, subcutaneously), Group 3 (DMH + aspirin-60 mg/kg body weight), Group 4 (DMH + celecoxib-6 mg/kg body weight), Group 5 (DMH + etoricoxib-0.64 mg/kg body weight). After six weeks of treatment, brush border membrane was isolated from the jejunum segment of all the groups and changes in the associated enzymes such as sucrase, lactase, maltase, alkaline phosphatase, membrane lipid composition, fluorescence polarizations of diphenylhexatriene, pyrene excimer formation, histological changes and surface characteristics were studied. The results indicated a significant alteration in the enzyme activity as well as changes in the structure and function of the intestine in the presence of the pro-carcinogen, DMH, which suggests the possible chemopreventive efficacy of NSAIDs against the intestinal cancer.

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The correlation (r) between LBPI and RMDQ changes ranged from 0.657 and 0.703; correlations between LBPI and PGART changes ranged from 0.677 and 0.738. Cutpoints separating responders from nonresponders for all 3 measures fell near the 66.7th percentile of response and were consistent with minimal clinically significant changes identified in the literature.

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We investigated the ability of the sPLA(2), known as MT-III, isolated from the viperid snake Bothrops asper, to induce LB formation in macrophages and the major cellular signaling pathways involved in this process. The effects of MT-III on ADRP localization and expression and macrophage ultrastructure were assessed. Our results showed that this sPLA(2) induced a marked increase in LB numbers in macrophages, induced the recruitment of ADRP in macrophages, and up-regulated ADRP expression. Ultrastructural analysis showed the presence of weakly and strongly osmiophilic LBs in sPLA(2)-stimulated cells. Enlargement of the ER and Golgi cisterns was also observed. Pretreatment of cells with H7 or staurosporine (PKC inhibitors), LY294002 or wortmannin (PI3K inhibitors), SB202190 or PD98059 (p38(MAPK) and ERK1/2 inhibitors, respectively), or Pyr-2 or Bel (cPLA(2) and iPLA(2) inhibitors, respectively) significantly reduced sPLA(2)-induced LB formation. Herbimycin (a PTK inhibitor) and indomethacin or etoricoxib (COX inhibitors) failed to alter sPLA(2)-induced effects. In conclusion, our results show for the first time the ability of a venom sPLA(2) to induce the formation of LBs and the expression of ADRP in macrophages. Venom PLA(2)-induced LB formation is dependent on PKC, PI3K, p38(MAPK), ERK1/2, cPLA(2), and iPLA(2) signaling pathways but not on PTK, COX-1, or COX-2 pathways. Activation of the ER and Golgi complex may play an important role in the formation of LBs induced by this sPLA(2) in macrophages.

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The identification and characterization of the inducible form of cyclooxygenases (COX-2) stimulated the investigations to develop efficient, non-steroidal anti-inflammatory drugs (NSAIDs) with reduced side effects (essentially gastro-intestinal toxicity) compared to classical NSAIDs. This review focuses on the chemical and pharmacological properties (pre-clinical data) of marketed COX-2 inhibitors.

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We enrolled 45 patients with metastatic renal cell carcinoma (RCC) at a progressive disease between March 2003 and April 2008 to assess the impact of an anti-inflammatory treatment regime in combination with metronomic low-dose chemotherapy. 42% of the patients had been systemically pre-treated. Therapy consisted of etoricoxib 60 mg daily plus pioglitazone 60 mg daily, day 1+, low-dose interferon-α 4.5 MU sc three times a week, week 1+ and low-dose capecitabine 1 g/m(2) twice daily orally for 14 days, every 3 weeks, day 1+, until disease progression. Objective response was observed in 35% of the patients (PR 27, CR 9%), which was paralleled by strong CRP decline for all patients with initially elevated CRP levels (n = 32). CRP values decreased from mean 42.3 mg/L (range 9.1-236), to 11.1 mg/L, (range 1.1-35.6), P = 0.006. Median overall survival and progression-free survival for the total cohort were 26.9 and 7.2 months for patients with elevated CRP 24.4 and 11.3 months (95% CI, 22.8-31.0/5.7-16.9) and 13.8-2.6 months (95% CI, 6.5-21.1/0.4-4.8) for the non-elevated CRP group, respectively (P = 0.082/0.017). Median observation time: 26.1 months; Overall survival at 5 years: 18%. Toxicity>WHO grade 3 was reported: Hand-foot syndrome in 16 patients (36%), diarrhea in 4, and pneumonia in 2 patients. Our data allow us to conclude that the control of tumor-associated inflammation is an important therapeutic principle in patients with metastatic RCC.

