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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:
Etoricoxib, Coxyveen, Nucoxia, Algix, Tauxib, Etorix

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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.

arcoxia tablets price

Cyclo-oxygenase (COX)-2-specific inhibitors form one of the most commonly prescribed groups of pain relief drugs. Despite the known reproductive toxicity of NSAIDs, which are nonspecific COX inhibitors, little is known about the differential role between COX-1 and COX-2 inhibition on reproduction. It has been suggested that COX-2 plays a prominent role in animals at all stages of reproduction, from ovulation to implantation to decidualisation and delivery. Both estrogen and progesterone have been shown to be involved in regulation of COX production in tissues of the reproductive tract. Similar to NSAIDs, warnings on reproduction have been included in the product labelling of marketed COX-2-specific inhibitors. Variations in the level of warnings in these labels are noted, with an order of stringency being celecoxib approximate, equals etoricoxib > rofecoxib approximate, equals valdecoxib. The specificity of etoricoxib for COX-2 has been found to be approximately 3-fold greater than that of rofecoxib and valdecoxib and approximately 14-fold more than celecoxib in human whole blood assays. There is growing evidence to suggest that the inducible COX-2, rather than the COX-1, is the main enzyme responsible for reproduction. It was demonstrated that the change in estrogen and progesterone levels during pregnancy contributes to the dramatic increase in COX-2 expression. This further strengthens the earlier findings that COX-2 activities are necessary to support pregnancy. It is also worth mentioning that although a definite correlation between the specificity of a COX-2-specific inhibitor and the level of precaution stated in the drug labels in UK was not obtained, a direct relationship between the specificity and the potential to result in teratogenicity has not been excluded. With growing interest of the pharmaceutical industry in developing more COX-2-specific inhibitors and the fact that reproductive toxicity is not tested in pregnant women before marketing, it is important for drug regulators to raise awareness of the potential reproductive adverse effects and provide guidance on the level of caution when using these drugs in pregnancy.

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Cyclooxygenase inhibitors were developed in the quest of enhanced analgesic efficacy devoid of gastric side effects. Etoricoxib is a second-generation cox-2 inhibitor and as its use increases so do the reports of side effects. We report a case of extoricoxib-induced pretibial erythema and edema; and review the literature.

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The objective of the present investigation was to study the influence of polyethylene glycol 4000 (PEG) and polyvinylpyrrolidone K30 (PVP) on in vitro dissolution of etoricoxib from solid dispersions. Preliminary studies were carried out using a physical mixture of the drug and carriers. Solid dispersions were prepared using the solvent evaporation method. A 32 factorial design was adopted in the solvent evaporation method using the concentration of PEG and PVP as independent variables. Full and reduced models were evolved for dependant variables, such as the percentage of drug release in 10 min (Q10), percentage of drug release in 30 min (Q30), percentage of drug release in 45 min (Q45) and percent dissolution efficiency (DE). The reduced models were validated using two check points. Q10 > 65%, Q30 > 75%, Q45 > 85% and DE > 80% were used as constraints for the selection of an optimized batch. Contour plots are presented for the selected dependant variables. PEG was found to be more effective in increasing the drug dissolution compared to PVP. Wettability study was carried out for the pure drug and optimized batch. FT-IR spectroscopy, microscopic study, differential scanning calorimetry and X-ray diffraction study were carried out in order to characterize the drug in solid dispersions. Improved dissolution was attributed to decreased crystallinity of the drug, improved wetting and solubilizing effects of carriers such as PEG and PVP from the solid dispersion of etoricoxib. In conclusion, dissolution of etoricoxib can be modulated using appropriate levels of hydrophilic carriers.

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The primary outcome measured was the number of patients with postoperative complications according to the Dindo-Clavien classification.

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The antitumorigenic mechanism of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib is still a matter of debate. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study investigates the impact of celecoxib on the expression of intercellular adhesion molecule 1 (ICAM-1) and cancer cell lysis by lymphokine-activated killer (LAK) cells. Celecoxib, but not other structurally related selective COX-2 inhibitors (i.e., etoricoxib, rofecoxib, valdecoxib), was found to cause a substantial upregulation of ICAM-1 protein levels. Likewise, ICAM-1 mRNA expression was increased by celecoxib. Celecoxib enhanced the susceptibility of cancer cells to be lysed by LAK cells with the respective effect being reversed by a neutralizing ICAM-1 antibody. In addition, enhanced killing of celecoxib-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen 1 (LFA-1), suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. Finally, celecoxib elicited no significant increase of LAK cell-mediated lysis of non-tumor bronchial epithelial cells, BEAS-2B, associated with a far less ICAM-1 induction as compared to cancer cells. Altogether, our data demonstrate celecoxib-induced upregulation of ICAM-1 on lung cancer cells to be responsible for intercellular ICAM-1/LFA-1 crosslink that confers increased cancer cell lysis by LAK cells. These findings provide proof for a novel antitumorigenic mechanism of celecoxib.

