From the generated design space, an optimal formulation was obtained and the results validated the experimental design. The QbD approach was an efficient manner of understanding formulation and process parameters at the freeze-dried orodispersible tablets preparation.
In vivo toxicity study. Horses were randomly assigned to 5 treatment groups, receiving placebo, PBZ (4.4 mg/kg PO q12h day 1, 2.2 mg/kg PO q12h for 4 days, 2.2 mg/kg PO q24h for 9 days), or 3 dose rates of meloxicam (0.6 mg/kg q24h, 1.8 mg/kg q24h, 3.0 mg/kg q24h) for 14 days. Sucrose permeability testing was performed on Day 0 (before treatment) and on Day 13. All personnel involved with data collection or analysis were blinded to treatment.
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The use of specific NSAIDs and the factors interfering with NSAIDs metabolism might associate with small intestinal injury, especially with diaphragm disease.
This prospective, observational study evaluated a multimodal analgesia clinical pathway for TSA.
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These experimental results bring data in favor of the (99m)Tc-NTP 15-5 radiotracer for assessing, in vivo, cartilage remodeling in RA that could be used to monitor therapy.
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Various anti-inflammatory drugs differ in their ability to regulate NF-kappaB activation in HEK293 cells, which indicates that NF-kappaB activation might be a potential useful target to study mechanism and for drug screening.
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Meloxicam (0.5 mg/kg, IV, or 1.0 mg/kg, PO) was administered in a randomized crossover design with a 10-day washout period. Blood samples were collected at predetermined times over 96 hours. Serum drug concentrations were determined by high-pressure liquid chromatography with mass spectrometry. Computer software was used to estimate values of pharmacokinetic parameters through noncompartmental methods.
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The objective of this study was to investigate the pharmacokinetics and tissue disposition of meloxicam after repeated oral administration in calves. Thirteen male British × Continental beef calves aged 4 to 6 months and weighing 297-392 kg received 0.5 mg/kg meloxicam per os once daily for 4 days. Plasma meloxicam concentrations were determined in 8 calves over 6 days after first treatment. Calves were randomly assigned to be euthanized at 5, 10, 15 (n = 3/timepoint), and 19 days (n = 4) after final administration. Meloxicam concentrations were determined in plasma (LOQ= 0.025 μg/mL) and muscle, liver, kidney, and fat samples (LOQ = 2 ng/g) after extraction using validated LC-MS-MS methods. The mean (± SD) Cmax , Cmin , and Caverage plasma meloxicam concentrations were 4.52 ± 0.87 μg/mL, 2.95 ± 0.77 μg/mL, and 3.84 ± 0.81 μg/mL, respectively. Mean (± SD) tissue meloxicam concentrations were highest in liver (226.67 ± 118.16 ng/g) and kidney samples (52.73 ± 39.01 ng/g) at 5 days after final treatment. Meloxicam concentrations were below the LOQ in all tissues at 15 days after treatment. These findings suggest that tissue from meloxicam-treated calves will have low residue concentrations by 21 days after repeated oral administration.
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Bone volume density increased significantly (P = 0.001) in both groups with a strong correlation between treatment and periods (P = 0.003). In the TG, a small amount of bone formation occurred compared with the CG between 3 and 21 days. No significant differences in the number of VEGF-positive cells per square millimeter (P = 0.07) and VEGF messenger RNA (mRNA) expression (P = 0.49) were found between groups. Immunostained cells per square millimeter and mRNA expression for VEGF receptor (VEGFR)-1 (P = 0.04 and P < 0.001) and VEGFR-2 (P < 0.001 for both analysis) showed a strong interaction between treatment groups and periods. In the TG, immunostained cells per square millimeter and mRNA expression for VEGFR-1 were, respectively, 89% and 37% lower from 3 to 10 days compared with the CG, whereas for VEGFR-2, these values were 252% and 60%, respectively, from 3 to 7 days.
