Abstract

BackgroundHyperthyroid cats might have a predisposition to arterial thrombus formation. The mechanism for thrombogenesis currently is unknown but could be associated with systemic hypercoagulability as seen in hyperthyroid humans.ObjectiveOur purpose was to evaluate markers of hemostasis in hyperthyroid cats compared to healthy cats, and in hyperthyroid cats before and after radioactive iodine treatment (RIT).AnimalsTwenty‐five cats with hyperthyroidism and 13 healthy euthyroid cats >8 years of age.MethodsProthrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, antithrombin (AT), D‐dimers, thrombin‐antithrombin complexes (TAT), von Willebrand Factor antigen (vWF : Ag), and activity of factors VIII and IX were measured. An echocardiogram was performed in all cats. Hemostatic markers and echocardiogram were evaluated again 6 to 9 months after successful RIT in 7 cats.ResultsHyperthyroid cats had higher fibrinogen concentration (P < .0001), AT activity (P < .0001), and vWF : Ag concentration (P = .01) than healthy control cats with all results decreasing significantly post‐RIT. Hyperthyroid cats were not more likely to be in a hypercoaguable state than euthyroid cats (P = .08). Serum T4 concentration was not a predictor of a hypercoagulable state (P = .53).Conclusions and Clinical ImportanceHyperthyroid cats have evidence of altered hemostasis that does not appear to be solely attributable to cardiac abnormalities, but no evidence of a hypercoagulable state. Findings suggest altered hemostasis resolves after RIT. Hyperthyroid cats could have endothelial dysfunction as indicated by increased vWF : Ag which could potentiate thrombogenesis.

Highlights

  • Hyperthyroid cats are predisposed to thrombus formation

  • The purpose of this study was to evaluate markers of hemostasis in hyperthyroid cats compared to healthy cats, and in hyperthyroid cats before and after treatments with radioactive iodine (RIT)

  • There is a significant likelihood of being in hypercoagulable state based on hyperthyroid state (P = 0.019) and serum T4 level is significantly associated with predicating hypercoagulability (P = 0.043)

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Summary

Introduction

Hyperthyroid cats are predisposed to thrombus formation. The mechanism for thrombogenesis is currently unknown, but could be associated with altered hemostasis as seen in hyperthyroid humans. Elevations in PK, HMWK, factor XIIa and bradykinin were demonstrated, which are markers of contact surface activation.[167] Thyroid hormone receptor b (THRB) expression in endothelial cells has been previously documented.[168] Unaltered parameters of fibrinolysis and coagulation have been seen in a cohort of patients with resistance to thyroid hormone despite circulating elevated thyroxine suggesting procoagulant effects mediated via a THRB-dependent pathway showing further alteration of the vascular endothelium.[77] Endothelial associated proteins, including vWF, have been demonstrated to be increased in hyperthyroid humans.

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