This study was presented in part at the 2012 American College of Veterinary Internal Medicine Forum, New Orleans, LA
Hypercoagulability and ACTH-Dependent Hyperadrenocorticism in Dogs
Version of Record online: 26 AUG 2013
Copyright © 2013 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 27, Issue 5, pages 1136–1142, September/October 2013
How to Cite
Park, F.M., Blois, S.L., Abrams-Ogg, A.C.G., Wood, R.D., Allen, D.G., Nykamp, S.G. and Downie, A. (2013), Hypercoagulability and ACTH-Dependent Hyperadrenocorticism in Dogs. Journal of Veterinary Internal Medicine, 27: 1136–1142. doi: 10.1111/jvim.12162
- Issue online: 13 SEP 2013
- Version of Record online: 26 AUG 2013
- Manuscript Accepted: 16 JUL 2013
- Manuscript Revised: 23 MAY 2013
- Manuscript Received: 18 JAN 2013
- Ontario Veterinary College Pet Trust Fund
- Cushing's disease;
Dogs with hyperadrenocorticism are at risk of thromboembolic disease, which might be caused by an underlying hypercoagulable state.
To assess hemostatic function in dogs with ACTH-dependent hyperadrenocorticism (ADHAC) before and after treatment.
Nineteen dogs with ADHAC and 40 normal dogs.
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).
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.