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Arcoxia (Etoricoxib)

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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.


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.


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.


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


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.


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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IFS causes important changes in the micturition physiology in rats, and the inhibition of the isoenzyme COX-2 could be an important event that could prevent the detrimental effects elicited by IFS-induced hemorrhagic cystitis.

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Osteoblasts were cultured from femoral heads obtained from five young otherwise healthy patients undergoing total hip replacement. The cells were cultured using techniques that have been previously described. A full factorial design was used to set up the experiment on samples obtained from the five donors. Normal therapeutic concentrations of the various DMARDs were added alone and in combination to the media. The cell proliferation was estimated after two weeks using spectrophotometric technique using Roche Cell proliferation Kit. Multilevel regression analysis was used to estimate which drugs or combination of drugs significantly affected cell proliferation.

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To evaluate the risk of first myocardial infarction (MI) associated with the use of various non-steroidal anti-inflammatory drugs (NSAIDs) in the general population.

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The effect of hepatic insufficiency on the pharmacokinetics of etoricoxib, a selective inhibitor of cyclooxygenase-2, was investigated following administration of single and multiple oral doses to mild hepatic insufficiency patients (Child-Pugh score of 5 to 6), multiple oral doses to moderate hepatic insufficiency patients (Child-Pugh score of 7 to 9), and single intravenous doses to both mild and moderate hepatic insufficiency patients. A trend of decreasing systemic clearance with increasing hepatic impairment was observed. Absorption of etoricoxib was unaffected by hepatic impairment. Binding of etoricoxib to plasma proteins was also found to be unaffected by hepatic disease. Etoricoxib was generally well tolerated by patients with mild and moderate hepatic insufficiency. Together, these results support a 60-mg once-daily dosing regimen for mild hepatic insufficiency patients and a 60-mg every-other-day dosing regimen for moderate hepatic insufficiency patients. There are no clinical or pharmacokinetic data in patients with severe hepatic insufficiency (Child-Pugh score > 9).

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The least squares (LS) mean (95% CI) differences from placebo for Pain Intensity Difference at Rest over Days 1-3 were -0.54 (-0.95, -0.14); -0.49 (-0.89, -0.08); and -0.45 (-0.85, -0.04) for etoricoxib 90 mg, etoricoxib 120 mg, and ibuprofen, respectively (p < 0.05 for etoricoxib vs. placebo). Differences in LS Geometric Mean Ratio morphine use over Days 1-3 from placebo were 0.66 (0.54, 0.82); 0.69 (0.56, 0.85); and 0.66 (0.53, 0.81) for etoricoxib 90 mg, etoricoxib 120 mg, and ibuprofen, respectively (p < 0.001 for etoricoxib vs. placebo). Differences in LS Mean Pain Intensity upon Knee Flexion were -0.37 (-0.85, 0.11); -0.46 (-0.94, 0.01); and -0.42 (-0.90, 0.06) for etoricoxib 90 mg, etoricoxib 120 mg, and ibuprofen, respectively. Opioid-related AEs occurred in 41.8%, 34.7%, 36.5%, and 36.3% of patients on placebo, etoricoxib 90 mg, etoricoxib 120 mg, and ibuprofen, respectively.

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The enzyme cyclooxygenase (COX) was shown to exist as two distinct isoforms about a decade ago. COX-1 is constitutively expressed as a 'housekeeping' enzyme in nearly all tissues, and mediates physiological responses (e.g. cytoprotection of the stomach, and platelet aggregation). On the other hand, COX-2, expressed by cells involved in inflammation (e.g. macrophages, monocytes, synoviocytes), has emerged as the isoform that is primarily responsible for the synthesis of prostanoids involved in acute and chronic inflammatory states. Consequently, the hypothesis that selective inhibition of COX-2 might have therapeutic actions similar to those of non-steroidal anti-inflammatory drugs, but without causing gastrointestinal side effects, was the rationale for the development of selective inhibitors of the COX-2 isoenzyme. Selective COX-2 inhibitors currently used in the clinic are the sulphonamides celecoxib and valdecoxib (parecoxib is a prodrug of valdecoxib), as well as the methylsulphones rofecoxib and etoricoxib. Furthermore, the phenylacetic acid derivative lumiracoxib has gained permission recently to be marketed in Europe. This review discusses the clinically relevant similarities and differences of these substances, with particular emphasis on their diverse pharmacokinetic characteristics.

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The primary outcome measure was the cumulative dose of intravenous and subcutaneous morphine required during the first postoperative 48 h to maintain a 10-point numerical pain rating scale value of 3 or less. Secondary outcomes measures were duration of analgesia from initiation of spinal anaesthesia until the first analgesic requirement and the side-effects of the treatment.

