Mixed Amiodarone-Induced Thyrotoxicosis Refractory to Medical Therapy and Plasmapheresis

Anupam Kotwal, Basel Touchan, Kavita Y. Seetharaman, Richard Allen Haas, Marie Lithgow, Samir Malkani


Amiodarone-induced thyrotoxicosis (AIT) is associated with increased mortality in older individuals with impaired ventricular function, underlying the importance of rapid restoration and maintenance of euthyroidism. Plasmapheresis for treating thyrotoxicosis has shown mixed results. A 61-year-old gentleman was hospitalized for progressively worsening dyspnea, palpitations, tremor and generalized weakness. He had a history of atrial fibrillation, coronary artery disease, heart failure and type 2 diabetes. He had been diagnosed with AIT 4 months prior to admission, after which amiodarone was discontinued, and he was started on prednisone and methimazole which was later changed to propylthiouracil. Physical examination revealed irregular tachycardia, lid lag, fine hand tremor, proximal muscle weakness, pedal edema and a small, smooth, non-tender thyroid gland without bruit. Hormonal investigations revealed low TSH of 0.02 mcr IU/mL (reference: 0.28 - 3.89), high free T4 of 4.88 ng/dL (reference: 0.58 - 1.64), high free T3 of 5.4 pg/mL (reference: 2.5 - 3.9) and normal total T3 of 114 ng/dL (reference: 87 - 178). Thyroglobulin antibody, thyroid peroxidase antibody and thyroid stimulating immunoglobulin were undetectable. Echocardiogram revealed reduced left ventricle ejection fraction of 25%. Ultrasound showed a bilaterally heterogeneous, hypovascular and hypoechoic thyroid. I-123 scan revealed very low uptake. These findings were suggestive of destructive type 2 AIT. However, the lack of a good response to steroids argued for type 1 AIT. Given his poor response to medical therapy and increased cardiovascular risk for an urgent thyroidectomy, plasmapheresis was instituted in an attempt to lower the thyroid hormone levels. Eight daily cycles provided only modest clinical and biochemical improvement. Subsequently, he underwent total thyroidectomy leading to improvement of thyrotoxicosis. Histopathology of the thyroid demonstrated intrafollicular histiocytes, patchy fibrosis and involuted follicles, suggestive of destructive thyroiditis. On follow-up 2 months later, he remained clinically euthyroid on levothyroxine replacement with stable cardiac status. This case represents mixed/indeterminate AIT of protracted duration refractory to thionamides and steroids. Plasmapheresis did not provide clinical improvement and only modestly lowered the free T4 level. Euthyroidism was finally achieved following total thyroidectomy. This finding suggests the limitations of utilizing plasmapheresis as a therapeutic modality prior to definitive treatment in AIT.

J Endocrinol Metab. 2015;5(3):220-223
doi: http://dx.doi.org/10.14740/jem278w


Amiodarone; Thyrotoxicosis; Plasmapheresis; Thyroidectomy; Euthyroidism

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