Phase of usual Graves' disease (first to fourth row of images)

A 73-year-old woman was referred for typical complaints suggesting thyrotoxicosis. Graves' hyperthyroidism was diagnosed and methimazole therapy was started. Considering the degree of thyroid enlargement we offered surgery, but the patient refused our suggestion. We mention that radioiodine therapy was contraindicated because the patient had urinary incontinency. The details of laboratory tests and therapy are presented in Table. 13 months after the initial examination the patient was well, euthyroid and we ended the thyrostatic therapy.

Two months after the discontinuation of the thyroid therapy the patient got a severe heart attack with a cardiac arrest. She had to be resuscitated. A congestive heart failure developed. Amiodarone was initiated 2 months after the myocardial infarction. TSH test just before starting with Amiodarone resulted in 0.87 mIU/L.

Phase of amiodarone induced thyrotoxicosis (fifth and sixth row of images)

Clinical data: The patient felt relatively well for 5 weeks. Thereafter the patient noticed signs of hyperthyroidism and her cardiac status worsened suddenly. She was admitted to the intensive care unit.

Palpation: Both lobes were firm and extremely enlarged

Laboratory examination: hyperthyroidism (TSH undetectable, FT4 >100 pM/L, TSAb 20.9 U/L). Erythrocyte sedimentation rate and CRP were in the normal range.

Ultrasonography: The thyroid became extremely enlarged and hypoechogenic. A so-called vascular inferno was detected on Doppler mode.

Cytology: benign with signs of hyperfunction.

Clinical diagnosis: type 1 amiodarone-induced thyrotoxicosis.

We suggested daily 60 mg methimazole and daily 0.8 g potassium-perchlorate and large dose of steroid. 4 days later the patient died.

Summary of thyroid therapy and thyroid function tests.

Date of examination	Volume of the thyroid (mL)	Therapy before actual examination	Laboratory tests			Suggestion after actual examination
			TSH (mIU/L)	FT4 (pM/L)	TSAb (U/L)
Initial examination	38.9	Nothing	0.001	50.1	7.2	30 mg methimazole
1.5 month after init. exam.	22.4	30 mg methimazole	0.06	18,5	-	15 mg methimazole
4 months after init. exam.	22.6	15 mg methimazole	2.01	11.1	-	10 mg methimazole
7 months after init. exam.	28.5	10 mg methimazole	17.2	7.08	-	10 mg methimazole + 50 ug levothyroxine
14 months after in. exam.	23.4	5 mg methimazole + 75 ug l-tiroxine	2.75	14.4	0	Nothing
18 months after in. exam.	132	Nothing	0.001	> 100	20.9	60 mg methimazole+0.8 g potassium-perchlorate

 

Comments.

1. Amiodarone-induced thyrotoxicosis type 1 is caused by the excess load of iodine released from Amiodarone. The cause for elevated thyroid hormones is not destruction but increased thyroid hormone synthesis. This form of thyrotoxicosis may occur in thyroids with pre-existing thyroid disorder like in this patient.

2. Note the significant difference in the vascularization and the size of the thyroid between the first "usual" and the second Amiodarone-induced attack of thyrotoxicosis. We never ever saw in our 25 years practice such difference in thyroid volume between first and recurrent hyperthyroidism in any of our patients. We suppose that the iodine excess itself and the iodine-induce relapse of Graves' disease were responsible for the second attack.

3. This patient presented the typical course of Graves' disease as regards the sonographic pattern, the size of the thyroid and the vascularization.