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Seven days prior to treatment, dogs were anesthetized for endoscopic evaluation of the upper portion of the gastrointestinal tract (ie, the gastric and duodenal mucosa). Five regions of the gastroduodenal area were scored by 2 investigators. Dogs were randomly assigned to 1 of 4 treatment groups as follows: saline-saline, dexamethasone-saline, saline-meloxicam, and dexamethasone-meloxicam groups. On days 1, 2, and 3, dogs received either dexamethasone or saline (0.9% NaCl) solution injections SC twice daily. On days 2, 3, and 4, dogs received either meloxicam or saline solution injections SC once daily. On day 2, dogs were anesthetized for a sham surgery (ie, electrostimulation). On day 5, the gastroduodenal area of each dog was reevaluated by use of endoscopic evaluation and histologic examination of biopsy specimens.
In summary, selective COX-2 inhibitor-meloxicam has a salutary effect on the tubular and interstitial response to UUO. TGF-beta and its receptor approaches partly explain some of the mechanism.
Specific inhibitors of Cytochrome P4502C9 enzyme (CYP2C9) viz. clopidogrel, fenofibrate fluvoxamine and sertraline at concentration of 50, 100, 150 and 200 µM were employed to investigate the nature of enzyme involved in bioconversion of meloxicam to its main metabolite 5-OH methyl meloxicam by Cunninghamella blakesleeana. Virtual screening for interaction of specific CYP2C9 inhibitors with human CYP2C9 enzyme was performed by molecular docking using Auto dock vina 4.2 version. The in silico studies were further substantiated by in vitro studies, which indicated fenofibrate to be a potent inhibitor of CYP2C9 enzyme followed by sertraline, clopidogrel and fluvoxamine, respectively. Two-stage fermentation protocol was followed to study metabolism of meloxicam and its inhibition by different CYP2C9 inhibitors. Meloxicam metabolites were identified using HPLC, LC-MS analysis and based on previous reports, as 5-OH methyl meloxicam (M1), 5-carboxy meloxicam (M2) and an unidentified metabolite (M3). All the inhibitors tested in the study showed a clear concentration dependent inhibition of meloxicam metabolism. The results suggest that the enzymes involved in metabolism of meloxicam in C. blakesleeana are akin to mammalian metabolism. Hence, C. blakesleeana can be used as a model organism in studying drug interactions and also in predicting mammalian drug metabolism.
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Massage combined CMM footbath fumigation and washing had better clinical efficacy on patients suffering from KOA.
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The effects of anti-inflammatory drugs on ileal 5-hydroxytryptamine (5-HT) metabolic dynamics at 72 h after a single administration of cisplatin were investigated in rats. Cisplatin 5 mg/kg i.p. caused pathological changes, with an inflammatory response occurring 72 h after its administration. The inflammatory response was associated with the induction of cyclooxygenase-2, but not cyclooxygenase-1, in the ileal mucosa at 72 h after the cisplatin administration. Daily treatment with meloxicam 3 mg/kg s.c. ameliorated the cisplatin-induced mucosal damage, whereas dexamethasone 1 mg/kg s.c. did not. Cisplatin administration also caused a significant increase in cyclooxygenase-2 mRNA expression at 72 h after administration, which was blunted by dexamethasone, but not by meloxicam. Cisplatin increased the content of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), but had no effect on 5-HT turnover (5-HIAA/5-HT ratio). Meloxicam and dexamethasone did not significantly decrease 5-HT and 5-HIAA content. Cisplatin significantly decreased monoamine oxidase activity but increased tryptophan hydroxylase (TPH) activity and TPH(1) mRNA expression in ileal tissue. Meloxicam and dexamethasone significantly restored the decreased monoamine oxidase activity and inhibited the cisplatin-induced increase in tryptophan hydroxylase activity toward the control levels. These drugs also decreased the cisplatin-induced increase in TPH(1) mRNA expression. Neither cisplatin nor the anti-inflammatory drugs had significant effect on mRNA expression of the serotonin re-uptake transporter. These results suggest that the inflammatory response associated with cyclooxygenase-2 induction is involved in the opposite change in ileal tryptophan hydroxylase and monoamine oxidase activities in the delayed phase after single administration of cisplatin to rats.
