Dogs with hyperadrenocorticism are at risk of thromboembolic disease, which might be caused by an underlying hypercoagulable state.Hypothesis/Objectives:
To assess hemostatic function in dogs with ACTH-dependent hyperadrenocorticism (ADHAC) before and after treatment.Animals:
Nineteen dogs with ADHAC and 40 normal dogs.Methods:
Prospective, 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).Results:
Dogs 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 Importance:
Dogs 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.