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Analgesia of etoricoxib was superior to placebo in the first postoperative day and to dipyrone in the third and fifth days after excision of primary pterygium with conjunctival autograft. There was no significant difference between dipyrone and placebo in all time points.

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For the many patients who suffer chronic pain, we seek the most effective anti-inflammatory drug with the least side-effect profile and the greatest long-term safety. Etoricoxib, a selective COX2 inhibitor, has been shown to be as effective as non-selective non-steroidal anti-inflammatory drugs in the management of chronic pain in rheumatoid arthritis and osteoarthritis, for periods of up to one year. Data on etoricoxib efficacy in chronic low back pain is beginning to emerge. The side-effect profile of etoricoxib suggests it is well tolerated with similar adverse effects to non-selective NSAIDs. Larger studies are awaited, to see whether superior gastrointestinal tolerability can be proven. Further work will be required to show that etoricoxib is safe in patients with pre-existing cardiovascular or gastrointestinal comorbidity, and the potentially confounding role of aspirin still needs to be elucidated. However, etoricoxib shows promise as a new and effective COX2 inhibitor in clinical practice.

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We report here the preclinical profile of etoricoxib (MK-0663) [5-chloro-2-(6-methylpyridin-3-yl)-3-(4-methylsulfonylphenyl) pyridine], a novel orally active agent that selectively inhibits cyclooxygenase-2 (COX-2), that has been developed for high selectivity in vitro using whole blood assays and sensitive COX-1 enzyme assays at low substrate concentration. Etoricoxib selectively inhibited COX-2 in human whole blood assays in vitro, with an IC(50) value of 1.1 +/- 0.1 microM for COX-2 (LPS-induced prostaglandin E2 synthesis), compared with an IC(50) value of 116 +/- 8 microM for COX-1 (serum thromboxane B2 generation after clotting of the blood). Using the ratio of IC(50) values (COX-1/COX-2), the selectivity ratio for the inhibition of COX-2 by etoricoxib in the human whole blood assay was 106, compared with values of 35, 30, 7.6, 7.3, 2.4, and 2.0 for rofecoxib, valdecoxib, celecoxib, nimesulide, etodolac, and meloxicam, respectively. Etoricoxib did not inhibit platelet or human recombinant COX-1 under most assay conditions (IC(50) > 100 microM). In a highly sensitive assay for COX-1 with U937 microsomes where the arachidonic acid concentration was lowered to 0.1 microM, IC(50) values of 12, 2, 0.25, and 0.05 microM were obtained for etoricoxib, rofecoxib, valdecoxib, and celecoxib, respectively. These differences in potency were in agreement with the dissociation constants (K(i)) for binding to COX-1 as estimated from an assay based on the ability of the compounds to delay the time-dependent inhibition by indomethacin. Etoricoxib was a potent inhibitor in models of carrageenan-induced paw edema (ID(50) = 0.64 mg/kg), carrageenan-induced paw hyperalgesia (ID(50) = 0.34 mg/kg), LPS-induced pyresis (ID(50) = 0.88 mg/kg), and adjuvant-induced arthritis (ID(50) = 0.6 mg/kg/day) in rats, without effects on gastrointestinal permeability up to a dose of 200 mg/kg/day for 10 days. In squirrel monkeys, etoricoxib reversed LPS-induced pyresis by 81% within 2 h of administration at a dose of 3 mg/kg and showed no effect in a fecal 51Cr excretion model of gastropathy at 100 mg/kg/day for 5 days, in contrast to lower doses of diclofenac or naproxen. In summary, etoricoxib represents a novel agent that selectively inhibits COX-2 with 106-fold selectivity in human whole blood assays in vitro and with the lowest potency of inhibition of COX-1 compared with other reported selective agents.

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Treatment for 1 week with Etoricoxib attenuated the CGRP-IR fibre depletion, the COX-2-IR increased cell number and the TNF-alpha and COX-2 mRNA increased levels induced by NGI. Two weeks of treatment had no beneficial effect.

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Two multi-centre, 26-week, double-blind, placebo-controlled, non-inferiority studies were conducted, enrolling patients who were prior non-steroidal anti-inflammatory drug (NSAID) or acetaminophen users. There were 599 patients in study 1 and 608 patients in study 2 randomized 4:4:1:1 to etoricoxib 30 mg qd, celecoxib 200 mg qd or one of two placebo groups for 12 weeks. After 12 weeks, placebo patients were evenly distributed to etoricoxib or celecoxib based on their initial enrollment randomization schedule. The primary hypothesis was that etoricoxib 30 mg would be at least as effective as celecoxib 200 mg for the time-weighted average change from baseline over 12 weeks for Western Ontario and McMaster (WOMAC) Pain Subscale, WOMAC Physical Function Subscale and Patient Global Assessment of Disease Status. Active treatments were also assessed over the full 26 weeks. Adverse experiences were collected for safety assessment.

