A Remote Assay for Measuring Canine Platelet Activation and the Inhibitory Effects of Antiplatelet Agents.

BACKGROUND: Antiplatelet medications are increasingly used in dogs. Remote analysis of platelet activity is challenging, limiting assessment of antiplatelet drug efficacy. HYPOTHESIS/OBJECTIVES: To evaluate a method used in humans for stimulation and remote analysis of canine platelet activity. ANIMALS: Forty-five dogs of various ages without a coagulopathy or thrombocytopenia. Six were receiving antiplatelet medication. METHODS: Prospective 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. RESULTS: Canine 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 IMPORTANCE: This 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.

Hypophysitis, Panhypopituitarism, and Hypothalamitis in a Scottish Terrier Dog.

A 6-year old male neutered Scottish Terrier was referred with a 1 week history of progressive lethargy and anorexia. Neurological examination localized a lesion to the forebrain and hormonal testing showed panhypopituitarism. Magnetic resonance imaging (MRI) of the brain revealed a rounded, well-defined, suprasellar central mass. The mass was slightly hyperintense to the cortical grey matter on T2-weighted (T2W), hypointense on T1-weighted (T1W) images and without T2* signal void. There was a central fusiform enhancement of the mass after contrast administration which raised the suspicion of a pituitary neoplasm. Rapid deterioration of the dog prevented further clinical investigations. Histopathologic examination revealed a lymphocytic panhypophysitis of unknown origin suspected autoimmune involving the hypothalamus (hypothalamitis). This is a unique case report of a dog presenting with inflammatory hypophysitis and hypothalamitis of suspected autoimmune origin with detailed clinical, MRI, histology and immunohistochemistry findings.

Preliminary investigation of urine N-telopeptide concentration as a biomarker of bone resorption in dogs receiving glucocorticoids.

OBJECTIVES: The influence of glucocorticoid therapy on bone resorption in dogs using a urine N-telopeptide assay was investigated. MATERIALS AND METHODS: Thirty-one dogs receiving oral glucocorticoids and 31 age-matched healthy control dogs were enrolled. Urine N-telopeptide concentration was measured using a commercially available immunoassay and results were expressed as a ratio against urinary creatinine concentration. Dogs receiving glucocorticoids were divided into three subgroups based on daily glucocorticoid dose and three subgroups based on treatment duration. Urine N-telopeptide concentration was then compared between groups. RESULTS: Urine N-telopeptide concentration was significantly higher in dogs receiving glucocorticoids compared to the control group. CLINICAL SIGNIFICANCE: 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.

Hypercalcaemia secondary to elevated 1,25 dihydroxycholecalciferol in a dog with immune-mediated polyarthritis.

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.