Peer-reviewed veterinary case report
Blood clotting risks in dogs with ACTH-related Cushing's disease
By Park, F M et al.·Published in Journal of veterinary internal medicine·2013·Department of Clinical Studies, Canada·View original on PubMed →
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Original publication title: Hypercoagulability and ACTH-dependent hyperadrenocorticism in dogs.
- Species:
- dog
Plain-English summary
Nineteen dogs with a condition called ACTH-dependent hyperadrenocorticism (ADHAC) were studied to see how their blood clotting ability was affected before and after treatment with a medication called trilostane. These dogs showed signs of increased blood clotting risk, which could lead to serious complications like blood clots. Even after starting treatment, they remained at a higher risk for clotting issues. The study found that while their platelet counts and certain blood proteins increased, a specific deficiency in antithrombin (a protein that helps prevent clots) was not a factor in their condition.
People also search for: dog hyperadrenocorticism treatment · dog blood clotting problems · trilostane for dog Cushing's disease
Abstract
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.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/24033421/