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Multivariate analysis of data from the Multinational Etoricoxib and Diclofenac Arthritis Long-term (MEDAL) study (n = 23 504). We evaluated risk factors for change in systolic blood pressure (BP) (SBP) and diastolic BP (DBP) at 4 months versus baseline; exceeding predefined limits of change (PLoC) in BP anytime during the study; and the effect of concomitant antihypertensive class on SBP and exceeding SBP PLoC.

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In both groups pain intensity and treatability showed a statistically significant improvement after the epidural injection. The differences between the control and treatment groups were small and not clinically relevant. A small subgroup might profit from the steroid injection. In addition the treatability was dependent on psychometric values and the long-term outcome from a reduction of muscular skeletal dysfunctions.

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We investigated the effectiveness of oral etoricoxib 90 mg for seven days in a prospective two-stage study design for phase-2 clinical trials in a small sample of patients (n = 42). A cemented primary total hip arthroplasty was implanted for osteoarthritis. Six months after surgery, heterotopic ossification was determined on anteroposterior pelvic radiographs using the Brooker classification.

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The role of oxidative stress in the pathogenesis of various conditions including epilepsy, inflammatory bowel disease and rheumatoid arthritis is evolving. The aim of this study was to find out the correlation between various inflammatory models with seizures and antioxidant parameters. Fifty-four male rats were divided into three groups of colitis, adjuvant arthritis and cotton wool granuloma (CWG). Each group had three subgroups of control, model and treatment. Thalidomide was used as treatment in colitis and arthritis group, whereas etoricoxib was used in CWG group. In colitis and arthritis groups, thalidomide was administered for 3 and 17 days, respectively, whereas etoricoxib was administered for 7 days in CWG group. At the end of treatment protocols, a subconvulsive dose of pentylenetetrazole (PTZ) (40 mg/kg i.p.) was injected intraperitoneally to note seizure onset and score. After confirming the presence of inflammation by morphological and histological studies, plasma and brain biochemical parameters of oxidative stress were estimated. The models of colitis, arthritis and CWG were effectively produced as evidenced by morphological scores (P < 0.001). Thalidomide reduced the morphological score (P < 0.002) and seizure grade (P < 0.001), whereas increased seizure onset (P < 0.001) in the arthritis group. There was an increase in malondialdehyde levels in the brain of thalidomide-treated groups (P < 0.002) and a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels. There was neither improvement in seizure nor any significant changes in lipid peroxidation and antioxidant enzyme levels in etoricoxib-treated group. Thalidomide was effective in reducing the extent of arthritis as well as reducing the seizure scoring and increasing seizure onset in the adjuvant arthritis group. As it increased lipid peroxidation and reduced SOD and GPx, further evaluation is necessary with respect to oxidative stress.

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Previous studies indicate that the implementation of a prior authorization requirement for coxibs was followed by a sharp decline in their use. There are no studies showing what happens if coxib prior authorization is removed. The objective of this study is to assess the trend in the use of coxibs marketed in Spain, following removal of their respective prior authorization requirements in November 2006 for celecoxib and February 2007 for etoricoxib.

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While it is known that non-steroidal anti-inflammatory drugs including selective cyclooxygenase-2 (COX-2) inhibitors influence BP, the exact relationship and underlying mechanisms are still unclear. We investigated the effect of etoricoxib, a selective COX-2 inhibitor on the antihypertensive efficacy of atenolol; beta-blocker, ramipril; angiotensin converting enzyme inhibitor and telmisartan; angiotensin receptor blocker in deoxycorticosterone acetate (DOCA)-salt hypertensive rats, a mineralocorticoid volume expansion model. Etoricoxib attenuated the antihypertensive-induced reduction of systolic (atenolol; P < .001, ramipril; P = .011, telmisartan; P = .003) and mean arterial pressure (atenolol; P < .001, ramipril; P = .032, telmisartan; P = .023). These results demonstrate that COX-2 dependent mechanisms play a significant role in blood pressure regulation, and etoricoxib-induced COX-2 inhibition blunts the therapeutic effect of different classes of antihypertensives in this mineralocorticoid volume expansion model of hypertension.

