Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 34 P396 | DOI: 10.1530/endoabs.34.P396

SFEBES2014 Poster Presentations Thyroid (51 abstracts)

A highly exaggerated response to Warfarin therapy in a patient with thyrotoxicosis

Tolulope Shonibare , Elizabeth Berkin , Bernard Chang & Ramzi Ajjan


Department of Endocrinology and Diabetes, St James University Hospital, Leeds, UK.


Case history: A 22-year-old lady was referred to the thyroid eye clinic with bilateral proptosis following a routine visit to the opticians. She had a 2-year history of thyrotoxic symptoms, which had been getting worse over the past 4 months.

She had signs of severe thyrotoxicosis and was clinically in atrial fibrillation (AF) with a central heart rate of 195 beats/min. Neck palpation revealed a moderate-sized smooth and symmetrical goitre with no bruits or lymphadenopathy. There was evidence of active thyroid eye disease with a clinical disease activity score of 3. Her investigations revealed a free T4 109.8 pmol/l, total T3>12.3 nmol/l and TSH < 0.05 mIU/l. Her TSH-R antibodies were positive at 100 U/l, consistent with a diagnosis of Graves’ disease, and her electrocardiogram (ECG) confirmed AF. She was commenced on carbimazole 20 mg three times daily and 40 mg/day of prednisolone was added for the management of thyroid eye disease. Following advice from cardiology, she was started on 5 mg bisoprolol and warfarin was added using the standard Fennerty protocol. Her INR after three doses of warfarin was 18.7 but the patient remained asymptomatic. Warfarin was stopped and the dose was subsequently adjusted to achieve an INR between 2 and 3. She became euthyroid in 6 weeks and reverted spontaneously into stable sinus rhythm, confirmed by 24 h ECG.

Discussion: A limited number of reports have shown an increased sensitivity to oral anticoagulants in thyrotoxicosis, but to our knowledge, this case represents the most extreme case described to date. The mechanism remains unclear, although some have suggested thyroxine induced alteration in clotting factor and/or altered metabolism of warfarin. In our patient, the INR was nearly tenfold above the therapeutic range, despite being induced on the standard Fennerty warfarin protocol. This highlights the need for a different anticoagulation regimen in patients with thyrotoxicosis and AF. We suggest more frequent and earlier checks of INR in cases where warfarin therapy is required in patients with hyperthyroidism, particularly in those with severe thyrotoxicosis.

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