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Electronic databases were searched up to November 2003. Industry submissions to the National Institute for Health and Clinical Excellence (NICE) in 2003 were also reviewed.

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In addition to the determination of clinical symptoms, investigations included radiography of the thorax, spine, hands and feet, arthrosonography, determination of laboratory parameters (including C-reactive protein levels and presence of antibodies against cyclic citrullinated peptide), cytogenetics and electrocardiography.

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Experimental animals were divided into four groups as liver I/R control (LIRC), 50 mg/kg etoricoxib + liver I/R (ETO-50), 100 mg/kg etoricoxib + liver I/R (ETO-100), and healthy group (HG). ETO-50 and ETO-100 groups were administered etoricoxib, while LIRC and HG groups were orally given distilled water by gavage. Hepatic artery was clamped for one hour to provide ischemia, and then reperfusion was provided for 6 hours. Oxidant, antioxidant, and COX-2 gene expressions were studied in the liver tissues. ALT and AST were measured.

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Religious fasting is associated with headache. This has been documented as "Yom Kippur headache" and "first of Ramadan headache." Etoricoxib, a Cox-2 inhibitor with a 22-hour half-life, has been shown effective in preventing fasting headache when taken just prior to the 25-hour Yom Kippur fast. We hypothesized that etoricoxib would also be effective in preventing headache during Ramadan, despite the different characteristics of the fast.

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Etoricoxib is a new COX-2 selective inhibitor under development for treatment of osteoarthritis, rheumatoid arthritis, and acute pain. In this study, etoricoxib 120 mg provided rapid and long-lasting pain relief to patients with moderate-to-severe postdental surgery pain. Etoricoxib was generally well tolerated.

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Etoricoxib is a potent selective COX-2 inhibitor in man. Ex vivo whole-blood assays assessed COX-2 inhibition after oral administration of etoricoxib in single (5-500 mg) and multiple (25-150 mg) once-daily doses to healthy human subjects. A separate study examined ex vivo gastric mucosal PGE2 synthesis after etoricoxib (120 mg qd), naproxen (500 mg bid), or placebo for 5 days. The effect of etoricoxib 120 mg qd on the COX-1-mediated antiplatelet effects of low-dose aspirin (ASA) was also assessed. The mean (time)-weighted average inhibition (WAI) of lipopolysaccharide (LPS)-stimulated PGE2 (COX-2 assay) vcrsus placebo was dose related after single (range: 3.1%-99.1%) and multiple doses (range: 52.5%-96.7%). PGE2 remained significantly inhibited 24 hours postdose at steady state. Inhibition of LPS-stimulated PGE2 showed a strong relationship with etoricoxib plasma concentrations; ex vivo, IC50 was almost identical to in vitro. Multiple dosing of etoricoxib (up to 150 mg qd) showed no important effects on serum TXB2, bleeding time, or platelet aggregation (COX-1-mediated effects). The nonselective nonsteroidal anti-inflammatory (NSAID) naproxen significantly inhibited (approximately 78%) ex vivo prostaglandin synthesis in gastric mucosa; etoricoxib had no effect. Etoricoxib did not interfere with the antiplatelet effects of low-dose ASA, as assessed by serum TXB2 and platelet aggregation. Etoricoxib was generally well tolerated, even at doses above the clinical dose range. Based on these results, etoricoxib is a potent selective inhibitor of COX-2 after single and multiple dosing regimens and does not inhibit prostaglandin synthesis in the gastric mucosa, even at doses above the clinical dose range of 60 to 120 mg.

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The out-patient pharmacies in Ramallah and Bethlehem, central Palestine, were evaluated for NSAIDs utilization and pattern of prescribing and dispensing of these commonly used medications across the whole country. In our study for this area that accounts for almost 25% of the inhabitants of all Palestine (459, 761 inhabitants according to 2011 census), we analyzed the use of NSAIDs whether were prescribed for the patient or were obtained without a prescription in the period of Sept 1(st) to Nov. 30, 2011. The number of defined daily doses, DDD/1000 inh/day, and the percentage utilization from total were determined and analyzed using the simple ATC/DDD model which was developed by WHO for assessment of quality prescribing of medications. From these data we calculated DU 90% for the drugs described in this study. Using a scale for GI toxicity and risk determination from a meta- analysis of controlled epidemiological studies, we determined the GI risk of the drugs in the study. Ketoprofen and piroxicam were found to be associated with the highest risk, on the other hand ibuprofen and diclofenac were associated with low risk of GI toxicity. The average Price/DDD was also determined for the purpose of comparison with the prices in other European countries. Our findings were both exciting and interesting with the total consumption of NSAIDs over the period of study was 31.26 DDD/1000 inh/day comparing to 51.02 DDD/1000 inh/day in the European countries included in the study. Only 5 drugs fell within DU 90% which are respectively along with their percentage NSAIDs consumption: (ibuprofen; 26.48%, diclofenac; 23.38%, etoricoxib; 21.24%, meloxiocam; 12.19%, and celecoxib; 7.16%). The drugs were obtained mostly by prescription except for the first 2 agents (ibuprofen and diclofenac) which were almost exclusively bought without a prescription as OTC with the pharmacist greatly influence their use and dispensing. The price of purchasing for the top DU 90% agents was almost twice the price in Europe for the same drugs taking into consideration the limitations of our study in determining the equipotency or the equivalency of the DDD doses in Palestine and Europe.