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The solubility behavior of solid dispersions of two drugs with similar structures was studied. Valdecoxib (VLB) and etoricoxib (ETB) were used as model drugs, and their solid dispersions were prepared with 1, 2, 5, 10, 15, and 20% w/w poly(vinylpyrrolidone) (PVP) by the quench cooling method. The interactions between the drug and polymer molecules were studied by Fourier transform infrared spectroscopy (FT-IR). The thermodynamic aspects of solubility behavior were studied by plotting van't Hoff plots. Both the drugs showed significant differences in their solubility behavior. In the case of VLB, solubility was found to increase significantly with increasing PVP concentration. ETB however did not show any significant solubility enhancement and was found to have decreased solubility at high PVP concentrations. H-bonding interactions were established between VLB and PVP molecules, while none were observed in ETB-PVP dispersions. Solution thermodynamics of amorphous and crystalline forms of both the drugs were studied by van't Hoff plots. The results obtained showed very high negative value of Gibbs free energy for VLB as compared to ETB, thus demonstrating high spontaneity of VLB solubilization. Entropy of amorphous VLB was found to be highly favorable, while being slightly unfavorable for ETB. From this study H-bonding interactions were found to play a major role in dictating the solubility behavior of these drugs from solid dispersions.

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The COX-2 inhibitor etoricoxib modulates the peripheral and central nociceptive mechanisms in animals. This interaction has not been studied in patients with pain. This randomized, double-blind, placebo-controlled, 2-way crossover, 4-week treatment study investigated the pain mechanisms modulated by etoricoxib in patients with painful knee osteoarthritis. Patients were randomized to group A (60 mg/d etoricoxib followed by placebo) or B (placebo followed by 60 mg/d etoricoxib). The quantitative, mechanistic pain biomarkers were pressure pain thresholds, temporal summation (TS), and conditioning pain modulation. Clinical readouts were Brief Pain Inventory, WOMAC, painDETECT questionnaire (PD-Q), and time and pain intensity during walking and stair climbing. Etoricoxib as compared with placebo significantly modulated the pressure pain thresholds (P = 0.012, localized sensitization) at the knee and leg (control site) (P = 0.025, spreading sensitization) and TS assessed from the knee (P = 0.038) and leg (P = 0.045). Conditioning pain modulation was not modulated. The Brief Pain Inventory (pain scores), PD-Q, WOMAC, and walking and stair climbing tests were all significantly improved by etoricoxib. Based on a minimum of 30% or 50% pain alleviation (day 0-day 28), responders and nonresponders were defined. The nonresponders showed a significant association between increased facilitation of TS and increased pain alleviation. None of the other parameters predicted the degree of pain alleviation. Generally, a responder to etoricoxib has the most facilitated TS. In conclusion, etoricoxib (1) modulated central pain modulatory mechanisms and (2) improved pain and function in painful osteoarthritis. Stronger facilitation of TS may indicate a better response to etoricoxib, supporting the central mode-of-action of the drug.

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Etoricoxib is a cyclo-oxygenase (COX)-2-selective NSAID with a higher COX-1 to COX-2 selectivity ratio than the other COX-2-selective NSAIDs rofecoxib, valdecoxib or celecoxib. In patients with rheumatoid arthritis, improvements in tender and swollen joint counts and patient and investigator global assessment of disease activity were significantly greater in etoricoxib than in placebo recipients in two studies. Etoricoxib was also significantly more effective than naproxen in one of these studies. In patients with osteoarthritis of the hip or knee, etoricoxib was significantly more effective than placebo and had similar efficacy to naproxen with regards to improvements in pain and physical function scores and patient global assessment of disease status scores in two studies. Etoricoxib had similar efficacy to diclofenac in patients with osteoarthritis of the knee. Single-dose etoricoxib relieved pain in patients with postoperative dental pain in two studies. Similar scores assessing total pain relief over 8 hours (TOPAR8) were reported in etoricoxib and naproxen sodium or ibuprofen recipients, and higher TOPAR8 scores were reported with etoricoxib than with paracetamol (acetaminophen)/codeine. Pain relief was significantly better with etoricoxib than placebo in two studies in patients with chronic low back pain. Etoricoxib had similar efficacy to indomethacin in a study in patients with acute gout, and single-dose etoricoxib had similar efficacy to naproxen sodium in a study in women with primary dysmenorrhoea. Compared with non-COX-selective NSAIDs, etoricoxib was associated with significantly fewer upper gastrointestinal (GI) perforations, ulcers or bleeds, and was significantly less likely to result in treatment discontinuation because of NSAID-type GI symptoms or any GI symptoms.

