mobic and deracoxib

To determine effects of anti-inflammatory doses of COX-2 selective NSAIDs carprofen, meloxicam, and deracoxib on platelet function in dogs and urine 11-dehydro-thromboxane B2.. Randomized, blocked, crossover design with a 14-day washout period.. Healthy intact female Walker Hounds aged 1-6 years and weighing 20.5-24.2 kg.. Dogs were given NSAIDs for 7 days at recommended doses: carprofen (2.2 mg kg(-1), PO, every 12 hours), carprofen (4.4 mg kg(-1), PO, every 24 hours), meloxicam (0.2 mg kg(-1), PO, on the 1st day then 0.1 mg kg(-1), PO, every 24 hours), and deracoxib (2 mg kg(-1), PO, every 24 hours). Collagen/epinephrine and collagen/ADP PFA-100 cartridges were used to evaluate platelet function before and during and every other day after administration of each drug. Urine 11-dehydro-thromboxane B(2) was also measured before and during administration of each drug.. All NSAIDs significantly prolonged PFA-100 closure times when measured with collagen/epinephrine cartridges, but not with collagen/ADP cartridges. The average duration from drug cessation until return of closure times (collagen/epinephrine cartridges) to baseline values was 11.6, 10.6, 11 and 10.6 days for carprofen (2.2 mg kg(-1) every 12 hours), carprofen (4.4 mg kg(-1) every 24 hours), meloxicam and deracoxib, respectively.. Oral administration of some COX-2 selective NSAIDs causes detectable alterations in platelet function in dogs. As in humans, PFA-100 collagen/ADP cartridges do not reliably detect COX-mediated platelet dysfunction in dogs. Individual assessment of platelet function is advised when administering these drugs prior to surgery, particularly in the presence of other risk factors for bleeding.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Platelets; Carbazoles; Dogs; Female; Hemostasis; Meloxicam; Platelet Aggregation; Sulfonamides; Thiazines; Thiazoles; Thromboxane B2

To determine the effects of nonsteroidal anti-inflammatory drugs of various cyclooxygenase selectivities on hemostasis and prostaglandin expression in dogs.. 8 client-owned dogs with clinical signs of osteoarthritis.. Dogs received aspirin (5 mg/kg, PO, q 12 h), carprofen (4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), and meloxicam (0.1 mg/kg, PO, q 24 h) for 10 days each, with an interval of at least 14 days between treatments. On days 0 and 10, blood was collected for platelet aggregation assays, thrombelastography, and measurement of lipopolysaccharide-stimulated prostaglandin E(2), platelet thromboxane B(2) (TXB(2)), and free serum TXB(2) and 6-keto-prostaglandin F (PGF)-1alpha concentrations.. Platelet aggregation decreased after treatment with aspirin and carprofen, whereas significant changes from baseline were not detected for the other drugs tested. Thrombelastograms obtained after treatment with carprofen revealed decreased maximum amplitude and alpha-angle, suggesting hypocoagulability. Maximum amplitude and coagulation index increased after treatment with deracoxib. Plasma concentrations of prostaglandin E(2) decreased after treatment with carprofen or deracoxib, and platelet TXB(2) production increased after treatment with aspirin. Serum concentrations of the prostacyclin metabolite 6-keto-PGF-1alpha did not change significantly after treatment with any of the drugs, although the ratio of free TXB(2) to 6-keto-PGF-1alpha decreased slightly after treatment with carprofen and increased slightly after treatment with deracoxib.. At the dosages tested, treatment with meloxicam affected platelet function minimally in dogs with osteoarthritis. Treatment with carprofen decreased clot strength and platelet aggregation. Clot strength was increased after treatment with deracoxib.

Topics: Animals; Aspirin; Carbazoles; Cross-Over Studies; Cyclooxygenase Inhibitors; Dog Diseases; Dogs; Female; Gene Expression Regulation; Hemostasis; Male; Meloxicam; Osteoarthritis; Platelet Aggregation; Prostaglandins; Sulfonamides; Thiazines; Thiazoles

This positive-control study evaluated the efficacy of firocoxib versus carprofen, deracoxib, and meloxicam for the prevention of pain and inflammation in a urate crystal synovitis model of lameness. Lameness scoring and force plate gait analysis were used to assess efficacy. The resulting lameness scores and force plate ground reaction forces after urate crystal injection were not significantly different among the groups. Relative to each group's baseline (nonlame) score, only the firocoxib group was not significantly lame, based on lameness score, at the model's peak effect.

Topics: 4-Butyrolactone; Animals; Carbazoles; Cyclooxygenase 2 Inhibitors; Dog Diseases; Dogs; Female; Lameness, Animal; Male; Meloxicam; Severity of Illness Index; Sulfonamides; Sulfones; Synovitis; Thiazines; Thiazoles; Treatment Outcome; Uric Acid

