Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new mobic research articles will be listed here shortly after becoming available to us.
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J Feline Med Surg. 2008 Apr 24;
Gunew MN, Menrath VH, Marshall RD
Osteoarthritis is a chronic, painful condition that is now recognised as affecting a large proportion of cats. Non-steroidal anti-inflammatory drugs (NSAIDs) have proven efficacy in dogs and humans but there are limited published data on the use of NSAIDs in the long-term management of this condition in cats. This prospective study aimed to assess the long-term safety and palatability of oral meloxicam and its efficacy in treating osteoarthritic pain in cats when given at a dose of 0.01-0.03mg/kg once daily. Forty cats diagnosed with osteoarthritis completed the trial with a mean treatment duration of 5.8 months. Gastrointestinal upset in 2/46 (4%) cats was the only adverse effect noted. No deleterious effect on renal function was detected in cats studied. Owners subjectively assessed treatment efficacy as good or excellent in 34/40 (85%) of cases. The results of this study showed oral meloxicam to be safe and palatable long-term treatment for osteoarthritis in cats when given with food at a dose of 0.01-0.03mg/kg.
Mechanism of calcium hydroxide-induced neutrophil migration into air-pouch cavity.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008 Apr 23;
Teixeira de Moraes Costa MM, Penha de Oliveira SH, Gomes-Filho JE
The aim of this study was to investigate cellular migration induced by calcium hydroxide to air-pouch cavities in mice. The migration was more specific to neutrophil and was dose and time dependent (peaking 96 h after stimulation). This migration was inhibited by pretreatment with thalidomide, indomethacin, MK886, meloxicam, dexamethasone, MK886 associated with indomethacin, and MK886 associated with indomethacin and dexamethasone. The air-pouch exudate from animals stimulated with calcium hydroxide showed an increase of leukotriene-B(4) (LTB(4)), interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) release. Pretreatment with 3% thioglycollate increased the macrophage population in the air pouch but did not change neutrophil migration. Depleting the resident mast cells through chronic pretreatment with compound 48/80 did not alter neutrophil migration in response to calcium hydroxide. It was possible to conclude that calcium hydroxide-induced neutrophil migration to the air-pouch cavity in mice is mediated by LTB(4), TNF-alpha, KC, MIP-2, and prostaglandins, but it was not dependent on macrophages or mast cells.
Renal effect of meloxicam versus ketoprofen in anaesthetized pseudo-normovolaemic piglets.
Can J Physiol Pharmacol. 2008 January/February; 86(1-2): 55-63
Junot S, Troncy E, Keroack S, Gauvin D, Del Castillo JR, Boivin R, Bonnet JM
Due to renal COX-2 constitutive expression, meloxicam is presumably deleterious for kidney function in critical situations. The present study investigates the influence of intravenous meloxicam on renal parameters and compares it with a nonselective COX inhibitor, ketoprofen. Piglets (n = 6 in each group) were treated with ketoprofen (2 mg.kg-1), meloxicam (0.2 mg.kg-1), or saline at the beginning of anaesthesia. Under intravenous anaesthesia, pigs were instrumented for cardiovascular, respiratory, and renal function evaluation, including urinary flow (UF), glomerular filtration rate (GFR), and renal blood flow (RBF). After baseline data collection (U0), data collection consisted of six 20-minute periods (U1 to U6). In all groups, the time course of cardiovascular and respiratory parameters remained within normal ranges. A small decrease in cardiac output and an increase in mean systemic arterial blood pressure (p = 0.002) occurred in all groups. In the placebo group, a similar decrease was observed for RBF and cardiac output, with troughs of -10.1% +/- 6.8%, and -12.9% +/- 3.2%, respectively. GFR and UF, however, remained stable over time in this group. Ketoprofen significantly decreased UF (-29.3% +/- 5.5% max at U3), with similar decreases in GFR and RBF. Meloxicam induced a transient (at U2) and small decrease in UF with no difference, at any time point, with the placebo group. The renal effects of meloxicam appear minimal and transient in anaesthetized piglets. This study demonstrates the safety of meloxicam for preemptive surgical analgesia under conditions of normovolaemia. Fluid therapy appears recommended to prevent any renal dysfunction.
