• F M Park, S L Blois, A C G Abrams-Ogg, R D Wood, D G Allen, S G Nykamp, and A Downie.
• Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON.
• J. Vet. Intern. Med. 2013 Sep 1; 27 (5): 1136-42.

BackgroundDogs with hyperadrenocorticism are at risk of thromboembolic disease, which might be caused by an underlying hypercoagulable state.Hypothesis/ObjectivesTo assess hemostatic function in dogs with ACTH-dependent hyperadrenocorticism (ADHAC) before and after treatment.AnimalsNineteen dogs with ADHAC and 40 normal dogs.MethodsProspective, observational study. Dogs with ADHAC were recruited from the referral hospital patient population; normal dogs were recruited from staff and students at the study's institution. Hemostasis was assessed before and at 3 and 6 months after treatment with trilostane (T0, T3, T6) by kaolin-activated thrombelastography with platelet mapping (TEG-PM), prothrombin time, activated partial thromboplastin time, fibrinogen concentration, and antithrombin activity (AT).ResultsDogs with ADHAC had statistically significantly increased α-angle (P < .01) and maximum amplitude (MA)(thrombin) (P < .01) on TEG-PM, and significantly decreased κ (P < .005) at T0, T3, and T6. Platelet count (P < .001) and fibrinogen concentration (P < .001), but not AT activity, were increased in dogs with ADHAC at T0, T3, and T6.Conclusions And Clinical ImportanceDogs with ADHAC have thrombelastographic evidence of hypercoagulability and remained hypercoagulable during treatment. AT deficiency does not appear to be involved in the pathogenesis of hypercoagulability in this population.Copyright © 2013 by the American College of Veterinary Internal Medicine.

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