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Is Thyroid Hormone Suppression Therapy Prothrombotic?

Department of Laboratory Medicine (M.K.H., K.G.R., P.K.M., A.C., R.C., G.C.), Pharmacy Department (K.K.S., F.P.), and Biostatistics and Clinical Epidemiology Service (R.W.), Warren G. Magnuson Clinical Center; the National Institute of Diabetes and Digestive and Kidney Diseases (M.C.S., T.E.); Office of the Director (A.P.); and the National Cancer Institute (D.M.B.), The National Institutes of Health, Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: McDonald Horne, M.D., Department of Laboratory Medicine, National Institutes of Health, Building 10, Room 2C-306, Bethesda, Maryland 20892. E-mail: MHorne{at}mail.cc.nih.gov.

The purpose of this study was to determine whether chronic thyroid hormone suppression therapy (THST) is prothrombotic.

We obtained blood samples from 14 thyroid cancer patients while on THST and after they had become hypothyroid for radioiodine whole-body scanning and therapy. Prothrombin fragment 1 + 2, fibrinogen, factor VIII, antithrombin, tissue plasminogen activator antigen (tPA), plasminogen activator inhibitor 1 (PAI-1), PAI-1/tPA, and C-reactive protein were significantly (P < 0.05) higher in the hyper- than in the hypothyroid state, whereas protein C and plasmin-antiplasmin complexes were significantly lower during the hyperthyroid period. When the 10 female patients were hyperthyroid, their levels of prothrombin fragment 1 + 2, fibrinogen, protein S, antithrombin, tPA, PAI-1, and PAI-1/tPA were significantly higher (P 0.05) than in healthy female controls, whereas when the female patients were hypothyroid, their antithrombin and plasmin-antiplasmin were lower and their protein S was higher than in controls. Factor II, plasminogen, and D-dimer were not significantly affected by the thyroid status in either assessment.

In conclusion, we found evidence that the majority of patients treated with THST have a prothrombotic profile.

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