Prostacyclin is an important mediator of peripheral pain sensation. Here, we investigated its potential participation in mediating neuropathic pain and found that prostacyclin receptor (IP) knockout mice exhibited markedly decreased pain behavior. Application of an IP antagonist to the injury site or selective IP deficiency in myeloid cells mimicked the antinociceptive effect observed in IP knockout mice. At the site of nerve injury, IP was expressed in interleukin (IL) 1β-containing resident macrophages, which were less common in IP knockout mice. Local administration of the IP agonist cicaprost inhibited macrophage migration in vitro and promoted accumulation of IP- and IL1β-expressing cells as well as an increase of IL1β concentrations at the application site in vivo. Fittingly, the IL1-receptor antagonist anakinra (IL-1ra) decreased neuropathic pain behavior in wild-type mice but not in IP knockout mice. Finally, continuous, but not single administration, of the cyclooxygenase inhibitor meloxicam early after nerve injury decreased pain behavior and the number of resident macrophages. Thus, early synthesis of prostacyclin at the site of injury causes accumulation of IL1β-expressing macrophages as a key step in neuropathic pain after traumatic injury.
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Enhancing drug loading onto ion-exchange resin via the formation of cyclodextrin inclusion complex is usable in the development of ion-exchange based drug delivery systems, which will beneficially reduce the use of harmful acidic or basic and organic chemicals.
Ibuprofen and naproxen inhibit ASA's antithrombocyte effect below the nonresponse threshold. Etoricoxib and meloxicam do not cause relevant change in ASA thrombocyte inhibition. Naproxen has an inherent weak thrombocyte inhibitory action below the ASA response threshold.
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Concomitant inhibition of both cyclooxygenase (COX) isoforms, COX-1 and COX-2, has been used to explain the therapeutic efficacy and gastrointestinal (GI) toxicity of nonsteroidal anti-inflammatory drugs (NSAIDs) in the treatment of rheumatic diseases. While COX-2 is induced during inflammatory responses, constitutively expressed COX-1 is cytoprotective in the GI tract. Newer inhibitors such as meloxicam, which have been shown to inhibit COX-2 preferentially in vitro, are expected to retain their efficacy while exhibiting decrease toxicity. Clinical trials have been performed with meloxicam to evaluate these parameters. Controlled trials showed that meloxicam is significantly more effective than the placebo for the treatment of both rheumatoid arthritis and osteoarthritis. In comparative studies with piroxicam, naproxen, and diclofenac, meloxicam was approximately as effective as the other drugs. Analysis of the safety profile of meloxicam indicated that the risk of GI adverse events, especially PUBs (perforation, ulceration, and bleeding) is significantly reduced with meloxicam compared with that of comparators. These data confirm that preferential COX-2 inhibitors such as meloxicam provide a significant advantage over standard NSAIDs in the treatment of rheumatic diseases.
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Interaction studies with inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) inhibitor have been conducted to assess the nature of interaction and the possible therapeutic advantage. The interaction between meloxicam--a selective COX-2 inhibitor--and aminoguanidine hydrochloride--a selective iNOS inhibitor-- was examined in carrageenan-induced paw edema in rats. Appropriate statistical method was applied to detect the nature of anti-inflammatory interaction. Different doses of meloxicam (1, 3, 10 and 30 mg/kg) or aminoguanidine hydrochloride (10, 30, 100 and 300 mg/kg) were administered orally to adult male albino rats. Higher doses of meloxicam (3, 10 and 30 mg/kg) showed statistically significant anti-inflammatory effect. However, aminoguanidine hydrochloride did not show any anti-inflammatory activity. Combination of sub-threshold dose of meloxicam (1 mg/kg) with increasing doses of aminoguanidine hydrochloride (30, 100 and 300 mg/kg) resulted in synergistic anti-inflammatory effect. Combined therapy with sub-threshold dose of aminoguanidine hydrochloride (30 mg/kg) with increasing doses of meloxicam (1, 3, 10 and 30 mg/kg) also resulted in synergistic anti-inflammatory effect. The possible mechanism of interaction could be the stimulation of COX-2 activity by nitric oxide (NO) by combining with heme component. These results suggest that co-administration of meloxicam and aminoguanidine hydrochloride may be an alternative in clinical control of inflammation.
