Cristina Costa-Farré

Objective: To demonstrate that a single dose of enflicoxib is noninferior to daily carprofen for the control of pain and inflammation in dogs undergoing soft tissue surgery. Methods: A prospective, multisite, blinded, randomized, controlled, parallel-group, noninferiority field study was performed to assess the efficacy and safety of enflicoxib in the control of pain and inflammation associated with soft tissue surgery. Two hundred fifteen dogs were randomized to receive 8 mg/kg of enflicoxib PO the day before surgery or 4 mg/kg of carprofen SC at induction and PO daily for 5 days. Veterinarians assessed efficacy with the short form of the Glasgow Composite Pain Scale (SF-GCPS) at 2, 5, 8, and 24 hours and 2, 3, and 5 days after surgery. The visual analog scale was used to assess inflammation. Demeanor, analgesia, and mobility were assessed daily by the owners. Results: Enflicoxib was noninferior to carprofen in the SF-GCPS area under the curve for the first 48 hours. Inflammation and SF-GCPS total scores were within the clinically relevant margin at each time point. No differences were observed in inflammation or in the owner assessment. Conclusions: Enflicoxib administered 24 hours before surgery is safe and efficacious for the control of postoperative pain associated with soft tissue surgery. Clinical Relevance: A single preoperative dose of enflicoxib is an alternative for postoperative management in dogs undergoing soft tissue surgery, offering a simplified treatment regimen without compromising outcomes.

A case of distal renal tubular acidosis occurring as a transient complication in a 13-year-old female greyhound dog with gastric-dilatation-volvulus was diagnosed. The acute renal ischemia and inflammatory condition associated with this syndrome could be considered the main underlying mechanisms responsible for the acute, severe, and complicating renal tubular dysfunction.

Summary: Background: Prostaglandin E₂ (PGE₂) has been proposed to exert antiasthmatic effects in patients, to prevent antigen‐induced airway pathology in murine models, and to inhibit mast cells (MC) activity in vitro.Objective: To assess in a murine model whether the protective effect of PGE₂ may be a consequence of its ability to activate the E‐prostanoid (EP)₂ receptor on airway MC.Methods: Either BALB/c or C57BL/6 mice were exposed intranasally (i.n.) to house dust mite (HDM) aeroallergens. Both strains were given PGE₂ locally (0.3 mg/kg), but only BALB/c mice were administered butaprost (EP₂ agonist: 0.3 mg/kg), or AH6809 (EP₂ antagonist; 2.5 mg/kg) combined with the MC stabilizer sodium cromoglycate (SCG: 25 mg/kg). Airway hyperresponsiveness (AHR) and inflammation, along with lung MC activity, were evaluated. In addition, butaprost's effect was assessed in MC‐mediated passive cutaneous anaphylaxis (PCA) in mice challenged with 2,4‐dinitrophenol (DNP).Results: Selective EP₂ agonism attenuated aeroallergen‐caused AHR and inflammation in HDM‐exposed BALB/c mice, and this correlated with a reduced lung MC activity. Accordingly, the blockade of endogenous PGE₂ by means of AH6809 worsened airway responsiveness in sensitive BALB/c mice, and such worsening was reversed by SCG. The relevance of MC to PGE₂‐EP₂ driven protection was further highlighted in MC‐dependent PCA, where butaprost fully prevented MC‐induced ear swelling. Unlike in BALB/c mice, PGE₂ did not protect the airways of HDM‐sensitized C57BL/6 animals, a strain in which we showed MC to be irrelevant to aeroallergen‐driven AHR and inflammation.Conclusions & Clinical Relevance: The beneficial effect of both exogenous and endogenous PGE₂ in aeroallergen‐sensitized mice may be attributable to the activation of the EP₂ receptor, which in turn acts as a restrainer of airway MC activity. This opens a path towards the identification of therapeutic targets against asthma along the ‘EP₂ ‐MC‐airway’ axis.