Clinical data: A 59-year-old man was referred for an evaluation of hyperthyroidism. The patient was treated with amiodarone for 2 years. Over this period the TSH gradually decreased. On the last occasion 3 month earlier, subclinical hyperthyroidism was detected (TSH 0.08 mIU/L and FT4 18.1 pM/L). The patient lost 5 kg in weight and had fatigue. He noticed neither TAO nor neck complaints.

Palpation: the thyroids were moderately firm and painless.

Laboratory examination: hyperthyroidism (TSH undetectable, FT4 63.9 pM/L). Anti-TPO and TSAb were normal. Erythrocyte sedimentation rate was not elevated (9 mm/H). Anti-TPO level was 49 U/mL, while TSAb was not detectable.

Ultrasonography: The thyroid was minimally hypoechogenic and contained numerous moderately hypoechogenic areas with ill-defined borders. The vascularization was decreased.

Cytology: benign lesion without signs of thyroiditis.

Clinical diagnosis: amiodarone-induced thyrotoxicosis (AIT) type II or combined form.

Suggestion: daily 32 mg methylprednisolone with decreasing the dose with 8 mg every fifth day.

Summary of follow-up

Four weeks later the FT4 level although decreased but was far from the normal (44.5 pM/L). The steroid was discontinued and daily 30 mg methimazole was given.

Another four weeks later the FT4 level was unchanged. 8 mg steroid and daily 10 to 20 mg methimazole was administered.

In the next six months the FT4 level was in all but one occasion in the normal range, while the TSH has gradually normalized. On the last visit the patient was already euthyroid on 8 mg methylprednisolone every second day and daily 10 mg methimazole. The ultrasound pattern remained unchanged.

Two months after the last visit the patient died of acute myocardial infarction.

Comment.

1. This patient had combined type 1 and type 2 amiodarone-induced thyrotoxicosis with great probability. The decreased vascularization and the effect of steroid stand for a destructive, type 2 form, while the degree of hyperthyroidism, the normal sedimentation rate and the lack of steroid therapy to completely resolve hyperthyroidism argue for type 1 form.

2. While the gray-scale mode was not fully convincing, the almost absent vascularity had significantly role in the differential diagnostic.