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.
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.
Authors: Jenna Woodman; Catherine R Wagg; Søren R Boysen; Renaud Leguillette; Kyle Mizen; Marie-France Roy Journal: Can Vet J Date: 2015-12 Impact factor: 1.008
Authors: Paula García San José; Carolina Arenas Bermejo; Irene Clares Moral; Pedro Cuesta Alvaro; María Dolores Pérez Alenza Journal: J Vet Intern Med Date: 2020-07-02 Impact factor: 3.333
Authors: Amy Dixon; Edward J Hall; Sophie Adamantos; Aarti Kathrani; Ciara McGrath; Vicki Black Journal: J Vet Intern Med Date: 2021-02-01 Impact factor: 3.333