To report which nonsteroidal anti-inflammatory drugs (NSAIDs) were associated with gastric or duodenal perforation (GDP) in dogs presented to a university teaching hospital and to report the frequency of prescription of NSAIDs by the corresponding referring veterinary community during the same time period.. Retrospective cohort study of dogs from January 2007 to March 2020.. Single university teaching hospital.. A total of 30 dogs met inclusion criteria.. Four dogs were administered more than 1 NSAID within 7 days of GDP, 3 dogs received a combination of an NSAID and a corticosteroid, and 1 dog received 2 NSAIDs and a corticosteroid. Four dogs received an overdose of an NSAID. One dog received an overdose of 1 NSAID and received an additional NSAID at the labeled dose within 7 days of GDP. Eighteen dogs received only 1 NSAID at the labeled dose. In these 18 dogs, meloxicam was administered in 44.4% (8/18), firocoxib in 27.8% (5/18), deracoxib in 16.7% (3/18), and piroxicam in 11.1% (2/18). One hundred and sixty surveys on NSAID prescribing practice were returned. Carprofen was the most commonly prescribed NSAID (70.6%), followed by meloxicam (10.6%), deracoxib (8.4%), firocoxib (7.8%), aspirin (1.5%), and other (0.9%).. NSAID administration, even at labeled doses, appears to be a precipitating factor for GDP. Despite carprofen being the most frequently prescribed NSAID over the study period, no case of GDP received it as a single therapeutic agent. Further prospective evaluation is needed to verify these findings.

Topics: Adrenal Cortex Hormones; Animals; Anti-Inflammatory Agents, Non-Steroidal; Dog Diseases; Dogs; Meloxicam; Peritonitis; Retrospective Studies

In vitro whole blood canine assays were used to quantify the inhibitory actions of the novel non-steroidal anti-inflammatory drug (NSAID) robenacoxib on the cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, in comparison with other drugs of the NSAID class. COX-1 activity was determined by measuring serum thromboxane (Tx)B(2) synthesis in blood samples allowed to clot at 37 degrees C for 1h. COX-2 activity was determined by measuring prostaglandin (PG)E(2) synthesis in blood samples incubated at 37 degrees C for 24h in the presence of lipopolysaccharide. The rank order of selectivity for inhibition of COX-2 versus COX-1 (IC(50) COX-1:IC(50) COX-2) for veterinary drugs was highest with robenacoxib (128.8) compared to deracoxib (48.5), nimesulide (29.2), S+ carprofen (17.6), meloxicam (7.3), etodolac (6.6), R- carprofen (5.8) and ketoprofen (0.88). Selectivity expressed as the clinically relevant ratio IC(20) COX-1:IC(80) COX-2 was highest for robenacoxib (19.8) compared to deracoxib (2.3), S+ carprofen (2.5), R- carprofen (2.1), nimesulide (1.8), etodolac (0.76), meloxicam (0.46) and ketoprofen (0.21). An in vivo pharmacokinetic ex vivo pharmacodynamic study in the dog established dosage and concentration-effect relationships for single oral doses of robenacoxib over the dosage range 0.5-8.0mg/kg. Values of C(max) and AUC were linearly related to dosage over the tested range. Robenacoxib did not inhibit serum TxB(2) synthesis (COX-1) ex vivo at dosages of 0.5-4.0mg/kg and produced only transient inhibition (at the 1h and 2h sampling times) at the 8mg/kg dosage. All dosages of robenacoxib (0.5-8mg/kg) produced marked, significant and dose related inhibition of PGE(2) synthesis (COX-2) ex vivo. The data demonstrate that in the dog robenacoxib is a highly selective inhibitor of the COX-2 isoform of COX, and significantly inhibits COX-2 and spares COX-1 in vivo when administered orally over the dosage range 0.5-4.0mg/kg.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Dogs; Etodolac; Isoenzymes; Ketoprofen; Kinetics; Lipopolysaccharides; Meloxicam; Prostaglandin-Endoperoxide Synthases; Sulfonamides; Thiazines; Thiazoles; Thromboxane B2

To determine effects of therapeutic dosages of aspirin, carprofen, deracoxib, and meloxicam on platelet function and systemic prostaglandin concentrations in healthy dogs.. 10 hound-crossbred dogs.. Aspirin (10 mg/kg, PO, q 12 h), carprofen (4.4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), meloxicam (0.1 mg/kg, PO, q 24 h), and a placebo were administered for 7 days in a random order to each of 10 healthy dogs; there was a 21-day washout period between subsequent treatments. One-stage prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, and plasma concentrations of thromboxane (TX)B(2) and 6-keto prostaglandin (PG)F(1alpha) were measured before and after treatment administration. Platelet function was assessed by use of a platelet-function analyzer and aggregation.. Aspirin, carprofen, and meloxicam did not significantly affect platelet function. Deracoxib caused a mild decrease in platelet aggregation induced by 50microM ADP. Platelet number, Hct, PT, aPTT, and plasma TXB(2) and 6-keto PGF(1alpha) concentrations were unchanged after NSAID administration. Meloxicam administration resulted in a significant decrease in fibrinogen concentration, but results remained within the laboratory reference interval.. Oral administration of commonly used NSAIDs at therapeutic dosages in healthy dogs did not alter plasma TXB(2) and 6-keto PGF(1alpha) concentrations. Deracoxib administration resulted in a minor abnormality in platelet aggregation. Anti-inflammatory doses of aspirin did not affect platelet function as measured by use of optical aggregometry and a platelet-function analyzer. Further evaluation of the effects of aspirin and cyclooxygenase-2-selective inhibitors on hemostasis should be performed.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Blood Coagulation; Blood Platelets; Carbazoles; Dogs; Female; Male; Meloxicam; Ovariectomy; Platelet Aggregation; Prostaglandins; Sulfonamides; Thiazines; Thiazoles