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First trimester abortions especially cervical dilation and suction aspiration are associated with pain, despite various methods of pain control.

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[(14)C]Etoricoxib (100 microCi/dose) was administered to six healthy male subjects (i.v., 25 mg; p.o., 100 mg). Following the i.v. dose, the plasma clearance was 57 ml/min, and the harmonic mean half-life was 24.8 h. Etoricoxib accounted for the majority of the radioactivity (approximately 75%) present in plasma following both i.v. and p.o. doses. The oral dose, administered as a solution in polyethylene glycol-400, was well absorbed (absolute bioavailability of approximately 83%). Total recovery of radioactivity in the excreta was 90% (i.v.) and 80% (p.o.), with 70% (i.v.) and 60% (p.o.) excreted in urine and 20% in feces after either route of administration. Radiochromatographic analysis of the excreta revealed that etoricoxib was metabolized extensively, and only a minor fraction of the dose (<1%) was excreted unchanged. Radiochromatograms of urine and feces showed that the 6'-carboxylic acid derivative of etoricoxib was the major metabolite observed (> or =65% of the total radioactivity). 6'-Hydroxymethyl-etoricoxib and etoricoxib-1'-N-oxide, as well as the O-beta-D-glucuronide conjugate and the 1'-N-oxide derivative of 6'-hydroxymethyl-etoricoxib, were present in the excreta also (individually, < or =10% of the total radioactivity). In healthy male subjects, therefore, etoricoxib is well absorbed, is metabolized extensively via oxidation (6'-methyl oxidation >1'-N-oxidation), and the metabolites are excreted largely in the urine.

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The least-squares mean time-weighted change from baseline LBP-IS score over 4 weeks was -32.94 mm (95% CI -36.25, -29.63) for etoricoxib, indicating substantial efficacy in relief of pain. The treatment difference for the primary outcome was 2.51 mm (95% CI -1.50, 6.51), fulfilling the prespecified equivalence criterion of 95% confidence interval wholly within +/- 10 mm. Etoricoxib improved all secondary and other efficacy outcomes. There were no statistically significant between-group differences in the proportion of patients with one or more clinical adverse events (AEs) (etoricoxib 35%, diclofenac 39%), or the proportion of patients who discontinued due to AEs (etoricoxib 7%, diclofenac 5%).

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Double-blind, placebo-controlled, randomized trial.

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Andrographis paniculata Nees (Acanthacae) is commonly used medicinal plant in the traditional. Unani and Ayurvedic medicinal systems. It has broad range of pharmacological effects such as hepatoprotective, antioxidant, antivenom, antifertility, inhibition of replication of the HIV virus, antimalarial, antifungal, antibacterial, antidiabetic, suppression of various cancer cells and anti-inflammatory properties. Andrographolide (AN) is one of the active constituent of the A. paniculata Nees extract (APE). They have been found in many traditional herbal formulations in India and proven to be effective as anti-inflammatory drug

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Study group included 76 patients suffering from IBD (ulcerative colitis (UC) (38), and Crohn's disease (CD) (38)). The control group included 70 patients known to have UC (35) and Crohn's disease (CD) (35). Patients of both groups were referred to the rheumatology clinic for rheumatic manifestations that require antiinflammatory therapy and were intolerable to the t-NSAIDs. The level of the IBD activity at the baseline visit, when drug/placebo therapy was initiated, was scored for all subjects included in the study. In the study group the dose of etoricoxib ranged from 60 to 120 mg tablet once a day according to their rheumatic condition. The control group received a placebo tablet once a day. Adverse events related to the use of the study medication in 1 and 3 months time were documented. Etoricoxib/placebo therapy was stopped once the patient experience flare up of their IBD.