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The continual use of selective cyclooxygenase-2 (COX-2) inhibitors may have a negative impact on bone repair around titanium implants. Because modified implant surfaces could be considered an important strategy to increase success rates in some conditions that interfere in bone healing, the aim of this study was to investigate whether an aluminum oxide (Al2O3)-blasted implant surface could reduce the negative action promoted by the continuous administration of selective COX-2 inhibitors on bone healing around implants.
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To compare triple vs. double nonopioid perioperative analgesic regimens in women undergoing abdominal hysterectomy.
Drugs belonging to the Non-steroidal anti-inflammatory (NSAID) group are not only used as anti-inflammatory, analgesic and anti-pyretic agents, but also show anti-cancer effects. Complexing them with a bioactive metal like copper, show an enhancement in their anti-cancer effects compared to the bare drugs, whose exact mechanism of action is not yet fully understood. For the first time, it was shown by our group that Cu(II)-NSAIDs can directly bind to the DNA backbone. The ability of the copper complexes of NSAIDs namely meloxicam and piroxicam to bind to the DNA backbone could be a possible molecular mechanism behind their enhanced anticancer effects. Elucidating base sequence specific interaction of Cu(II)-NSAIDs to the DNA will provide information on their possible binding sites in the genome sequence. In this work, we present how these complexes respond to differences in structure and hydration pattern of GC rich sequences. For this, binding studies of Cu(II) complexes of piroxicam [Cu(II)-(Px)2 (L)2] and meloxicam [Cu(II)-(Mx)2 (L)] with alternating GC (polydG-dC) and homopolymeric GC (polydG-polydC) sequences were carried out using a combination of spectroscopic techniques that include UV-Vis absorption, fluorescence and circular dichroism (CD) spectroscopy. The Cu(II)-NSAIDs show strong binding affinity to both polydG-dC and polydG-polydC. The role reversal of Cu(II)-meloxicam from a strong binder of polydG-dC (Kb=11.5×10(3) M(-1)) to a weak binder of polydG-polydC (Kb=5.02×10(3) M(-1)), while Cu(II)-piroxicam changes from a strong binder of polydG-polydC (Kb=8.18×10(3) M(-1)) to a weak one of polydG-dC (Kb=2.18×10(3) M(-1)), point to the sensitivity of these complexes to changes in the backbone structures/hydration. Changes in the profiles of UV absorption band and CD difference spectra, upon complex binding to polynucleotides and the results of competitive binding assay using ethidium bromide (EtBr) fluorescence indicate different binding modes in each case.
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Meloxicam is a cyclo-oxygenase-2 (COX-2) preferential non-steroidal anti-inflammatory drug with very effective analgesic and anti-inflammatory effects in swine. Previous reports in piglets have demonstrated that meloxicam also inhibits COX-1 and reduces production of thromboxane significantly. We use preinjury analgesia in our immature swine (3-5-day-old piglets) model of brain injury using rapid head rotations without impact. In 23 consecutive subjects we found that premedication with meloxicam (n = 6) produced a significantly higher mortality rate (5/6 or 83%) than buprenorphine (n = 17, 1/17 or 6%, P < 0.02). On gross neuropathological examination of the meloxicam-treated swine, we observed massive subdural and subarachnoid bleeding which were not present in buprenorphine-premedicated animals. To our knowledge there are no previous reports in swine of increased bleeding or platelet inhibition associated with meloxicam administration and further research is needed to define mechanisms of action in piglets. We caution the use of meloxicam in swine when inhibition of platelet aggregation might adversely affect refinement of experimental research protocols, such as in stroke, trauma and cardiac arrest models.
