A 68-year-old man comes to the office due to a 4-week history of progressive fatigue, trem… — USMLE Step 2 CK

A $68$ -year-old man comes to the office due to a $4$ -week history of progressive fatigue, tremors, and a $5$ -kg ( $11$ -lb) weight loss. His medical history is significant for ischemic cardiomyopathy with a left ventricular ejection fraction of $35\%$ and recurrent sustained ventricular tachycardia. His medications include amiodarone, metoprolol, lisinopril, and spironolactone. His pulse is $112$ /min and irregular, and blood pressure is $134/82$ mm Hg. Physical examination reveals a fine bilateral hand tremor and hyperreflexia. The thyroid gland is normal in size and non-tender on palpation. There is no proptosis or pretibial myxedema.

Laboratory results are as follows:

Laboratory Test	Result	Reference Range
Thyroid-stimulating hormone (TSH)	$<0.01$ $\mu$ U/mL	$0.4-4.0$ $\mu$ U/mL
Free thyroxine (T4)	$4.2$ ng/dL	$0.7-1.9$ ng/dL
Free triiodothyronine (T3)	$6.8$ pg/mL	$2.0-4.4$ pg/mL

Color flow Doppler ultrasonography of the thyroid shows a structurally normal gland with markedly decreased vascularity. A $24$ -hour radioactive iodine uptake scan reveals $<1\%$ uptake.

Which of the following is the most appropriate next step in the management of this patient's thyroid condition?

Initiation of oral prednisone therapyAnswer
B
Initiation of methimazole therapy
C
Immediate discontinuation of amiodarone and observation
D
Administration of radioactive iodine 131
E
Initiation of levothyroxine therapy

Answer

Initiation of oral prednisone therapy

This patient has amiodarone-induced thyrotoxicosis (AIT) Type 2. Amiodarone can cause thyrotoxicosis via two distinct mechanisms. Type 1 AIT occurs in patients with underlying autonomous thyroid tissue (e.g., nodular goiter) where the massive iodine load fuels excess hormone synthesis; this presents with normal or increased vascularity on Doppler ultrasound. In contrast, Type 2 AIT is a destructive thyroiditis occurring in normal thyroid glands, causing the release of preformed thyroid hormones. It is characterized by structurally normal glands with decreased or absent vascular flow on color Doppler. Because Type 2 is an inflammatory, destructive process, the first-line treatment is systemic glucocorticoids (e.g., prednisone) to reduce inflammation. Note that a

24

-hour radioactive iodine uptake scan is low (

<1\%

) in both types due to saturation of the iodine pool by amiodarone, making the Doppler ultrasound the critical distinguishing test.

Step-by-Step Solution

Interpret the laboratory findings.

The patient has a suppressed TSH with elevated free T4 and free T3, confirming thyrotoxicosis.

Establishing the biochemical diagnosis is the first step in localizing the pathology.

Identify the underlying etiology based on medication history.

The patient is taking amiodarone, an iodine-rich antiarrhythmic drug that can cause amiodarone-induced thyrotoxicosis (AIT).

Amiodarone is a common trigger for thyroid dysfunction and alters standard diagnostic and treatment pathways.

Differentiate between AIT Type 1 and AIT Type 2 using imaging results.

Color flow Doppler ultrasound shows decreased vascularity, which confirms AIT Type 2 (destructive thyroiditis) rather than Type 1 (hyperthyroidism/increased vascularity).

Radioactive iodine uptake is low in both types due to the massive iodine load, making Doppler ultrasound the crucial distinguishing test.

Select the appropriate targeted therapy for AIT Type 2.

Glucocorticoids (such as prednisone) are indicated to treat the inflammatory destructive process.

Unlike Type 1 which requires antithyroid drugs to block synthesis, Type 2 is driven by preformed hormone release from tissue destruction, which responds to steroids.

Key Concept

Amiodarone-induced thyrotoxicosis (AIT) Type 2 is a destructive thyroiditis characterized by decreased vascularity on color Doppler ultrasound, and it is managed primarily with systemic glucocorticoids.

Estimated Time:1m 30s

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