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Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
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Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
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Hypercoagulability and ACTH-dependent hyperadrenocorticism in dogs.

F M Park1, S L Blois, A C G Abrams-Ogg

  • 1Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON.

Journal of Veterinary Internal Medicine
|September 17, 2013
PubMed
Summary
This summary is machine-generated.

Dogs with ACTH-dependent hyperadrenocorticism (ADHAC) show hypercoagulability, increasing their risk of blood clots. This hypercoagulable state persists even after treatment with trilostane.

Keywords:
Cushing's diseaseHemostasisPlateletThrombelastographyThromboembolism

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Area of Science:

  • Veterinary Internal Medicine
  • Canine Endocrinology
  • Hemostasis and Thrombosis

Background:

  • Hyperadrenocorticism (Cushing's disease) in dogs is linked to an increased risk of thromboembolic disease.
  • The underlying cause may involve a hypercoagulable state, affecting blood clotting.
  • Understanding hemostatic changes is crucial for managing affected dogs.

Purpose of the Study:

  • To evaluate hemostatic function in dogs with ACTH-dependent hyperadrenocorticism (ADHAC).
  • To assess changes in coagulation parameters before and after treatment with trilostane.
  • To investigate the role of antithrombin (AT) in the hypercoagulable state of ADHAC.

Main Methods:

  • A prospective, observational study involving 19 dogs with ADHAC and 40 healthy controls.
  • Hemostasis was assessed using kaolin-activated thrombelastography with platelet mapping (TEG-PM), prothrombin time, activated partial thromboplastin time, fibrinogen, and antithrombin activity.
  • Assessments were performed before treatment (T0) and at 3 (T3) and 6 (T6) months post-trilostane therapy.

Main Results:

  • Dogs with ADHAC exhibited significant thrombelastographic evidence of hypercoagulability (increased α-angle, maximum amplitude; decreased κ) at all time points.
  • Elevated platelet counts and fibrinogen concentrations were observed in dogs with ADHAC.
  • Antithrombin activity did not differ significantly and was not found to be deficient.

Conclusions:

  • Dogs with ADHAC demonstrate a persistent hypercoagulable state, detectable by thrombelastography.
  • This hypercoagulability continues throughout trilostane treatment.
  • Antithrombin deficiency is unlikely to be a primary factor in the hypercoagulability associated with ADHAC.