Hypercoagulability and ACTH-dependent hyperadrenocorticism in dogs.

BACKGROUND

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.