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Twenty eight male Spraque-Dawley rats were randomized into four groups as dexketoprofen trometamol (Group I), meloxicam (Group II), diclofenac sodium (Group III) and control group. Nonsteroidal anti-inflammatory drugs (NSAID) were administered after a fibula fracture for 10 days. Untreated alveolar bone was histopathologically examined for spongious bone density, osteoclastic density and osteoblastic density.
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Multicenter, multinational, double-blind, double-dummy, three parallel groups, randomized trial, phase IIb, 337 patients. Treatment group comparisons of continuous variables were carried out using the Kruskal-Wallis test and Wilcoxon signed rank tests. Efficacy was analyzed using Fisher and chi(2)-tests.
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Meloxicam is a non-steroidal anti-inflammatory drug (NSAID) that primarily has an antiproteinuric effect and is used for the treatment of chronic glomerular diseases. In chronic glomerular disease (CGD), proteinuria is involved in the production of tubulo-interstitial lesions and has an important role in their progression. CGD improves with steroid therapy and immunosuppression. In the case of a favorable outcome, a reduction in proteinuria is also attained. In some situations, this therapy is prohibited, requiring alternative medication. NSAIDs are one class of these alternative drugs; in addition to having anti-inflammatory actions, they also have antiproteinuric effects. The aim of the study has been to assess the effect of the anti-inflammatory treatment with meloxicam upon proteinuria as well as upon tubular lesions by determining urinary NAG in its dynamics. The study was performed on 12 patients with CGD, 6 of them with nephrotic syndrome. On all patients we administered treatment with meloxicam 15 mg/day, 30 days. On all patients we performed proteinuria and urinary N-acetyl b D glucosaminidase (NAG) at the beginning, after 7 days and after 30 days of treatment. A 24-hour urine collection was taken from all patients. The urinary protein concentration was determined with the use of the Dimension (Dade Behring, Inc., Newark, DE, USA) clinical chemistry system UCFP method. We found a decrease of proteinuria under treatment from 2.85 +/- 1.69 g/24h to 1.53 +/- 0.83 g/24h, which was significantly lower, compared to the initial measurement (p = 0.01878). After 30 days of treatment with meloxicam, urinary NAG decreased from 10.6 +/- 12.56 U/g creatinine to 6.44 +/- 7 U/g, a decrease that was statistically non-significant. We observed a strong correlation between initial urinary NAG and initial proteinuria ri = 0.924, p < 0.001 and between final urinary NAG and final proteinuria rf = 0.856, p < 0.001. Our study revealed the favorable effect of meloxicam on patients with CGD on a 30-day treatment phase reflected on the evolution of proteinuria. Only in one case we did reveal a possible deleterious effect of this treatment. The assessment of the effect on tubulo-interstitial lesions in this short treatment period through urinary NAG assessment indicated only a modest and statistically non-significant response. We consider that meloxicam can be a useful drug in the treatment of proteinuric glomerular diseases.
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NSAIDs remain the principal pharmacological agents used for symptom relief in patients with rheumatic disease. They represent the largest single group of drugs used worldwide. Given the large number of available NSAIDs, it is unsurprising that some differences exist among them with regard to mechanism of action, pharmacokinetics, and tolerability. How these differences affect the overall risks and benefits of treatment continues to be examined in clinical trials. Meloxicam is COX-2 selective NSAID with favourable gastrointestinal and thromboembolic safety profile.
We studied 36 patients, allocated randomly to receive meloxicam 15 mg rectally (n = 18) or placebo suppository (n = 18) before total abdominal hysterectomy in a double-blind study. Visual analogue scores for pain at rest (P < 0.005), on movement (P < 0.05) and on coughing (P < 0.05) were significantly decreased in the meloxicam group during the first 24 h after surgery. Mean 24-h PCA morphine requirements were 33.2 (SD 16.9) mg and 38.2 (20.8) mg in the meloxicam and placebo groups, respectively (ns). There was no difference in the incidence of nausea, vomiting or sedation between groups.