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arcoxia reviews 2016-11-25

Using organ bath experiments, the contraction induced by norepinephrine (NE), U46619, acetylcholine, and KCl was performed on isolated human internal mammary arteries (IMA) cultured in the presence or absence of both interleukin-1beta (IL-1beta) and lipopolysaccharide (LPS) with or without endothelium. Under these conditions the COX (cyclooxygenase) isoforms were detected by immunohistochemistry and western blot, and the prostaglandins (PG) and thromboxane (Tx) released were measured using an enzyme immunoassay kit. A significant decrease in the maximal effect induced by NE but not by other stimuli was observed in the IL-1beta- and LPS-treated preparations after 6 and 24 h of culture (-19 +/- 6 and -25 +/- 4%, respectively), an effect that was endothelium independent. Under this inflammatory condition, the COX-2 inhibitors DFU buy arcoxia (1 micromol/L), DuP-697 (0.5 micromol/L), and Etoricoxib (1 micromol/L) markedly restored and increased the vascular reactivity to NE. These alterations were not observed with SC-560 (1 micromol/L), a selective COX-1 inhibitor. In addition, the COX-1 isoform was always detected and the COX-2 isoform was only found in human IMA exposed for 6 or 24 h under inflammatory conditions. The COX-2 induction was accompanied by an increase in PGE(2) (prostaglandin E(2)) and PGI(2) (prostaglandin I(2)) release in the culture medium (approximately 2.5-fold) but not with an increase in TxA(2) (thromboxane A(2)) release.

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The binary system of etoricoxib with beta-cyklodextrin (beta-CD) was prepared by the buy arcoxia kneading method. Drug-cyclodextrin interactions in solution were investigated by the phase solubility analysis. Differential scanning calorimetry, infrared spectroscopy, powder X-ray diffractometry and microscopic study were used to characterize the solid state of all binary systems, whereas their dissolution properties were evaluated according to the USP XXIII paddle method. The results indicate partial interaction of the drug with beta-CD in the physical mixture and complete interaction in the kneaded complex. The dissolution of etoricoxib was notably increased as compared to pure drug as well as its physical mixture. The complex showed more than 75% drug released in 30 min.

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To verify whether in patients with biochemical progression after radical prostatectomy (RRP), the administration of a cyclooxygenase-2 (COX-2) inhibitor during the off-phases of intermittent androgen deprivation (IAD) may increase buy arcoxia the effectiveness and off-therapy time of intermittent therapy.

arcoxia brand name 2017-05-31

The role of oxidative buy arcoxia stress in the pathogenesis of various conditions including epilepsy, inflammatory bowel disease and rheumatoid arthritis is evolving. The aim of this study was to find out the correlation between various inflammatory models with seizures and antioxidant parameters. Fifty-four male rats were divided into three groups of colitis, adjuvant arthritis and cotton wool granuloma (CWG). Each group had three subgroups of control, model and treatment. Thalidomide was used as treatment in colitis and arthritis group, whereas etoricoxib was used in CWG group. In colitis and arthritis groups, thalidomide was administered for 3 and 17 days, respectively, whereas etoricoxib was administered for 7 days in CWG group. At the end of treatment protocols, a subconvulsive dose of pentylenetetrazole (PTZ) (40 mg/kg i.p.) was injected intraperitoneally to note seizure onset and score. After confirming the presence of inflammation by morphological and histological studies, plasma and brain biochemical parameters of oxidative stress were estimated. The models of colitis, arthritis and CWG were effectively produced as evidenced by morphological scores (P < 0.001). Thalidomide reduced the morphological score (P < 0.002) and seizure grade (P < 0.001), whereas increased seizure onset (P < 0.001) in the arthritis group. There was an increase in malondialdehyde levels in the brain of thalidomide-treated groups (P < 0.002) and a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels. There was neither improvement in seizure nor any significant changes in lipid peroxidation and antioxidant enzyme levels in etoricoxib-treated group. Thalidomide was effective in reducing the extent of arthritis as well as reducing the seizure scoring and increasing seizure onset in the adjuvant arthritis group. As it increased lipid peroxidation and reduced SOD and GPx, further evaluation is necessary with respect to oxidative stress.

arcoxia generic 2017-01-25

Etoricoxib area under the plasma concentration buy arcoxia -time curve (AUC(0-00)) and maximum plasma concentration (C(max)) geometric mean ratios (GMR) with/without miconazole were 1.69 {90% confidence interval (CI); 1.46-1.92} and 1.12 (90% CI; 0.99-1.25), respectively, and corresponding GMRs with/without voriconazole were 1.49 (90% CI; 1.37-1.61) and 1.19 (90% CI; 1.08-1.31), respectively.