Health Technol Assess. 2008 Apr; 12(11): 1-178
Chen YF, Jobanputra P, Barton P, Bryan S, Fry-Smith A, Harris G, Taylor RS
OBJECTIVES: To review the clinical effectiveness and cost-effectiveness of cyclooxygenase-2 (COX-2) selective non-steroidal anti-inflammatory drugs (NSAIDs) (etodolac, meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib and lumiracoxib) for osteoarthritis (OA) and rheumatoid arthritis (RA). DATA SOURCES: 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. REVIEW METHODS: Systematic reviews of randomised controlled trials (RCTs) and a model-based economic evaluation were undertaken. Meta-analyses were undertaken for each COX-2 selective NSAID compared with placebo and non-selective NSAIDs. The model was designed to run in two forms: the 'full Assessment Group Model (AGM)', which includes an initial drug switching cycle, and the 'simpler AGM', where there is no initial cycle and no opportunity for the patient to switch NSAID. RESULTS: Compared with non-selective NSAIDs, the COX-2 selective NSAIDs were found to be equally as efficacious as the non-selective NSAIDs (although meloxicam was found to be of inferior or equivalent efficacy) and also to be associated with significantly fewer clinical upper gastrointestinal (UGI) events (although relatively small numbers of clinical gastrointestinal (GI) and myocardial infarction (MI) events were reported across trials). Subgroup analyses of clinical and complicated UGI events and MI events in relation to aspirin use, steroid use, prior GI history and Helicobacter pylori status were based on relatively small numbers and were inconclusive. In the RCTs that included direct COX-2 comparisons, the drugs were equally tolerated and of equal efficacy. Trials were of insufficient size and duration to allow comparison of risk of clinical UGI events, complicated UGI events and MIs. One RCT compared COX-2 (celecoxib) with a non-selective NSAID combined with a gastroprotective agent (diclofenac combined with omeprazole); this included arthritis patients who had recently suffered a GI haemorrhage. Although no significant difference in clinical GI events was reported, the number of events was small and more such studies, where patients genuinely need NSAIDs, are required to confirm these data. A second trial showed that rofecoxib was associated with fewer diarrhoea events than a combination of diclofenac and misoprostol (Arthrotec). Previously published cost-effectiveness analyses indicated a wide of range of possible incremental cost per quality-adjusted life-year (QALY) gained estimates. Using the simpler AGM, with ibuprofen or diclofenac alone as the comparator, all of the COX-2 products are associated with higher costs (i.e. positive incremental costs) and small increases in effectiveness (i.e. positive incremental effectiveness), measured in terms of QALYs. The magnitude of the incremental costs and the incremental effects, and therefore the incremental cost-effectiveness ratios, vary considerably across all COX-2 selective NSAIDs. The base-case incremental cost per QALY results for COX-2 selective NSAIDs compared with diclofenac for the simpler model are: celecoxib (low dose) 68,400 pounds; celecoxib (high dose) 151,000 pounds; etodolac (branded) 42,400 pounds; etodolac (generic) 17,700 pounds; etoricoxib 31,300 pounds; lumiracoxib 70,400 pounds; meloxicam (low dose) 10,300 pounds; meloxicam (high dose) 17,800 pounds; rofecoxib 97,400 pounds; and valdecoxib 35,500 pounds. When the simpler AGM was run using ibuprofen or diclofenac combined with proton pump inhibitor (PPI) as the comparator, the results change substantially, with the COX-2 selective NSAIDs looking generally unattractive from a cost-effectiveness point of view (COX-2 selective NSAIDs were dominated by ibuprofen or diclofenac combined with PPI in most cases). This applies both to 'standard' and 'high-risk' arthritis patients defined in terms of previous GI ulcers. The full AGM produced results broadly in line with the simpler model. CONCLUSIONS: The COX-2 selective NSAIDs examined were found to be similar to non-selective NSAIDs for the symptomatic relief of RA and OA and to provide superior GI tolerability (the majority of evidence is in patients with OA). Although COX-2 selective NSAIDs offer protection against serious GI events, the amount of evidence for this protective effect varied considerably across individual drugs. The volume of trial evidence with regard to cardiovascular safety also varied substantially between COX-2 selective NSAIDs. Increased risk of MI compared to non-selective NSAIDs was observed among those drugs with greater volume of evidence in terms of exposure in patient-years. Economic modelling shows a wide range of possible costs per QALY gained in patients with OA and RA. Costs per QALY also varied if individual drugs were used in 'standard' or 'high'-risk patients, the choice of non-selective NSAID comparator and whether that NSAID was combined with a PPI. With reduced costs of PPIs, future primary research needs to compare the effectiveness and cost-effectiveness of COX-2 selective NSAIDs relative to non-selective NSAIDs with a PPI. Direct comparisons of different COX-2 selective NSAIDs, using equivalent doses, that compare GI and MI risk are needed. Pragmatic studies that include a wider range of people, including the older age groups with a greater burden of arthritis, are also necessary to inform clinical practice.
Neurosci Lett. 2008 May 9; 436(2): 205-9
Chae SW, Kang BY, Hwang O, Choi HJ
Cyclooxygenase (COX) is the rate-limiting enzyme that catalyzes the formation of prostaglandins from arachidonic acid. The inducible isoform COX-2 is upregulated in the dopaminergic neurons of the substantia nigra of postmortem Parkinson's disease (PD) patients and in neurotoxin-induced Parkinsonism models. COX-2 has attracted significant attention as an important source of oxidative stress in dopaminergic neurons due to its potential to oxidize catechols including dopamine. However, the role of COX-2 in the pathogenesis of PD has not been fully evaluated. Here, we show that COX-2 induces dopamine oxidation, as evidenced by the findings that COX-2 can facilitate dopamine oxidation in a cell-free system and in COX-2-overexpressing SH-SY5Y cells, and that this can be completely abolished by the selective COX-2 inhibitor meloxicam. Increased COX-2 expression causes oxidative protein modification and alpha-synuclein accumulation in dopaminergic cells. These data suggest that an abnormal increase in COX-2 expression causes dopamine oxidation and contributes to the preferential vulnerability of dopaminergic cells as in PD.