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Previous studies suggest that endothelial progenitor cells (EPCs) contribute to vascular repair processes. In contrast, circulating microparticles (MPs) are reported to be part of a process that is damaging to vascular cells. Numerous studies suggest that the "balance" between EPCs and MPs is important for the integrity of vascular cells and preservation of endothelial function. In the present study, we assess the impact of acetylsalicylate (ASA) - which is, beside statins and physical exercise, a third basic column in the preventive therapy of coronary artery disease (CAD) - on EPCs and MPs in patients with CAD. We investigated the effect of treatment (8 weeks) with ASA (100 mg/d) on endothelial function (flow-mediated vasodilation, FMD), number of circulating EPCs, and endothelial- and platelet-derived microparticles (eMP, pMP) in 15 male patients (age 59.5 ± 12.3 years) with CAD but nonsignificant stenosis. The number of pMPs and eMPs decreased by 62.7% (p < 0.05) and 28.4% (p < 0.05), respectively. The number of circulating EPCs (VEGFR2(+)CD34(+)), expressed as ‰ of circulating polymorphonuclear leukocytes, remained unchanged. Despite the reduced number of pMPs and eMPs in response to the ASA therapy, the FMD responses and the maximal dilator effects of nitroglycerin were unaffected. In a control experiment, patients (n = 6) treated with the selective COX-2 inhibitor etoricoxib (90 mg/day) for 8 weeks showed no changes in the number of pMPs, eMPs, and EPCs and in FMD. We report on a novel effect of ASA treatment on the number of circulating endothelial- and platelet-derived microparticles in patients with cardiovascular disease. The mechanism remains elusive, and appears not to be associated with the COX-2 pathway.

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The neurodegeneration in colchicine induced AD (cAD) rats is linked with neuroinflammation. The inducible cox-2 present in the brain may participate in the neuroinflammatory process related to progressive neurodegeneration in cAD rats. The aim of this study is to investigate the role of cox-2 in the neurodegeneration and cognitive impairments in cAD rats. The parameters of memory (working and reference memory), inflammatory markers [IL-1β, TNF-α, prostaglandin E2 (PGE2), cox-2 level] and histopathology of hippocampus were measured after 21-day of i.c.v. colchicine injection in rats and compared with that of control and sham operated rats. These parameters were also measured in these 3 different groups of rats after p.o. administration of 3 different doses of etoricoxib, a cox 2 inhibitor. The impairments of working and reference memory were associated with neuroinflammation and neurodegeneration in the hippocampus and increased cox-2 and PGE2 levels in hippocampus in cAD. Administration of etoricoxib in cAD rats resulted in recovery of memory impairments, neurodegeneration and neuroinflammation in hippocampus and inhibition of cox-2 and PGE2 levels in hippocampus. It appears from the results that activation of cox-2 in cAD is related to neuroinflammation involved in neurodegeneration. Colchicine induced initial neurodegeneration may trigger cascade of events for a progressive neurodegeneration where cox-2 activation plays a critical role. Moreover, this cox-2 mediated neurodegeneration is related to impairments of memory parameters. Thus, the present study showed that the impairments of memory and neurodegeneration in the hippocampus of cAD in 21-day study are mediated by cox-2 induced neuroinflammation.

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The sCOX-2 inhibitors are associated with an increased risk for rapid eGFR decline and hyperkalemia in both the short term and in the long term after sCOX-2 inhibitors were terminated in the setting of a community-based CKD population. For CKD patients, these results suggest that sCOX-2 inhibitors should be closely monitored and chronic exposure to any sCOX-2 inhibitors should be avoided.