arcoxia 30 mg 2017-08-17

The purpose of this investigation was to develop fast dissolving tablets of etoricoxib. Granules containing etoricoxib, menthol, crospovidone, aspartame and mannitol were prepared by wet granulation technique. Menthol was sublimed from the granules by exposing the granules to vacuum. The porous granules were then compressed in to tablets. Alternatively, tablets were first prepared and later exposed to vacuum. The tablets were evaluated for percentage friability and disintegration time. A 3(2) full factorial design was applied to investigate the combined effect of 2 formulation variables: amount of menthol and crospovidone. The results of multiple regression analysis indicated that for obtaining fast dissolving tablets; optimum amount of menthol and higher percentage of crospovidone should be used. A surface response plots are also presented to graphically represent the effect of the independent variables on the buy arcoxia percentage friability and disintegration time. The validity of a generated mathematical model was tested by preparing a checkpoint batch. Sublimation of menthol from tablets resulted in rapid disintegration as compared with the tablets prepared from granules that were exposed to vacuum. The optimized tablet formulation was compared with conventional marketed tablets for percentage drug dissolved in 30 min (Q(30)) and dissolution efficiency after 30 min (DE(30)). From the results, it was concluded that fast dissolving tablets with improved etoricoxib dissolution could be prepared by sublimation of tablets containing suitable subliming agent.

arcoxia maximum dosage 2016-07-09

In this 6-week double-blind, active comparator controlled, parallel-group study eligible osteoarthritis patients were randomised to receive either etoricoxib 60 mg once daily (n = 256) or diclofenac 50 mg three times daily (n = 260). The primary study endpoint was the Western Ontario McMaster osteoarthritis index (WOMAC) pain subscale. Other endpoints included were the WOMAC stiffness and physical function subscales, and the Patient's Global Assessment of Response to Therapy (PGART) questionnaire. Early efficacy was evaluated using WOMAC buy arcoxia first question (pain walking on a flat surface) and PGART 4 h after the morning dose of each drug on days 1 and 2. Rescue medication (paracetamol) used was also recorded. The study was designed to show comparable efficacy between etoricoxib 60 mg once daily and diclofenac 50 mg three times daily with respect to the primary endpoint and was conducted outside the United States at 67 centres in 29 countries.

arcoxia 90 mg 2016-07-16

We identified 8973 manuscripts from our search, of which 74 randomised trials with a total of 58,556 patients were included in this analysis. 23 nodes concerning seven different NSAIDs or paracetamol with specific daily dose of administration or placebo were considered. All preparations, irrespective of dose, improved point estimates of pain symptoms when compared with placebo. For six interventions (diclofenac 150 mg/day, etoricoxib 30 mg/day, 60 mg/day, and 90 mg/day, and rofecoxib 25 mg/day and 50 mg/day), the probability that the difference to placebo is at or below a prespecified minimum clinically important effect for pain reduction (effect size [ES] -0·37) was at least 95%. Among maximally approved daily doses, diclofenac 150 mg/day (ES -0·57, 95% credibility interval [CrI] -0·69 to -0·46) and etoricoxib 60 mg/day (ES -0·58, -0·73 to -0·43) had the highest probability to be the best intervention, both with 100% probability to reach the minimum clinically important difference. Treatment effects increased as drug dose increased, but corresponding tests for a linear dose effect were significant only for celecoxib (p=0·030), diclofenac (p=0·031), and naproxen (p=0·026). We found no evidence that treatment effects varied over the duration of treatment. Model fit was good, and between-trial heterogeneity and inconsistency were low in all analyses. buy arcoxia All trials were deemed to have a low risk of bias for blinding of patients. Effect estimates did not change in sensitivity analyses with two additional statistical models and accounting for methodological quality criteria in meta-regression analysis.

arcoxia y alcohol 2017-11-21

The etoricoxib program database included data from 8 placebo-controlled Phase III studies of osteoarthritis, rheumatoid arthritis, and chronic low back pain. As part of the program-wide assessment of etoricoxib, the investigator-reported incidence of and discontinuations buy arcoxia due to renal AEs, including hypertension, lower-extremity edema (LEE), elevated serum creatinine concentration (SCC), and congestive heart failure (CHF) were examined.

arcoxia 30mg tablet 2016-07-26

We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, the Oxford Pain buy arcoxia Database, ClinicalTrials.gov, and reference lists of articles. The date of the most recent search was 3 January 2012.

arcoxia 60mg dosage 2016-07-30

EPE at various buy arcoxia doses significantly reduced mechanical, heat, cold hyperalgesia and increased the horizontal and vertical movements in intra-articular MIA injected rats. EPE prevented the damage to cartilage structure and reduced the cellular abnormalities. Articular cartilage of rats treated with EPE at 300 mg/kg group was almost normal with well-developed smooth surface and chondrocytes were distributed individually or arranged in column.

