Peer-reviewed veterinary case report
Perzinfotel and PLA2 inhibitor effects on lameness in dogs with joint
By Budsberg, Steven C et al.·Published in American journal of veterinary research·2011·Department of Small Animal Medicine and Surgery, United States·View original on PubMed →
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Original publication title: Effect of perzinfotel and a proprietary phospholipase A(2) inhibitor on kinetic gait and subjective lameness scores in dogs with sodium urate-induced synovitis.
- Species:
- dog
Plain-English summary
An adult dog with joint pain caused by sodium urate-induced inflammation was treated with either perzinfotel, a phospholipase A(2) inhibitor, carprofen (a common pain medication), or no treatment. After the treatment, the dog showed some improvement with the phospholipase A(2) inhibitor, but it wasn't as effective as carprofen. The perzinfotel did not help reduce the lameness significantly. Overall, while the phospholipase A(2) inhibitor showed some benefits, carprofen was the most effective option for relieving the dog's pain.
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Abstract
OBJECTIVE: To investigate the ability of perzinfotel (an N-methyl-d-aspartate receptor antagonist) and a proprietary phospholipase A(2) (PLA(2)) inhibitor to attenuate lameness in dogs with sodium urate (SU)-induced synovitis. ANIMALS: 8 adult dogs. PROCEDURES: A blinded 4-way crossover study was performed. Dogs received perzinfotel (10 mg/kg), a proprietary PLA(2) inhibitor (10 mg/kg), carprofen (4.4 mg/kg; positive control treatment), or no treatment (negative control treatment). On the fourth day after initiation of treatment, synovitis was induced via intra-articular injection of SU 1 hour before administration of the last treatment dose. Ground reaction forces were measured and clinical lameness evaluations were performed before (baseline [time 0]) and 2, 4, 6, 8, 12, and 25 hours after SU injection. There was a 21-day washout period between subsequent treatments. Data were analyzed via repeated-measures ANOVAs. RESULTS: Peak vertical force (PVF) and vertical impulse (VI) values for negative control and perzinfotel treatments were significantly lower at 2 and 4 hours, compared with baseline values. Values for PVF and VI for the PLA(2) inhibitor and positive control treatments did not differ from baseline values at any time points. Between-treatment comparisons revealed significantly higher PVF and VI values for the positive control treatment than for the negative control and perzinfotel treatments at 2 and 4 hours. Values for VI were higher for PLA(2) inhibitor treatment than for negative control treatment at 2 hours. CONCLUSIONS AND CLINICAL RELEVANCE: Perzinfotel did not significantly alter SU-induced lameness. The proprietary PLA(2) inhibitor attenuated lameness but not as completely as did carprofen.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/21627521/