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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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A practicable and selective liquid chromatography-mass spectrometry assay for the determination of two cyclooxygenase-2 inhibitors, etoricoxib and valdecoxib, in human plasma is presented. The analytical technique is based on reversed-phase high-performance liquid chromatography (HPLC) coupled to atmospheric pressure chemical ionisation (APCI) mass spectrometry (Finnigan Mat LCQ ion trap). Mass analysis was performed in the positive ion mode. The ion trap was operated in the tandem MS mode (MS2) and the transitions of etoricoxib (m/z 359.2 --> 280.3) and valdecoxib (m/z 315.1 --> 235.1) were followed by selected reaction monitoring. Retention times of etoricoxib and valdecoxib were 1.05 and 1.08 min, respectively. The method was validated over a linear range 10-2500 and 5-1000 microg/L using the other substrate as internal standard. After validation, the method was used to study the pharmacokinetic pro fi le of etoricoxib or valdecoxib in a healthy volunteer after administration of a single oral dose (valdecoxib, 20 mg; etoricoxib, 90 mg). The presented method was suf fi cient to cover more than 90% of the area under the plasma concentration time curve.

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TRPV-1 antagonism appears promising in the management of clinical pain, but requires further investigation.

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University hospital, between January and September, 2014.

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To determine the effectiveness and safety of NSAIDs in the treatment of primary dysmenorrhoea.

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arcoxia drug classification 2016-02-05

The recent demonstration that platelets express a functional toll-like receptor 4 (TLR4) prompted us to explore the influence of TLR4 polymorphisms (Asp299Gly alone or in combination with Thr399Ile) on thromboxane A(2) (TXA(2)) biosynthesis in vivo. In 17 subjects with TLR4 polymorphisms versus 17 wild type (untreated with aspirin, matched for age, sex, and cardiovascular risk factors), intima-media thickness in the common carotid arteries was significantly lower. Average urinary excretion of 11-dehydro-TXB(2), an index of systemic biosynthesis of TX, was significantly reduced by 65%. The urinary excretion of Aciphex Dosage Forms 2,3-dinor-6-keto-prostaglandin F(1alpha), an index of systemic biosynthesis of prostacyclin, was marginally depressed but the prostacyclin/TXA(2) biosynthesis ratio was significantly higher than in wild type. Selective inhibition of cyclooxygenase 2-dependent prostacyclin (by rofecoxib or etoricoxib) was associated with increased urinary excretion of 11-dehydro-TXB(2) in carriers of TLR4 polymorphisms, but not in wild-type, suggesting a restrainable effect of prostacyclin on platelet function in vivo in this setting. Reduced TXA(2) biosynthesis may contribute to the protective cardiovascular phenotype of TLR4 polymorphisms.

arcoxia dosage mims 2015-12-28

Our study confirmed the good long-term tolerability of etoricoxib in patients with a history of hypersensitivity to other NSAIDs without differences between single and multiple reactors. Nonetheless, in Atarax 20 Mg NSAID-intolerant subjects this drug should be first challenged in specialised centres due to the risk ofsevere reactions.

ingredients arcoxia tablets 2016-07-21

Celecoxib, a COX-2 (cyclooxygenase-2)-selective inhibitor (coxib), is the only NSAID (non-steroidal anti-inflammatory drug) that has been approved for adjuvant Avodart Generic Equivalent treatment of patients with familial adenomatous polyposis. To investigate if the anti-proliferative effect of celecoxib extends to other coxibs, we compared the anti-proliferative potency of all coxibs currently available (celecoxib, rofecoxib, etoricoxib, valdecoxib, lumiracoxib). Additionally, we used methylcelecoxib (DMC), a close structural analogue of celecoxib lacking COX-2-inhibitory activity. Due to the fact that COX-2 inhibition is the main characteristic of these substances (with exception of methylcelecoxib), we conducted all experiments in COX-2-overexpressing (HCA-7) and COX-2-negative (HCT-116) human colon cancer cells, in order to elucidate whether the observed effects after coxib treatment depend on COX-2 inhibition. Cell survival was assessed using the WST proliferation assay. Apoptosis and cell cycle arrest were determined using flow cytometric and Western blot analysis. The in vitro results were confirmed in vivo using the nude mouse model. Among all coxibs tested, only celecoxib and methylcelecoxib decreased cell survival by induction of cell cycle arrest and apoptosis and reduced the growth of tumor xenografts in nude mice. None of the other coxibs (rofecoxib, etoricoxib, valdecoxib, lumiracoxib) produced anti-proliferative effects, indicating the lack of a class effect and of a role for COX-2. Our data emphasize again the outstanding anti-proliferative activity of celecoxib and its close structural analogue methylcelecoxib in colon carcinoma models in vitro and in vivo.

