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Difficulty: HardEndocrinology and Metabolism

An occupational health physician evaluates a 28-year-old registered nurse who recently transitioned to working night shifts. She complains of persistent palpitations, a 4-kg (8.8-lb) weight loss over the past month, and severe anxiety. The patient states she has felt immense pressure to maintain a slim physique for an upcoming family event. Her temperature is 37.1°C (98.8°F), blood pressure is 138/78 mm Hg, and resting pulse is 112/min. On physical examination, her skin is warm and moist. Extraocular movements are intact, and there is no lid lag or proptosis. The thyroid gland is nonpalpable and non-tender. A fine tremor is noted when her arms are outstretched.

Initial laboratory testing demonstrates:

TestPatient ValueReference Range
Thyroid-stimulating hormone (TSH)<0.01 mU/L0.4–4.0 mU/L
Free thyroxine (T4)0.5 ng/dL0.9–1.7 ng/dL
Total triiodothyronine (T3)280 ng/dL80–200 ng/dL

What is the most likely explanation for this patient's clinical and laboratory findings?

  1. Surreptitious ingestion of liothyronineAnswer
  2. B
    Surreptitious ingestion of levothyroxine
  3. C
    Autoantibody stimulation of the thyrotropin receptor
  4. D
    Release of preformed hormone due to viral inflammation
  5. E
    Autonomous hormone release from ectopic ovarian tissue

Answer

Surreptitious ingestion of liothyronine (synthetic T3)
The correct answer is surreptitious ingestion of liothyronine. This patient, a healthcare worker with pressure to lose weight, presents with classic signs of thyrotoxicosis (tachycardia, weight loss, anxiety, tremor). Her laboratory profile reveals a highly specific pattern: elevated T3, suppressed TSH, and abnormally low free T4. Liothyronine is synthetic T3. When taken exogenously, it rapidly enters the bloodstream and causes systemic thyrotoxicosis. It also exerts strong negative feedback on the hypothalamus and anterior pituitary, leading to profound suppression of TSH. Without TSH stimulation, the endogenous thyroid gland ceases its normal production of thyroxine (T4). Consequently, the patient will have a high circulating T3 level but a subnormal free T4 level. The absence of a palpable goiter further supports an exogenous source.

Step-by-Step Solution

1
Analyze the patient's clinical presentation.
The patient exhibits systemic signs of thyrotoxicosis, including tachycardia, significant weight loss, fine tremor, and severe anxiety.
Identifying the clinical hypermetabolic state sets the context for interpreting the laboratory findings.
2
Interpret the thyroid laboratory panel in the context of her symptoms.
TSH is profoundly suppressed, total T3 is significantly elevated, but free T4 is abnormally low.
A complete thyroid panel is necessary to differentiate the primary source of the thyrotoxicosis.
3
Synthesize the clinical and laboratory data with the physical exam findings.
The combination of thyrotoxicosis with high T3, low TSH, low T4, and a nonpalpable thyroid points to an exogenous T3 source.
Exogenous T3 suppresses pituitary TSH secretion, which halts endogenous thyroid gland production of T4, resulting in low serum T4 levels.

Key Concept

Exogenous liothyronine (T3) ingestion causes thyrotoxicosis with elevated T3, suppressed TSH, and suppressed endogenous free T4 due to negative feedback on the hypothalamic-pituitary-thyroid axis.
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Topics

Endocrinology and Metabolism

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