A 28-year-old female nurse is evaluated in the clinic for a 6-week history of palpitations… — USMLE Step 2 CK

A 28-year-old female nurse is evaluated in the clinic for a 6-week history of palpitations, insomnia, irritability, and a $4$ -kg ( $8.8$ -lb) weight loss. She denies any preceding viral illnesses, neck pain, or changes in vision. Her temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure is $134/74\ \text{mmHg}$ , and pulse is $112/\text{min}$ . Physical examination reveals an anxious-appearing woman with a fine resting tremor of the outstretched hands. Her skin is warm and diaphoretic. The thyroid gland is nonpalpable and nontender. There is no proptosis or extraocular muscle weakness. Laboratory studies show the following:

Thyroid-stimulating hormone (TSH): $< 0.01\ \mu\text{U/mL}$ (Normal: $0.5$ - $5.0\ \mu\text{U/mL}$ )
Free thyroxine (T4): $0.4\ \text{ng/dL}$ (Normal: $0.9$ - $1.7\ \text{ng/dL}$ )
Total triiodothyronine (T3): $310\ \text{ng/dL}$ (Normal: $80$ - $200\ \text{ng/dL}$ )

Which of the following is the most likely cause of this patient's symptoms?

Ingestion of exogenous triiodothyronineAnswer
B
Pituitary thyrotroph failure
C
Autoimmune thyrotropin receptor stimulation
D
Viral-induced thyroid follicular destruction
E
Ingestion of exogenous thyroxine

Answer

Ingestion of exogenous triiodothyronine

The correct answer is ingestion of exogenous triiodothyronine (liothyronine). This patient has undeniable clinical thyrotoxicosis (weight loss, palpitations, tremor, suppressed TSH). However, the etiology of the thyrotoxicosis must be deduced from the specific hormone profile. A suppressed TSH with an elevated T3 but a low free T4 is the classic signature of exogenous T3 ingestion. The ingested T3 enters the circulation, causing systemic thyrotoxicosis and exerting strong negative feedback on the hypothalamus and pituitary. This suppresses TSH secretion. Without TSH to stimulate the endogenous thyroid gland, endogenous production of T4 ceases, resulting in a subnormal serum free T4 level. The lack of a palpable goiter further points toward an exogenous source (factitious thyrotoxicosis), which is more commonly seen in healthcare workers.

Step-by-Step Solution

Identify the patient's clinical metabolic state.

The patient exhibits classic signs and symptoms of thyrotoxicosis, including tachycardia, weight loss, tremor, and diaphoresis.

Establishing the clinical state is essential to differentiate between true thyrotoxicosis and laboratory artifacts or other endocrine disorders.

Interpret the thyroid function tests.

The TSH is profoundly suppressed, Free T4 is abnormally low, and Total T3 is markedly elevated.

The combination of these three values forms a specific pattern that identifies the source of the thyroid hormone excess.

Integrate the clinical presentation with the laboratory pattern.

The thyrotoxicosis is driven exclusively by high T3. The low TSH indicates appropriate negative feedback, and the low T4 indicates that the thyroid gland is not actively producing hormone.

If the thyroid were hyperactive (e.g., Graves disease or toxic nodule) or releasing preformed hormone (e.g., thyroiditis), both T4 and T3 would be elevated.

Determine the etiology based on the isolated T3 excess and nonpalpable thyroid.

The findings are diagnostic of exogenous triiodothyronine (liothyronine) ingestion.

Exogenous T3 causes thyrotoxic symptoms and suppresses pituitary TSH. Without TSH stimulation, endogenous thyroid gland T4 production ceases, leading to the characteristic low Free T4 level.

Key Concept

Factitious thyrotoxicosis due to exogenous triiodothyronine (T3) abuse presents with clinical thyrotoxicosis, a suppressed TSH, an elevated T3 level, and characteristically low free T4 levels due to suppressed endogenous thyroid function.

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