arcoxia tablet adalah 2015-06-11

To further assess Celebrex Renal Dosing the clinically active dose range of etoricoxib, a COX-2 selective inhibitor, in rheumatoid arthritis (RA).

arcoxia 750 mg 2015-11-11

Plasma concentrations of etoricoxib, miconazole, voriconazole, and thromboxane B(2) generation were followed after Abilify 2mg Cost ingestion of 60 mg etoricoxib without pretreatment, after topical administration of miconazole oral gel (85 mg x 3, 3 days), or after oral voriconazole (400 mg x 2, 1st day, 200 mg x 2, 2nd day).

arcoxia with alcohol 2016-08-11

Etoricoxib at doses of 90 mg Detrol Dosage Forms and 120 mg demonstrated superior efficacy compared with placebo over 6 weeks, and compared with naproxen over 1 year. These study results demonstrate that etoricoxib is generally safe, well-tolerated, and efficacious for the treatment of AS.

arcoxia overdose 2016-11-28

We determined cyclo-oxygenase-1 and cyclo-oxygenase-2 inhibition in healthy middle-aged subjects (41-65 years) randomly assigned to four 7-day treatment sequences of etoricoxib 90 mg every day, celecoxib 200 mg twice a day, diclofenac 75 mg twice a day, or placebo in a double-blind, randomized, 4-period crossover study. Maximum inhibition of thromboxane B(2) (cyclo-oxygenase-1 activity) in clotting whole blood Priligy 80 Mg on day 7 (0-24 hours postdose) was the primary endpoint. Inhibition of lipopolysaccharide-induced prostaglandin E(2) in whole blood (cyclo-oxygenase-2 activity) was assessed on day 7 (0-24 hours postdose) as a secondary endpoint. Diclofenac had significantly greater maximum inhibition of thromboxane B(2) versus each comparator (P < .001); placebo 2.4% (95% confidence interval: -8.7% to 12.3%), diclofenac 92.2% (91.4% to 92.9%), etoricoxib 15.5% (6.6% to 23.5%), and celecoxib 20.2% (11.5% to 28.1%). Prostaglandin E(2) synthesis was inhibited with a rank order of potency of diclofenac > etoricoxib > celecoxib. In summary, at doses commonly used in rheumatoid arthritis, diclofenac significantly inhibits both cyclo-oxygenase-1 and cyclo-oxygenase-2, whereas etoricoxib and celecoxib significantly inhibit cyclo-oxygenase-2 and do not substantially inhibit cyclo-oxygenase-1.

arcoxia 45 mg 2016-06-06

The demand for mouth dissolving tablets has been growing during the last decade especially for elderly and children who have swallowing difficulties. Etoricoxib is a new non-steroidal anti-inflammatory drug (NSAID) with selective cox-2 inhibitory activity, selective inhibition of cox-2 provides anti-inflammatory and analgesic activity it is commonly used for osteo-arthritis, rheumatoid arthritis, primary dysmenorrhoea, post operative dental pain and acute gout. The main criteria for mouth dissolving tablets are to disintegrate or dissolve rapidly in oral cavity with saliva in 15 sec to 60 sec with need of water. The disintegrants used should fulfill the criteria by disintegrating the tablets in specified time limit.in the present investigation variety of super disintegrants like primogel, kollidone, Ac-Di-sol, L-HPMC, L-HPC, were selected and tablets were prepared by direct compression method in different concentration like 4% and 8%. The prepared tablets were evaluated for weight variation, hardness, friability, in vitro disintegration time, wetting time, in vitro dissolution study, etc. formulation f-9 shows the lowest disintegration time (44 sec) and wetting time ( Augmentin Iv Dose 52 sec). In vitro dissolution studies revealed that formulation F-9 containing 8% L-HPC showed 97% drug release at the end of 20 min.

arcoxia drug 2017-04-02

Nonsteroidal anti-inflammatory drugs (NSAIDs) are first-line therapies in the management of patients with ankylosing spondylitis. This chronic inflammatory skeletal disorder, a subtype of spondyloarthritis, is characterized by inflammatory back pain and affects young adults causing important suffering and disability. Long-term use of conventional NSAIDs is associated with a risk of gastrointestinal complications. Etoricoxib is a specific cyclooxygenase 2 inhibitor with strong anti-inflammatory effects and a favorable pharmacokinetic profile for the management of inflammatory disorders. The drug has been associated with reduced severe gastrointestinal adverse events. However, the cardiovascular safety of cyclooxygenase 2 inhibitors Motilium Tablets Uses has been debated.

