arcoxia 240 mg
There were 239 patients (89.5% female; mean age: 63.3 years) randomized to etoricoxib 30 mg (n = 120) and celecoxib 200 mg (n = 119). The differences (etoricoxib vs celecoxib) in least square (LS) mean change (95% CI) for WOMAC Pain, WOMAC Physical Function, and PGAD were -1.63 mm (-5.37, 2.10), -1.32 mm (-4.88, 2.23), and -1.09 mm (-5.48, 3.30), respectively. Drug-related clinical AEs occurred in 6.7% (etoricoxib) and 2.5% (celecoxib) of patients. This study was limited because it was not designed or powered to adequately capture and evaluate rare AEs associated with NSAID treatment.
34 701 patients (24 913 with osteoarthritis and 9 787 with rheumatoid arthritis) were enrolled. Average treatment duration was 18 months (SD 11.8). 320 patients in the etoricoxib group and 323 in the diclofenac group had thrombotic cardiovascular events, yielding event rates of 1.24 and 1.30 per 100 patient-years and a hazard ratio of 0.95 (95% CI 0.81-1.11) for etoricoxib compared with diclofenac. Rates of upper gastrointestinal clinical events (perforation, bleeding, obstruction, ulcer) were lower with etoricoxib than with diclofenac (0.67 vs 0.97 per 100 patient-years; hazard ratio 0.69 [0.57-0.83]), but the rates of complicated upper gastrointestinal events were similar for etoricoxib (0.30) and diclofenac (0.32).
arcoxia 90mg tablet
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 NSAID-intolerant subjects this drug should be first challenged in specialised centres due to the risk ofsevere reactions.
The authors analyzed 40 patients treated for radicular pain syndrome (RPS) caused by disk protrusion or herniation at the lumbar spine with the pain intensity of up to 9 points on digital rank scale of pain. As a clinical model they used a pathogenetically sound therapeutic blockade method including glucocorticosteroids for the therapy of acute neuralgia and basic medical therapy with Arcoxia 120 mg/day. Investigations were conducted to study the specific features of early recovery of test H-reflex caused in pair with a conditioning H-reflex in both healthy volunteers and patients with obvious RPS.
These results confirm that most NSAID-sensitive individuals with cutaneous reactions to classic NSAIDs will tolerate specific COX-2 inhibitors, supporting the use of thesedrugs after careful oral provocation in such patients.
arcoxia 90 mg
Alzheimer's disease (AD) is the most common form of dementia. The incidence of AD rises exponentially with age and its prevalence will increase significantly worldwide in the next few decades. Inflammatory processes have been suspected in the pathogenesis of the disease.
arcoxia drug classification
O(6)-Benzylguanine; (-)-Gossypol; Abatacept, AC-2592, Adalimumab, AIDSVAX gp120 B/E, Alemtuzumab, Aliskiren fumarate, ALVAC E120TMG, Ambrisentan, Amlodipine, Anakinra, Aripiprazole, Armodafinil, Atomoxetine hydrochloride, Avotermin; Bevacizumab, BIBW-2992, Bortezomib, Bosentan, Botulinum toxin type B; Canakinumab, CAT-354, Ciclesonide, CMV gB vaccine, Corifollitropin alfa, Daptomycin, Darbepoetin alfa, Dasatinib, Denosumab; EndoTAG-1, Eplerenone, Esomeprazole sodium, Eszopiclone, Etoricoxib, Everolimus, Exenatide, Ezetimibe, Ezetimibe/simvastatin; F-50040, Fesoterodine fumavate, Fondaparinux sodium, Fulvestrant; Gabapentin enacarbil, Golimumab; Imatinib mesylate, Inhalable human insulin, Insulin glargine, Ivabradine hydrochloride; Lercanidipine hydrochloride/enalapril maleate, Levosimendan, Liposomal vincristine sulfate, Liraglutide; MDV-3100, Mometasone furoate/formoterol fumavate, Multiepitope CTL peptide vaccine, Mycophenolic acid sodium salt, Nabiximols, Natalizumab, Nesiritide; Obeticholic acid, Olmesartan medoxomil, Omalizumab, Omecamtiv mecarbil; Paclitaxel-eluting stent, Paliperidone, Pegfilgrastim, Peginterferon alfa-2a, Peginterferon alfa-2b, Peginterferon alfa-2b/ ribavirin, Pemetrexed disodium, Polymyxin B nonapeptide, PORxin-302, Prasugrel, Pregabalin, Pridopidine; Ranelic acid distrontium salt, Rasagiline mesilate, rDEN4delta30-4995, Recombinant human relaxin H2, rhFSH, Rilonacept, Rolofylline, Rosiglitazone maleate/metformin hydrochloride, Rosuvastatin calcium, Rotigotine; Salcaprozic acid sodium salt, Sirolimus-eluting stent, Sitagliptin phosphate monohydrate, Sitaxentan sodium, Sorafenib, Sunitinib malate; Tadalafil, Tapentadol hydrochloride, Temsirolimus, Tenofovir, Tenofovir disoproxil fumarate, Teriparatide, Tiotropium bromide, Tocilizumab, Tolvaptan, Tozasertib, Treprostinil sodium; Ustekinumab; Vardenafil hydrochloride hydrate, Varenicline tartrate, Vatalanib succinate, Voriconazole, Vorinostat; Zotarolimus-eluting stent.
