Comparison of coagulation patterns in dogs with Cushing syndrome and prednisolone treatment assessed by thromboelastography.

Both Cushing syndrome and prednisolone therapy cause hypercoagulability in dogs, but via distinct coagulation mechanisms.

This cross-sectional study compared coagulation profiles in dogs with naturally occurring hyperadrenocorticism (Cushing syndrome, CS) versus dogs receiving exogenous prednisolone (PDS ≥0.25 mg/kg/d for ≥3 weeks) using thromboelastography (TEG). Twenty-nine dogs were divided into control (n=8), CS (n=12), and PDS (n=9) groups. TEG parameters assessed included reaction time (R), clot formation time (K), α-angle, maximum amplitude (MA), and clot strength (G). Both the CS and PDS groups demonstrated hypercoagulable states compared to controls, evidenced by significantly elevated MA and G values, indicating increased clot strength. Both experimental groups also showed shorter K values than controls, reflecting accelerated clot formation kinetics. Notably, the PDS group exhibited uniquely shorter R times compared to both controls and the CS group, suggesting faster initiation of coagulation in exogenous glucocorticoid excess. Platelet count showed opposing correlations with MA and G between the two groups, implying different underlying mechanisms driving hypercoagulability in endogenous versus exogenous glucocorticoid excess. These findings suggest that while both conditions predispose dogs to thrombosis, the pathophysiological mechanisms differ, with exogenous steroid administration producing more rapid clot initiation. Clinicians should consider functional coagulation monitoring, such as TEG, rather than relying solely on standard coagulation panels, to better characterize thrombotic risk and tailor thromboprophylactic strategies in dogs with either CS or receiving long-term glucocorticoid therapy.

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