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There were 588 patients randomized to placebo (n=46),etoricoxib (90 mg (n=191)), etoricoxib (120 mg (n=97)), ibuprofen(2400 mg (n=192)), and A/C (n=62). The overall analgesic effect (TOPAR6) of etoricoxib (90, 120 mg) was significantly greater than that of placebo (P ≤ 0.001), and not inferior to that of ibuprofen; no discernible difference was observed between etoricoxib 90 and 120 mg. Both etoricoxib doses were superior to A/C (P ≤ 0.001). Etoricoxib (90 and 120 mg) and ibuprofen(2400 mg) were generally well tolerated and had a similar incidence of adverse events (AEs). A/C was associated with significantly more AEs that led to discontinuation (ie, nausea and vomiting).

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All large scale randomised controlled trials comparing any non-steroidal anti-inflammatory drug with other non-steroidal anti-inflammatory drugs or placebo. Two investigators independently assessed eligibility.

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This double-blind study randomized OA patients to etoricoxib 90 mg, then to 60 mg once daily vs diclofenac 75 mg twice daily; RA patients were randomized to etoricoxib 90 mg once daily or diclofenac 75 mg twice daily. The primary endpoint was non-inferiority of etoricoxib vs diclofenac for thrombotic CV events (95% CI upper bound of hazard ratio <1.30). Other safety and efficacy parameters were evaluated in cohorts of patients based on etoricoxib dose and disease.

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This study portrays the potential CV risk of selective COX-2-Is; confirms and re-evaluate the results of earlier studies in this regard.

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This first study of COX-2 inhibition in provoked asthma found no negative effects of etoricoxib on allergen-induced airflow obstruction and sputum eosinophils, basal lung function, or methacholine responsiveness. The study suggests that short-term use of COX-2 inhibitors is safe in subjects with asthma.

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In this randomized, double-blind, placebo-controlled, multicenter study we assessed the analgesic effect of etoricoxib (a new cyclooxygenase-2 inhibitor) in patients having had knee or hip replacement surgery. A total of 228 patients with moderate or severe pain were randomly allocated within 72 h after surgery to receive etoricoxib 120 mg, controlled-release naproxen sodium 1100 mg, or placebo (1:1:1) on day 1 followed by etoricoxib and placebo (1:2) on days 2 to 7. Patients reported pain scores, rescue (opioid-combination) medication use, and the response to study drug. On day 1, etoricoxib provided an analgesic effect superior to placebo and similar to controlled-release naproxen sodium as demonstrated by the total pain relief score over 8 h, the primary end-point; least-squares mean scores were 11.0, 11.5, and 5.6, respectively (P < 0.001 versus placebo). Similarly, a larger percentage of patients receiving etoricoxib and naproxen sodium than those receiving placebo reported good to excellent responses to study drug: 53%, 60%, and 26% respectively. On days 2-7, etoricoxib demonstrated a significant reduction of rescue medication use, 35% (P < 0.001 versus placebo). The clinical relevance of the decrease was confirmed by Patient's Global Evaluation (P < 0.05 versus placebo). Patients receiving etoricoxib also experienced significantly less "worst" and "average" pain than did those on placebo. Etoricoxib was generally well tolerated in this study; the incidence of adverse experiences was infrequent and similar across treatment groups. In summary, etoricoxib provided analgesia that was similar to controlled-release naproxen sodium on day 1 and superior to placebo with reduced supplemental opioid use over 7 days.

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Non-steroidal anti-inflammatory drugs (NSAIDs), such as non-selective NSAIDs (nsNSAIDs) or selective cyclooxygenase-2 (COX-2) inhibitors, are commonly prescribed for arthritic pain relief in patients with osteoarthritis (OA), rheumatoid arthritis (RA), or ankylosing spondylitis (AS). Treatment guidelines for chronic NSAID therapy include the consideration for gastroprotection for those at risk of gastric ulcers (GUs) associated with the chronic NSAID therapy. The United States Food and Drug Administration has approved naproxen/esomeprazole magnesium tablets for the relief of signs and symptoms of OA, RA, and AS, and to decrease the risk of developing GUs in patients at risk of developing NSAID-associated GUs. The European Medical Association has approved this therapy for the symptomatic treatment of OA, RA, and AS in patients who are at risk of developing NSAID-associated GUs and/or duodenal ulcers, for whom treatment with lower doses of naproxen or other NSAIDs is not considered sufficient. Naproxen/esomeprazole magnesium tablets have been compared with naproxen and celecoxib for these indications in head-to-head trials. This systematic literature review and network meta-analyses of data from randomized controlled trials was performed to compare naproxen/esomeprazole magnesium tablets with a number of additional relevant comparators. For this study, an original review examined MEDLINE(®), Embase(®), and the Cochrane Controlled Trials Register from database start to April 14, 2009. Using the same methodology, a review update was conducted to December 21, 2009. The systematic review and network analyses showed naproxen/esomeprazole magnesium tablets have an improved upper gastrointestinal tolerability profile (dyspepsia and gastric or gastroduodenal ulcers) over several active comparators (naproxen, ibuprofen, diclofenac, ketoprofen, etoricoxib, and fixed-dose diclofenac sodium plus misoprostol), and are equally effective as all active comparators in treating arthritic symptoms in patients with OA, RA, and AS. Naproxen/esomeprazole magnesium tablets are therefore a valuable option for treating arthritic symptoms in eligible patients with OA, RA, and AS.

