A 78-year-old man had a history of atrial fibrillation since 1997 and
was placed on amiodarone 200 mg per day in 2005. He was admitted earlier this
year with mild congestive heart failure associated with rapid AF. His initial
evaluation revealed biochemical changes of hyperthyroidism but, aside from the
AF, the only other clinical manifestation of hyperthyroidism was a 4 lb weight
loss during the last month. In the elderly, it is not unusual for
hyperthyroidism to present with only a few of the classic symptoms of an
A radionuclide scan failed to demonstrate any uptake in the thyroid
consistent with amiodarone-induced thyroiditis an acute inflammation of
the thyroid with outpouring of triiodothyronine and thyroxine. The mechanism is
an overload of iodine stores and may occur in patients with or without known
Everything about this case is straightforward. Problems arise when
considering management, and opinions among my colleagues were diametrically
opposed to each other. Should the acute inflammation be controlled with
steroids? Should the hyperthyroidism be controlled with anti-thyroid
medication? Should the patient receive therapy with both? Should amiodarone be
continued, gradually tapered, or abruptly stopped?
From the patients perspective at least one answer was easy
he was so troubled by his AF that he was reluctant to discontinue amiodarone,
but he did agree to tapering therapy.
The literature1, 2 on this topic is confusing. You can find articles to
support all of the proposed approaches. I elected to taper amiodarone (the
cardiologist had no concerns with this), begin methimazole, and 10 mg
He was a very patient patient and put up with frequent lab testing and
adjustments to therapy just as long as his AF was not symptomatic. There is as
little consensus about discontinuing therapy as the thyroiditis abates as there
is about initiating therapy. Amiodarone was first to go, followed by the
prednisone, and much more gradually, the methimazole. The graphs below attest
to the time it took to restore a euthyroid state. For now the patient still has
AF but not to a point where he is worried by symptoms, nor where his
cardiologist is considering intervention.
Will he ultimately become hypothyroid? Unlikely, but by no means
For more information:
1. Tsang W. Can J Cardiol. 2009;25(7):421-424. PMID: 19584973.
2. Piga M. Minerva Endocrinol. 2008;33(3):213-228. PMID: 18846027.