Rheumatology (Oxford). 2008 May; 47(5): 627-33
Alvarez-Soria MA, Herrero-Beaumont G, Sánchez-Pernaute O, Bellido M, Largo R
OBJECTIVES: Synoviocytes play a crucial role in the inflammatory response leading to structural damage in OA. Our aim was to assess the effects of diacerein and NSAIDs on cellular responses of synoviocytes associated with inflammation and structural integrity of cartilage in OA. METHODS: The effects of diacerein, celecoxib, diclofenac, meloxicam and indomethacin on prostaglandin (PG) E2 production, cyclo-oxygenase-2 (COX-2) protein expression, nitrite levels, presence of MMP-1 and -13, and activation of nuclear factor-kappaB (NF-kappaB) were studied on stimulated OA synoviocytes and chondrocytes. RESULTS: Diacerein and NSAIDs inhibited IL-1beta-stimulated NF-kappaB activation in synoviocytes and chondrocytes except indomethacin in synoviocytes. Diacerein further increased COX-2 protein expression and PGE2 synthesis in synoviocytes stimulated with IL-1beta, while no effect was observed on stimulated chondrocytes. NSAIDs diminished until almost basal levels PGE2 release in both cells and, surprisingly, these drugs also diminished COX-2 protein expression both in synoviocytes and chondrocytes. With regard to structural mediators, diacerein decreased MMP-13 levels in synoviocytes but did not modify MMP-1 presence. NSAIDs induced a significant increase in MMP-1 levels in both cell types and in MMP-13 levels in chondrocytes. CONCLUSIONS: Diacerein does not seem to reduce but rather increase inflammatory mediators in synoviocytes, while it does not overall affect chondrocyte inflammatory profile.
Acta Cir Bras. 2008 Apr; 23(2): 140-148
Silva RA, Fagundes DJ, Silva AC, Sisti KE, Carvalho TM, Silva DN
PURPOSE: To study the repair of bone defect filled with autograft or bovine bone devitalized matrix in rats under anti-inflammatory action. METHODS: Two hundred and forty Wistar rats were distributed to two groups of 120 animals each. A 2mm-diameter defect was created in the femoral diaphysis. Animals of Group I had the bone defect filled with autograft and those of Group II, with bovine bone devitalized matrix. Animals of each group were redistributed to four subgroups according to the intramuscular administration of anti-inflammatory drug or saline solution: A - diclofenac sodium; B - dexamethasone; C - meloxicam; D - saline solution. Evaluation periods were 7, 14 and 30 days. Histological evaluation consisted of quantifying the inflammatory process, the bone neoformation, the collagen formation and the presence of macrophages. RESULTS: Animals of Group I did not show significant difference considering inflammatory reaction. Significant and progressive increase of bone neoformation was observed in both groups. The animals that received meloxicam and autograft showed less collagen formation at 14 and 30 days. The number of macrophages was higher in Group II than in Group I. The animals treated with dexamethasone and saline solution did not show statistically significant difference. CONCLUSIONS: Diclofenac sodium and meloxicam delayed bone graft repair and dexamethasone did not interfere in it.
Ther Clin Risk Manag. 2007 Jun; 3(2): 225-30
Raber A, Heras J, Costa J, Fortea J, Cobos A
The objective was to compare the incidence of adverse reactions reported with three nonsteroidal anti-inflammatory drugs with different cyclo-oxygenase (COX)-2 selectivity. All spontaneous adverse reaction notifications in the pharmacovigilance database of the World Health Organisation Collaborating Centre for International Drug Monitoring with aceclofenac, meloxicam, and rofecoxib that were recorded during the first year of marketing were included. The incidence rate (adverse reactions/10(6) defined daily dose) and 95% confidence interval for total adverse reactions was 8.7 (6.1-12.0) for aceclofenac, 24.8 (23.1-26.6) for meloxicam, and 52.6 (49.9-55.4) for rofecoxib. Aceclofenac had a lower incidence of gastrointestinal bleeding, abdominal pain, and arterial hypertension than meloxicam and a lower incidence of gastrointestinal bleeding, abdominal pain, liver toxicity, thromboembolic cardiovascular events, arterial hypertension, and edema than rofecoxib. The incidence of total and gastrointestinal adverse reactions was significantly lower with aceclofenac than with meloxicam or rofecoxib, thus raising doubts about the hypothetical advantage of COX-2 selective inhibitors.
Reumatizam. 2007; 54(2): 81-2
Kaliterna DM
What is your diagnosis? Squamous cell carcinoma of the uropygial gland.
J Avian Med Surg. 2007 Dec; 21(4): 321-4
Beaufrère H, Brasseur G, Heimann M