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Although adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) occur in only a small proportion of users, the widespread use of these drugs has resulted in a substantial overall number of affected persons who experience serious gastrointestinal complications. Dyspeptic symptoms are estimated to occur in 10-60% of NSAID users and lead to discontinuation of treatment in 5-15% of rheumatoid arthritis patients taking NSAIDs. It is now well established that the point prevalence of peptic ulcer disease in patients receiving conventional NSAID therapy ranges between 10 and 30%, representing a 10-30-fold increase over that found in the general population. One of 175 users of conventional NSAIDs in the USA will be hospitalized each year for NSAID-induced gastrointestinal damage. The mortality of hospitalized patients remains about 5-10%, with an expected annual death rate of 0.08%. The selective COX-II inhibitors (rofecoxib, celecoxib, parecoxib, etoricoxib, valdecoxib, lumiracoxib) show consistently comparable efficacy to that of conventional non-steroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis and osteoarthritis, but have a significantly reduced propensity to cause gastrointestinal toxicity. In many cases, the gastric effects of therapeutically active doses of COX-II inhibitors are indistinguishable from placebo. The safety benefits of COX-2 inhibitors given alone appear similar to combined therapy with conventional NSAIDs and gastroprotective agents. These findings warrant the consideration of COX-II inhibitors as first-line therapy in patients requiring long-term pain control.

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arcoxia 30 mg 2017-02-16

Five studies (880 participants) were included in the review. All five studies reported on 120 mg, with 655 participants in a comparison with placebo. At least 50% pain relief was reported by 64% with etoricoxib 120 mg and 10% with placebo (NNT 1.9 (1.7 to 2.1)). For dental studies only the NNT was 1.6 (1.5 to 1.8). Two studies also reported on higher doses of 180 and 240 mg, with 249 participants. At least 50% pain relief was reported by 79% with etoricoxib 120 mg and 12% with placebo (NNT 1.5 (1.3 to 1.7)).Significantly fewer participants used rescue medication when taking etoricoxib 120 mg than those taking placebo (NNT to prevent buy arcoxia online remedication 2.4 (2.1 to 2.9)), and the median time to use of rescue medication was 20 hours. Adverse events were reported at a similar rate to placebo, with no serious events.

arcoxia 220 mg 2016-05-21

We performed a nested case-control study in a cohort of 486,378 persons registered within the United Kingdom General Practice Research Database with at least 1 prescription of an NSAID between June 1, 2000, and October 31, 2004. A total of 3643 cases with acute myocardial infarction (AMI) were matched to 13,918 controls on age, sex, year of cohort entry, and general practice. Rate ratios (RRs) of AMI associated with use of COX-2-selective and -nonselective NSAIDs were calculated. Current use of etoricoxib was associated with a 2.09-fold (95% confidence interval [CI], 1.10 to 3.97) risk of AMI compared with no use of NSAIDs during the prior year. Current use of rofecoxib (RR=1.29; 95% CI, 1.02 to 1.63), celecoxib (RR=1.56 buy arcoxia online ; 95% CI, 1.22 to 2.00), and diclofenac (RR=1.37; 95% CI, 1.17 to 1.59) also significantly increased the AMI risk. For current use of valdecoxib, the RR was 4.60 (95% CI, 0.61 to 34.51). RRs appeared to increase with higher daily doses of COX-2 inhibitors and were also increased in patients without major cardiovascular risk factors.

etoricoxib drug arcoxia 2016-12-10

To evaluate the efficacy and tolerability of the highly selective cyclooxygenase-2 (COX-2) inhibitor etoricoxib for the treatment of rheumatoid buy arcoxia online arthritis (RA).