arcoxia medication 2017-06-17

Cyclo-oxygenase (COX)-2-specific inhibitors form one of the most commonly prescribed groups of pain relief drugs. Despite the known reproductive toxicity of NSAIDs, which are nonspecific COX inhibitors, little is known about the differential role between COX-1 and COX-2 inhibition on reproduction. It has been suggested that COX-2 plays a prominent role in animals at all stages of reproduction, from ovulation to implantation to decidualisation and delivery. Both estrogen and progesterone have been shown to be involved in regulation of COX production in tissues of the reproductive tract. Similar to NSAIDs, warnings on reproduction have been included in the product labelling of marketed COX-2-specific inhibitors. Variations in the level of warnings in Requip Maximum Dosage these labels are noted, with an order of stringency being celecoxib approximate, equals etoricoxib > rofecoxib approximate, equals valdecoxib. The specificity of etoricoxib for COX-2 has been found to be approximately 3-fold greater than that of rofecoxib and valdecoxib and approximately 14-fold more than celecoxib in human whole blood assays. There is growing evidence to suggest that the inducible COX-2, rather than the COX-1, is the main enzyme responsible for reproduction. It was demonstrated that the change in estrogen and progesterone levels during pregnancy contributes to the dramatic increase in COX-2 expression. This further strengthens the earlier findings that COX-2 activities are necessary to support pregnancy. It is also worth mentioning that although a definite correlation between the specificity of a COX-2-specific inhibitor and the level of precaution stated in the drug labels in UK was not obtained, a direct relationship between the specificity and the potential to result in teratogenicity has not been excluded. With growing interest of the pharmaceutical industry in developing more COX-2-specific inhibitors and the fact that reproductive toxicity is not tested in pregnant women before marketing, it is important for drug regulators to raise awareness of the potential reproductive adverse effects and provide guidance on the level of caution when using these drugs in pregnancy.

arcoxia 200 mg 2016-02-29

COX-1 plays a previously unrecognized part in the neuroinflammation. Genetic ablation or pharmacological inhibition of COX-1 activity attenuates the inflammatory response and neuronal loss. In this context, the effects of selective COX-1 inhibitors (P6, P10, SC-560, aspirin) and coxibs (celecoxib and etoricoxib) on LPS-stimulated microglial cell function (a worldwide accepted neuroinflammation model) were investigated, and the effects on COX-1/COX-2, cPGES mRNA and iNOS expression, PGE(2) and NO production and NF-κB activation by IκBα phosphorylation were evaluated. The total suppression of the expression of both COX-1 and COX-2 by their respective selective inhibitors occurred. NF-κB remained almost completely inactive in the presence of coxibs, as expected, and totally inactive in the presence of P6. P6 also markedly counteracted LPS enhancing cPGES mRNA expression and PGE(2) production. Since COX-1 is predominantly localized in microglia, its high selective inhibition rather than COX-2 (by coxibs) is more likely to reduce neuroinflammation and has been further investigated as a potential therapeutic approach and prevention in neurodegenerative diseases with a marked inflammatory component.

cut arcoxia tablets 2017-01-28

Etoricoxib, 120 mg, provided analgesic efficacy superior to that of the placebo for the summed pain intensity difference over 8 hours (p = 0.005), and total pain relief over 8 hours (p < 0.05), and all primary and secondary end points were similar to those of mefenamic acid. No serious or unexpected adverse events were reported, and no subjects withdrew from the study because of an adverse event. However, the incidence of nausea and epigastic pain in the mefenamic acid group was significantly higher than in the etoricoxib group.

arcoxia y alcohol 2017-02-11

Treatment of rheumatic conditions is limited in patients with asthma owing to concerns of nonsteroidal anti-inflammatory drugs potentially provoking asthma. Cross-sensitivity to all anti-inflammatory drugs that inhibit cyclooxygenase enzymes occurs in these individuals.

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A total of 36 patients with RA and leg ulcers were identified. Three patients presented with necrotizing vasculitis and 2 with pyoderma gangrenosum. Chronic venous insufficiency was diagnosed as the underlying cause of leg ulcers in 8 patients, peripheral arterial disease in 4 patients, and combined arterial and venous malfunction in 3 patients. Five patients suffered from pressure ulcers. Interestingly, in 11 patients (31%) other underlying causes besides constricted mobility followed by secondary lymphedema could not be identified, and these ulcers were classified as 'inactivity leg ulcers'.