Our results indicate that gastroprotective drugs are not prescribed to elderly NSAID users according to guidelines. Furthermore, COX-2-selective inhibitors were used with gastroprotective drugs more often than were traditional NSAIDs. Greater awareness of factors contributing to NSAID/COX-2-selective inhibitor-induced GI complications is warranted, particularly with respect to advanced age and concurrent use of anticoagulants.
cut arcoxia tablets
A new, simple HPTLC method for determination of etoricoxib (ETO) and thiocolchicoside (THIO) in combined tablet dosage form has been developed and validated. The pharmaceutical dosage form used in this study was Nucoxia-MR tablets. Sample solutions were prepared at concentrations of 25 and 20 microg/mL for ETO and THIO, respectively. The separation was carried out on 20 x 10 cm Merck aluminum sheets precoated with a 250 microm layer of silica gel 60F254 using ethyl acetate-methanol (8 + 2, v/v) as the mobile phase. The calibration curve was linear over a range of 50-250 and 100-500 ng/band for ETO and THIO, respectively. Quantitative determination was done by densitometric scanning of bands at 290 nm. LOD and LOQ values were 10.993 and 33.314 ng/band, respectively, for ETO and 25.133 and 76.161 ng/band, respectively, for THIO. The method was validated with respect to linearity, accuracy, precision, and robustness in accordance with the International Conference on Harmonization guidelines. The method has been successfully applied to the analysis of drugs in the pharmaceutical formulation.
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
Of 141 patients who underwent challenge testing with etoricoxib, only 2 (1.4%) had positive test results; both developed wheals on the extremities. These 2 patients were treated with chlorpheniramine maleate (10 mg intravenously), and the symptoms completely resolved within 2 hours. None of the patients experienced adverse reactions to the placebo challenge.
Etoricoxib 120 mg provided superior overall analgesic effect with a smaller percentage of patients experiencing nausea versus both oxycodone/acetaminophen 10 mg/650 mg and codeine/acetaminophen 60 mg/600 mg.
arcoxia 80 mg
This paper discusses the treatment of pain in the palliative care patient, specifically the use of meloxicam and recent advances in agents with cyclooxygenase-2 (COX-2) selectivity. Meloxicam is a nonsteroidal anti-inflammatory drug (NSAID) that preferentially inhibits COX-2 more than cyclooxygenase-1 (COX-1), especially at low doses, thereby offering advantages over traditional nonselective NSAIDs. New COX-2 selective agents are discussed, including valdecoxib, parecoxib, etoricoxib, and COX-189.
arcoxia 6o mg
The role of nonsteroidal anti-inflammatory drugs (NSAIDs) was studied on the antioxidant defense system and nitric oxide-derived damage in a 1,2-dimethylhydrazine (DMH)-induced rat colon carcinogenesis. Early precancerous lesions were established in the proximal and distal regions of the colon by morphological and histopathological examinations that were greatly regressed by the simultaneous treatment of the three NSAIDs, such as aspirin, celecoxib, and etoricoxib, along with the procarcinogen DMH. The intestinal brush border membrane (BBM) was isolated from the two regions and the colon-specific marker enzyme cysteine-sensitive alkaline phosphatase was assayed, which showed considerable elevation by DMH but reverted back to normal level by all the three NSAIDs. DMH also caused a higher level of lipid peroxidation as measured by malonyldialdehyde production, which was also found to be corrected by the NSAIDs, in both the region of the colonic tissue. The antioxidant activities were further established by a higher level of superoxide dismutase, catalase, glutathione reductase, and glutathione S-transferase in the NSAID treatment as compared to the DMH. The nonenzyme tripeptide, glutathione content was also recovered similarly as an antioxidant defense mechanism. To elucidate whether nitric oxide (NO) also plays an important role in the pathophysiology of colon cancer, the NO and citrulline levels were measured. The results show that the NO was lowered in DMH treatment and elevated by the administration of the NSAIDs while the citrulline level could not be recovered back. The findings of the present investigation indicate the chemopreventive modalities of the NSAIDs, particularly the COX-2 inhibitors.