arcoxia maximum dosage 2016-04-25

Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetylsalicylic acid (ASA) are often prescribed concurrently in patients with nociceptive pain and cardiovascular comorbidity. NSAIDs and ASA inhibit the same COX-enzymes, and thus may interact. ASA's cardioprotective antiplatelet effect is entirely COX-1 dependent. NSAIDs can be either non-COX-1 and COX-2 selective or COX-2 selective. The aim of this study was to examine the interaction between ASA and different selective and nonselective NSAIDs on thrombocyte function buy arcoxia online .

arcoxia dosage mims 2016-06-28

The aim of the study is to assess the effects of celecoxib and sulfasalazine on the risk of coronary artery disease (CAD) in patients with ankylosing spondylitis (AS).Using the claims data of Taiwan National Health Insurance (NHI) database, a nationally representative data that contain the medical records of 23 million Taiwan residents, we randomly selected 1 million cohort from the database, and then we enrolled only patients who were newly diagnosed with AS (n = 4829) between year 2001 and 2010, excluding patients who had CAD (ICD-9- CM codes: 410-414) before the diagnosis of AS (n = 4112). According to propensity score matched 1:2 on age, gender, AS duration, Charlson comorbidity index, hypertension, and hyperlipidemia, 236 and 472 patients were included in buy arcoxia online the case (AS with CAD) and control (AS without CAD) groups, respectively. We used the WHO defined daily dose (DDD) as a tool to assess the dosage of sulfasalazine and celecoxib exposure. Conditional logistic regression was used to estimate the crude and adjusted odds ratios (ORs) and 95% confidence interval (CI) for the risk of CAD associated with use of sulfasalazine and celecoxib.Among 4112 AS patients, 8.4% (346/4112) developed CAD. CAD in AS patients were positively associated with age of 35 to 65, Charlson comorbidities index (CCI), hypertension, and hyperlipidemia. There was no gender difference between case and control groups. After adjustment for age, gender, CCI, hypertension, and hyperlipidemia, sulfasalazine users with an average daily dose ≥ 0.5 DDD (0.5 gm/day) had negative association with CAD events as compared to sulfasalazine nonusers (OR 0.63; 95% CI, 0.40-0.99, P < 0.05). NSAIDs, including celecoxib, etoricoxib, but no naproxen and diclofenac were negatively associated with CAD. Celecoxib users, with an average daily dose > 1.5 DDD, were negatively associated with CAD events, compared to celecoxib nonusers (OR 0.34; 95% CI, 0.13-0.89; P < 0.05).In this 10-year population-based case-control study, 8.4% of AS patients developed CAD. Sulfasalazine usage at an average dose of ≥ 0.5 gm/day demonstrated negative association with CAD events in patients with AS.

arcoxia 750 mg 2016-07-06

Compared with nonselective NSAIDs, COX-2s produced significantly fewer gastroduodenal ulcers (relative risk, 0. buy arcoxia online 26; 95% confidence interval, 0.23-0.30) and clinically important ulcer complications (relative risk, 0.39; 95% confidence interval, 0.31-0.50), as well as fewer treatment withdrawals caused by GI symptoms. The co-administration of acetylsalicylic acid appears to reduce the GI safety of COX-2s in subgroup analyses.

arcoxia y alcohol 2017-06-16

Intracerebroventricular (ICV) administration of streptozotocin (STZ) causes degeneration of hippocampal neurons through unknown mechanisms that further lead to dementia. On assumption that enzyme cyclooxygenase (COX), which catalyzes the production of pro-inflammatory prostaglandins, may be involved in ICV-STZ induced neurodegeneration, the present study was designed to investigate the effects of chronic treatment with selective inhibitor of COX-1, COX-2 or COX-3 on hippocampal neuronal density in ICV-STZ treated rats. Drugs were administered daily for 21 days, intraperitoneally, in sham control as well as ICV-STZ treated rats. After 21 days of treatment, rats were sacrificed and histological changes were observed in Cornus Ammonis (CA)-1 region of hippocampus at light microscopic level. Histopathological evaluation showed that valeryl salicylate (selective COX-1 inhibitor; 5 and 10 mg/kg; i.p.) and etoricoxib (selective COX-2 inhibitor; 5 and 10 mg/kg; i.p.) significantly buy arcoxia online increased the survival of hippocampus CA1 neurons in a dose dependent manner. On the contrary, phenacetin (selective COX-3 inhibitor; 20 and 40 mg/kg; i.p.) treatment had no effect on reduced neuronal density in ICV-STZ treated rats. In summary, these findings provide the first comprehensive description about the differential role of COX isozymes in ICV-STZ induced neuronal death in hippocampal CA1 regions of the rat brain.