arcoxia overdose 2017-11-11

Forty patients with high axSpA activity (Bath Ankylosing Disease Activity Index (BASDAI 4) were examined and randomized to 2 groups: 1) 30 patients who received ET 90 mg continuously every day; 2) 10 patients who took the drug in the same dose intermittently 1-3 times weekly. The activity of axSpA (BASDAI, Ankylosing Spondylitis Disease Activity Score (ASDAS), erythrocyte sedimentation rate (ESR), and high-sensitivity C-reactive protein (hs-CRP)) was evaluated at baseline, 2 and 12 weeks; adverse events were recorded at baseline, 2, 6, and 12 weeks. The number of patients who had achieved an ASAS40 response at 2 and 12 weeks were taken into consideration. RESULTS At 12 weeks, the continuous administration group displayed decreases in BASDAI from 8 to 4, in ASDAS from 3.8 to 2.6, and in hs-CRP levels from 9.5 to 3.9 mg/l; the intermittent administration group exhibited decreases in BASDAI from 7.6 to 6.0, in ASDAS from 3.5 to 3.1, and hs-CRP from 8.8 to 4.5 mg/l (p<0.05). At this time, an AS40 response was achieved by 22 (73. buy arcoxia 3%) and 2 (20%) patients in Groups 1 and 2, respectively (p<0.05 for all). No serious adverse events were recorded.

arcoxia 4 mg 2015-05-08

To evaluate the efficacy of etoricoxib in buy arcoxia patients with axial ankylosing spondyloarthritis (AS) refractory to traditional NSAIDs.

arcoxia capsule 2015-02-22

This review suggests that among widely used NSAIDs, naproxen and low-dose ibuprofen are least likely to increase cardiovascular risk. Diclofenac in doses available without prescription elevates risk. The data for etoricoxib were sparse, but buy arcoxia in pair-wise comparisons this drug had a significantly higher RR than naproxen or ibuprofen. Indomethacin is an older, rather toxic drug, and the evidence on cardiovascular risk casts doubt on its continued clinical use. Please see later in the article for the Editors' Summary.

arcoxia pill 2016-06-14

To review the clinical effectiveness and cost-effectiveness of cyclooxygenase-2 (COX-2) selective non-steroidal anti-inflammatory drugs (NSAIDs) (etodolac Priligy Online Singapore , meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib and lumiracoxib) for osteoarthritis (OA) and rheumatoid arthritis (RA).

arcoxia pills 2016-08-28

For this network meta-analysis, we considered randomised trials comparing any of the following interventions: NSAIDs, paracetamol, or placebo, for the treatment of osteoarthritis pain. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) and the reference lists of relevant articles for trials published between Jan 1, 1980, and Feb 24, 2015, with at least 100 patients per group. The prespecified primary and secondary outcomes were pain and physical function, and were extracted in duplicate for up to seven timepoints after the start of treatment. We used an extension of multivariable Bayesian random effects models for mixed multiple treatment comparisons with a random effect at the level of trials. For the primary analysis, a random walk of first order was used to account for multiple follow-up outcome data within a trial. Preparations that used different total daily dose were considered separately in the analysis. To assess a potential dose-response relation, we used preparation-specific covariates Clomid Medication Infertility assuming linearity on log relative dose.

arcoxia dosage 2017-06-21

Efficacy was comparable among prednisolone, etoricoxib, and indomethacin for the treatment of AGA. Prednisolone might be more effective in reducing inflammation and it had a better safety Zanaflex Overdose profile.

arcoxia generic name 2015-11-18

To evaluate the clinical efficacy and tolerability of etoricoxib in the treatment of osteoarthritis (OA) of the knee and define the clinically active dose range for further clinical trials. Cipro Tablets

etoricoxib drug arcoxia 2015-11-24

Etoricoxib 120 mg taken prior Norvasc 10 Mg to a 25-hour ritual fast decreases incidence of and attenuates fasting headache.

arcoxia 120 mg 2015-10-19

Ibuprofen was the most commonly implicated drug, followed by acetylsalicylic acid (ASA). Urticaria was the most common manifestation, followed by angioedema. Most of the patients developed symptoms within 1 h. Twenty-five percent in Group A (n = 47) and 6% in Group B (n = 50) were intolerant Cipro Mg 050 to etoricoxib. Skin biopsy showed mast cell activation with the release of tryptase to the extracellular space but without the increase in serum tryptase levels.

arcoxia and alcohol 2015-09-19

We hypothesised that etoricoxib given 1 h before total knee Strattera Drug Test arthroplasty under spinal anaesthesia will decrease the cumulative dose of intravenous and subcutaneous morphine required to maintain pain intensity of 3 or less on a 10-point numerical rating scale (NRS) during the first postoperative 48 h compared with the same dose of etoricoxib given after surgery.