arcoxia 4 mg
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 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 200 mg
We conducted a population-based matched case-control study over the years 2000-3 in outpatient residents of Finland. In the nationwide Hospital Discharge Register 33 309 persons with first time MI were identified. A total of 138 949 controls individually matched for age, gender, hospital catchment area, and index day were selected from the Population Register. For combined NSAIDs, the adjusted odds ratio for the risk of first MI with current use was 1.40 (95% CI, 1.33-1.48). The risk was similar for conventional (1.34; 1.26-1.43), semi-selective (etodolac, nabumetone, nimesulide, and meloxicam) (1.50; 1.32-1.71), and cyclo-oxygenase-2 (COX-2) selective NSAIDs (rofecoxib, celecoxib, valdecoxib, and etoricoxib) (1.31; 1.13-1.50). Age of current user did not consistently modify the risk. No NSAID was associated with an MI-protective effect. All durations from 1 to 180 days of conventional NSAIDs and from 31 to 90 days duration of COX-2 selective NSAIDs were associated with an elevated risk of MI.
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Forty trials (88 116 patients) were included in the meta-analysis. The overall pooled OR for CVE for any coxib against placebo was 1.03 (95% CI: 0.71, 1.50). Comparing individual coxibs against placebo, we found that celecoxib, rofecoxib, etoricoxib and lumiracoxib were associated with higher CVE risks and valdecoxib was associated with a lower CVE risk, although there were no significant differences detected. There was also no significant difference in risk of CVE when comparing coxibs against any non-selective NSAIDs; the corresponding pooled OR was 0.86 (95% CI: 0.64, 1.16).
arcoxia tablet indication
Patients > or = 18 years of age with onset of acute gout within 48 h associated with moderate, severe, or extreme pain involving less than four joints were eligible for inclusion in the primary studies, and were randomized to etoricoxib 120 mg once daily (N = 178) or indomethacin 50 mg three times daily (N = 161). The primary and secondary efficacy endpoints were analyzed using an analysis of covariance model to detect potential differential treatment responses across several subgroups: joint involvement (mono-articular vs. oligo-articular), baseline pain severity (moderate vs. severe), concomitant allopurinol and/or colchicine use (users vs. nonusers), age (< 45, 45-55, and > 55 years), gender, and race (white or other).
arcoxia 40 mg
An open-label study was undertaken at multiple centers in Mexico to assess the impact of treatment with etoricoxib - a selective cyclo-oxygenase-2 (COX-2) inhibitor - on quality of life (QoL) and pain relief among patients with osteoarthritis (OA), rheumatoid arthritis (RA) or chronic low-back pain (CLBP). The study involved 191 adult patients (aged > 18 years old) who had used non-selective non-steroidal antiinflammatory drugs (NSAIDs) for the treatment of OA, RA or CLBP during the month prior to study enrolment. After discontinuation of prior therapy, patients were treated with etoricoxib 60 mg for OA and CLBP,or 90 mg for RA once daily for 2 weeks. Patient and physician questionnaires were used to collect information about drug treatments, patients' QoL (Short Form-8 Health Survey [SF8] and EQ-5D VAS), patients' pain assessment, and physicians' and patients' satisfaction with treatment at baseline and at follow-up visits. Relative to prior NSAID use, etoricoxib use was associated with improvements in all SF-8 QoL domains and component scores as well as in measures of pain and physical functioning. Current pain was reduced from 59.1 mm (0-100mm VAS) at baseline to 27.1mm at follow-up and the physical component score of the SF-8 improved from 33.3 to 46.3 (on a scale from 0 to100). At follow-up, 91% of patients were satisfied with the pain control provided by etoricoxib compared with 34% who were satisfied with the pain control provided by previous NSAIDs. Among physicians, 93% reported satisfaction with the analgesic effect, 95% with the anti-inflammatory profile, and 82% with the side-effect profile of etoricoxib relative to pre-study NSAID treatment. During etoricoxib therapy, use of concomitant medications was reduced. The results of this study are limited due to the lack of a control group, the un-blinded design, and the small number of patients. Large naturalistic trials are needed to confirm the results.
arcoxia 9 mg
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.
arcoxia with alcohol
Although the causative antibodies were drug dependent usually leading to abrupt and intravascular hemolysis, the patient only gradually developed anemia. These findings together with a positive direct and indirect antiglobulin test may lead to confusion with autoimmune hemolytic anemia of warm type. A nonreactive eluate was the key serologic finding in identifying drug-induced immune hemolytic anemia in this case.
arcoxia 220 mg
Celecoxib, a COX-2 (cyclooxygenase-2)-selective inhibitor (coxib), is the only NSAID (non-steroidal anti-inflammatory drug) that has been approved for adjuvant 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.
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A single daily dose of etoricoxib, 120 mg, was as efficacious as mefenamic acid in the management of secondary dysmenorrhea, with a lower incidence of epigastric pain, and was well tolerated for the treatment of secondary dysmenorrhea.