arcoxia with alcohol 2016-02-04

NSAID hypersensitivity was diagnosed in all 31 patients: 3 displayed positive results to pyrazolone skin tests and the other 28 to challenges with culprit NSAIDs. None reacted to either placebos or buy arcoxia online etoricoxib.

arcoxia drug classification 2016-04-22

The method is based on baseline manipulation (difference) buy arcoxia online spectroscopy where the amplitudes at 274 and 351 nm were selected to determine ETR and DRT, respectively, in combined formulation and methanol was used as solvent. Both the drugs obey Beer's law in the concentration ranges of 4-20 μg/mL for DRT and 4.5-22.5 μg/mL for ETR.

arcoxia tablet adalah 2017-01-05

Pain intensity levels in the etoricoxib group were lower than in the placebo group at the 2-, 3-, 4-, 5-, 6-, and 7-hour periods after surgery (Kruskal-Wallis test; P <0 buy arcoxia online .05). There was no statistically significant difference between celecoxib and etoricoxib. Discomfort in the celecoxib group was significantly lower than in the placebo group only at the 3-hour period (P = 0.03). Rescue medication intake was significantly less frequent in the etoricoxib group than in the placebo and celecoxib groups (analysis of variance; P = 0.009).

arcoxia medicine 2017-01-13

Twenty-four randomized controlled trials (2273 participants; 997 male, 1276 female; mean age, 18.2 years; SD, 4.4 years) were included in buy arcoxia online this network meta-analysis. A total of 26 interventions were identified and classified into 6 classes based on their mechanism of action. Compared with placebo-class, nonsteroidal anti-inflammatory drug analgesics and lasers were the most effective intervention classes with a shared median rank of 2 (95% credible interval [CrI], 1-3), followed by "other" analgesics (median rank, 3; 95% CrI, 1-4), behavior therapy (median rank, 4; 95% CrI, 3-6), and miscellaneous (median rank, 5; 95% CrI 3-6). The most effective individual interventions in the nonsteroidal anti-inflammatory drug analgesics and lasers classes were etoricoxib (median rank, 1; 95% CrI, 1-3) and gallium-arsenide superpulsed lasers (median rank, 3; 95% CrI, 1-13), respectively. Assessment of transitivity and consistency assumption showed no threat to the network meta-analysis estimates. There was no evidence of significant publication bias. Heterogeneity was mild to moderate (tau-square, 0.044; 95% CrI, 0.040-0.055).

arcoxia 60 mg 2015-08-14

There has been renewed interest in the treatment of gout with recent reported intervention buy arcoxia online studies of new agents such as etoricoxib, febuxostat and pegylated-uricase. However, these studies have highlighted the relative paucity of validated outcome measures with which to judge efficacy. This review outlines the published information regarding which endpoints have been measured in randomized clinical trials, what should be measured, what tools or instruments are available for this and the technical properties of such instruments. It highlights recent work that validates measures of tophi, radiographic damage and patient-reported outcomes. The absence of a valid definition of gout-flare or how flare reduction defines response is problematic; this forms the basis for a current ACR-EULAR sponsored project.

arcoxia tab 2017-01-08

The majority of leg ulcers in patients with RA are due to underlying venous/arterial malfunction while vasculitic or traumatic ulcers are less common. Additionally, we identified a relevant subgroup of patients with ' buy arcoxia online inactivity ulcers' due to impaired mobility and consecutive lymphedema. Morphology and localization of ulcerations as well as duplex sonography provide the most important clues for accurate diagnosis, ensuring adequate treatment.

arcoxia 70 mg 2015-04-21

The most common and leading cause of cancer-related death in men is lung cancer. Despite the recent advances in chemotherapy, advanced lung cancer still remains incurable. For this, the understanding of molecular mechanisms involved in lung carcinogenesis is necessary to provide potentially effective therapeutic targets for the treatment of lung cancer, and thus the therapeutic limitations can be overcome. Cyclooxygenase-2 (COX-2) is an important inflammation factor that is reported to be up-regulated in different cancers. A number of COX-2 inhibitors have been developed, but most of them are restricted due to the different risk factors. Currently, the FDA has allowed celecoxib to remain on the market but advised physicians to apply this drug with alternative therapies or to use at a low dosage. Some other COX-2 inhibitors, such as, apricoxib and etoricoxib are under critical investigation currently. Celecoxib is being tested in clinical trials against lung cancer, as a single agent or in combination with other agents. Recent studies have suggested celecoxib as a feasible and clinically active regimen in the treatment of patients with lung cancer. However, more clinical trials are necessary for the better understanding of the role of selective COX-2 inhibitors in the prevention and treatment of lung cancer along with their assessment of toxicity. In this review, we have discussed the mechanism of actions buy arcoxia online of COX-2 in cancer progression and the therapeutic use of COX-2 inhibitors in the treatment of lung cancer with subsequent clinical studies and future management.

