BackgroundAntiplatelet medications are increasingly used in dogs. Remote analysis of platelet activity is challenging, limiting assessment of antiplatelet drug efficacy.Hypothesis/ObjectivesTo evaluate a method used in humans for stimulation and remote analysis of canine platelet activity.AnimalsForty‐five dogs of various ages without a coagulopathy or thrombocytopenia. Six were receiving antiplatelet medication.MethodsProspective observational study. Platelets were stimulated with combinations of arachidonic acid (AA) and epinephrine (Epi) or adenosine diphosphate (ADP) and the thromboxane A2‐mimetic U46619 (U4). PAMFix was added to the blood samples to facilitate delayed analysis of platelet activity. Activity was assessed by flow cytometric measurement of surface P‐selectin (CD62P) expression.ResultsCanine platelets could be stimulated with both AA/Epi and ADP/U4. The levels of P‐selectin were significantly greater than paired, unstimulated samples (P < 0.001). Inhibition of P‐selectin expression occurred after this stimulation by adding antiplatelet drugs in vitro. The efficacy of antiplatelet drugs in samples from treated dogs was also measurable ex vivo using this method. Delayed analysis of platelet activity at time points up to 22 days demonstrated excellent correlation between respective mf values at each time point (r2 = 0.92, P < 0.0001).Conclusions and Clinical ImportanceThis study evaluated a new method to remotely assess canine platelet activity. It shows that PAMFix can be used for this purpose. This provides opportunities to interrogate the inhibitory action of antiplatelet drugs in clinical settings.

Case summaryA 5-year-old male neutered Persian cat was referred for investigation of a 4 week history of weight loss, inappetence and intermittent vomiting. Chronic kidney disease (CKD) and inflammatory bowel disease were diagnosed, and despite immunosuppressive therapy and assisted enteral nutrition, the cat experienced persistent anorexia, vomiting and severe weight loss. After 2 additional weeks of treatment, the cat developed acute-onset neurological signs associated with severe hyperammonaemia and was euthanased. Plasma amino acid assessment revealed deficiency of several amino acids involved in the urea cycle, including arginine.Relevance and novel informationTo our knowledge, this is the first reported case of an acquired urea cycle amino acid deficiency without nutritional deprivation in a cat. Several contributing factors were suspected, including intestinal malabsorption and CKD. This case demonstrates the importance of urea cycle amino acids in feline metabolism and possible necessity for parenteral supplementation, particularly in the context of persistent weight loss despite adequate enteral nutrition.

A seven-year-old male entire Bearded Collie was referred following a three-week history of pyrexia, lethargy and stiffness, which was poorly responsive to antibiotic therapy. The most significant laboratory abnormalities included marked neutrophilia and ionised hypercalcaemia. The dog was diagnosed with primary immune-mediated polyarthritis, which responded to prednisolone and azathioprine, and resulted in resolution of the elevated 1,25 hydroxycholecalciferol, hypercalcaemia and neutrophilia. To the authors' knowledge, this represents the first case report of hypercalcaemia secondary to immune-mediated polyarthritis.

In chick embryos, limited carbohydrate in‐ovo necessitates high rates of gluconeogenesis from amino acids and/or triglyceride‐glycerol for glycogen synthesis and other metabolic functions. The aim was to quantify gluconeogenesis and glucose carbon recycling during the latter stages of development in small versus large eggs. [U‐13C]Glucose (15 mg in 75 μL water) was injected into the amniotic fluid of small (54 to 58 g) and large (66 to 70 g) eggs for three consecutive days prior to tissue and blood collection on d 12, 14, 16 and 18 embryonic (5 eggs/age group). Blood was analyzed by GC‐MS for 13C‐mass isotopomer distribution in glucose, alanine, aspartate and glutamate. On d 16 and 18, embryo weights of small eggs were less than large eggs (17.8 and 20.6 g vs. 23.4 and 27.8 g; P<0.05). Gluconeogenesis (0.97 to 1.38 g/d) and glucose carbon recycling (30%) did not differ between small and large embryos; however, there was an increase (P < 0.01) in these fluxes from d 12 onwards. There was a significant contribution of glucose carbon to alanine flux (5 to 65%; P< 0.01), but only a small portion of aspartate (0.2 to 10%) and no glutamate derived from glucose. The latter indicates limited entry of glucose carbon into the Krebs cycle. In summary, small egg‐embryos maintained similar rates of gluconeogenesis compared to large egg‐embryos, despite their small embryonic size.

This preliminary study demonstrates significant increase in urine N-telopeptide concentration in dogs receiving glucocorticoid therapy compared to control dogs. Further studies are needed to assess whether this increase in urine N-telopeptide concentration correlates with decreases in bone mineral density as has been identified in humans.