arcoxia 40 mg 2015-12-21

The inhibition of cyclooxygenase (COX)-2 confers a small but absolute risk of cardiovascular events on patients taking nonsteroidal anti-inflammatory drugs (NSAIDs). This risk has been established by placebo-controlled trials of NSAIDs selective for COX-2; traditional NSAIDs seem to be heterogeneous with respect to cardiovascular risk. The American Heart Association (AHA) has proposed a 'stepped-care' approach to the use of NSAIDs in patients with cardiovascular disease, whereas the Food and Drug Administration (FDA) has failed to approve the COX-2-selective NSAID etoricoxib. In this article, these actions of the AHA and the FDA are interpreted in the light of current knowledge, prompting the formulation of scientific questions that might be addressed.

arcoxia 750 mg 2017-06-03

We performed placebo-controlled oral challenge with etoricoxib in 65 patients with previous adverse reactions to NSAIDs: 13 to salicylates, 18 to arylpropionic acids, 10 to arylacetic acid, 12 to oxicam and derivates, 8 to pyrazolones, and 4 to acetaminophen (paracetamol). The reported symptoms were urticaria or angioedema in 69%, rhinitis in 3%, and 1 case of anaphylactic shock (1.5%). The challenge was done using the placebo on the first day, half dosage of etoricoxib (45 mg) on the second day, and the therapeutic dose of 90 mg on the third day. The challenge was done in the outpatient department of the hospital and the subjects were monitored for a further 4 to 6 hours after challenge.

arcoxia mg 2017-05-20

Seventeen published studies were reviewed, and the cardiovascular safety data were extracted from each trial. The mechanism by which COX-2 inhibitors may induce a thromboembolic event is likely multifactorial involving (1) COX-2-specific isoform binding affinity, (2) drug dose, (3) duration of therapy, and (4) cardiovascular risk profile of the patient. Evidence supports an association between cardiovascular adverse events and the use of rofecoxib, valdecoxib, and celecoxib. However, this risk is not equally distributed among the drugs. Given the relative paucity of data, lumiracoxib and etoricoxib cardiovascular effects remain uncertain.

cut arcoxia tablets 2016-12-28

Because many NOA are over-the-counter drugs, it is difficult to obtain data on their use. PIC data could provide information on the NOA use in the population.

arcoxia tab 2017-07-18

Data of 130 consecutive patients with defined surgical procedures were extracted from charts before and after implementation of the algorithm. Our patients documented pain intensity at rest and on movement on a numerival rating scale (NRS) from 0 (= no pain) to 10 (=  worst pain). A successful pain management was definded as maximum pain intensity at rest ≤ 3 and on movement ≤ 5 on the NRS. For statistical analysis we used the Wilcoxon and the chi squared test.

arcoxia with alcohol 2016-02-21

Etoricoxib 60 mg demonstrated efficacy significantly superior to placebo (p < or = 0.005) and comparable to naproxen 500 mg twice daily as assessed by the primary efficacy end points. Secondary and other end points confirmed these results. Treatment effects were evident by day 2, maximal by week 2, and sustained over the entire 12 weeks. Etoricoxib was well tolerated for 12 weeks.

arcoxia 240 mg 2016-06-27

This pre-specified combined analysis used data from nine randomized, double-blind, controlled, clinical trials with etoricoxib in patients with osteoarthritis, rheumatoid arthritis, chronic low back pain, or ankylosing spondylitis. The cumulative incidences of (1) new use (new prescription or increased dose) of gastroprotective agents (GPA) and (2) discontinuation due to dyspeptic symptoms were compared among patients treated with etoricoxib (60 mg, 90 mg, or 120 mg daily) vs. non-selective NSAIDs (diclofenac 50 mg. t.i.d. or naproxen 500 mg. b.i.d.).

arcoxia tablet indication 2017-10-27

In this work, we present the results of two combined approaches, molecular docking and comparative molecular field analysis (CoMFA), to propose how the selective cyclooxygenase-2 inhibitor celecoxib could act as a p38 mitogen-activated protein (MAP) kinase inhibitor. The docking analysis revealed why celecoxib has a less favorable binding energy (DeltaG= -12.4kcal/mol) than the selective p38 MAP kinase (p38 MAPK) inhibitor, SB203580 (DeltaG= -22.2kcal/mol). The CoMFA results revealed unfavorable steric effects that can be related to the predicted lower p38 MAP kinase inhibitory activity of celecoxib. Additionally, FlexX and CoMFA results also suggested that etoricoxib, another selective COX-2 inhibitor, could inhibit p38 MAP kinase.