arcoxia capsule 2016-03-11

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 Paracetamol 500mg Syrup 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 (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.

arcoxia 6o mg 2015-08-17

Data collected during all phase IIb/III etoricoxib clinical trials > or = 4 weeks in duration were evaluated. The pooled data set includes clinical information from approximately 6500 patient-years (PYs) of drug exposure in patients diagnosed with rheumatoid Lioresal Dosage arthritis (RA), osteoarthritis (OA), ankylosing spondylitis (AS), or chronic low back pain (CLBP). Patients were treated with either etoricoxib (> or = 60 mg/day), the traditional NSAIDs naproxen (1000 mg/day), ibuprofen (2400 mg/day), diclofenac (150 mg/day), or placebo. The Relative risks (RRs) based on time to first occurrence of a thrombotic event in the etoricoxib group versus the comparator traditional NSAIDs or versus placebo were determined using patient-level data.

arcoxia 80 mg 2017-10-22

The purpose of Diamox Max Dose this review is to highlight the recent developments in the management of gout.

arcoxia 45 mg 2017-12-24

There were different features of paired H-reflex recovery in healthy individuals and patients with RPS Detrol Drug Classification during different treatment options. Recovery of test H-reflex in the range of 150-200 msec can be a criterion for a pain state.

arcoxia 4 mg 2016-07-22

We found that baseline systolic BP (SBP) was associated with significantly higher risk of all events (P < 0.001). Baseline diastolic BP (DBP) was Requip Xl Tablets inversely and significantly associated with risk of all events (P < 0.001 to P = 0.016) except CV/CHF mortality (P = 0.054). There was no significant differential effect between etoricoxib and diclofenac in relation to CVEs, except for confirmed CHF, for which the risk was significantly higher with etoricoxib (P = 0.019). Only CHF risk (P = 0.020 for both SBP and DBP change), but not thrombotic endpoints, was significantly associated with change in BP from months 0 to 4. These findings were not meaningfully altered after covariate adjustment for baseline CV risk.

arcoxia dosage 2017-12-30

Randomized, double-blind, and controlled trials, as well as case- Pamelor Drug Interactions control and retrospective cohort studies, that assessed the cardiovascular safety of COX-2 inhibitors were reviewed.

arcoxia tablet indication 2017-05-26

Naproxen/esomeprazole was a dominant strategy (more effective and less costly) compared to celecoxib, etoricoxib and diclofenac+PPI. Celecoxib+PPI and etoricoxib+PPI were more effective. Considering a cost-effectiveness Bactrim Ss Dosing threshold of €30,000 per additional QALY, naproxen/esomeprazole was cost-effective compared to ibuprofen+PPI and naproxen+PPI with incremental cost-effectiveness ratios (ICER) of €15,154 and €5,202 per additional QALY, respectively.

arcoxia mg 2017-11-27

Etoricoxib is a non-steroidal anti-inflammatory drug (NSAID) that inhibits the inducible cyclooxygenase (COX-2) with a good safety profile. We describe the first case of two mucosal adverse events to etoricoxib Duricef Drug Class in the same patient.

arcoxia 240 mg 2016-07-05

We searched the following databases from inception to 19 September 2013: PubMed, EMBASE, MEDLINE and CENTRAL. The search was not limited Hytrin Tablets Uses by language. Additional trials were identified by manually searching the reference lists of relevant papers and conference proceedings and through correspondence with experts and pharmaceutical companies.

arcoxia 200 mg 2016-10-31

Single dose oral etoricoxib produces Zithromax Online Usa high levels of good quality pain relief after surgery. The 120 mg dose is as effective as, or better than, other commonly used analgesics.

arcoxia 90 mg 2016-05-19

To evaluate the clinical literature on cyclooxygenase-2 (COX-2) inhibitors to determine whether a greater incidence of thromboembolic events is universal within the drug class.

arcoxia 30mg tablet 2017-06-18

Median follow-up was 62 weeks. In group A 5 of 22 (22.7%) cases and in group B 2 of 22 (9.1%) cases failed to respond to IAD (P >0.05). Comparing the two groups, in all three cycles of IAD the time of the cycles and the time of the off-phases were significantly (P <0.0001) longer in group B than in group A. The highest PSA value reached during the off-phases in each cycle was significantly (P <0.001) lower in group B than in group A. Withdrawal from treatment owing to side effects was not necessary in any of the 44 patients.