Question

Difficulty: HardEndocrinology and Metabolism

A 29-year-old woman comes to the clinic due to a 3-month history of intermittent heart palpitations, excessive sweating, and a 6-kg (13-lb) weight loss. She feels anxious and has had difficulty sleeping. The patient has no significant past medical history and takes no prescription medications. She works as a fitness instructor and admits to taking several online dietary supplements to "boost her metabolism." Her temperature is 37.1°C (98.8°F), blood pressure is 135/85 mm Hg, and pulse is 112/min. Physical examination reveals a fine tremor of the outstretched hands. Her thyroid gland is nonpalpable, and there is no exophthalmos or pretibial myxedema. Laboratory results show:

Laboratory TestResultReference Range
Thyroid-stimulating hormone (TSH)0.01 µU/mL0.4 - 4.0 µU/mL
Free T40.5 ng/dL0.9 - 1.7 ng/dL
Free T37.2 pg/mL2.0 - 4.4 pg/mL

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

  1. A
    Exogenous ingestion of thyroxine
  2. B
    Autoantibody stimulation of the thyrotropin receptor
  3. Exogenous ingestion of triiodothyronineAnswer
  4. D
    Inflammatory destruction of thyroid follicles
  5. E
    Compression of thyrotroph cells by a sellar mass

Answer

Exogenous ingestion of triiodothyronine
The correct answer is exogenous ingestion of triiodothyronine (T3). This patient presents with clinical signs of thyrotoxicosis (tachycardia, tremor, sweating, weight loss). The laboratory results show a suppressed TSH and elevated Free T3, confirming hyperthyroidism. However, the Free T4 is surprisingly low. This specific pattern—suppressed TSH, low Free T4, and high Free T3—is the hallmark of factitious thyrotoxicosis caused by liothyronine (T3) abuse, often found in 'metabolism-boosting' weight loss supplements. The high circulating exogenous T3 exerts negative feedback on the anterior pituitary, severely suppressing TSH secretion. Without TSH stimulation, the endogenous thyroid gland halts production of both T4 and T3, leading to glandular atrophy (resulting in a nonpalpable thyroid on exam). Because T3 cannot be reverse-converted to T4 in the periphery, the serum Free T4 level falls below normal, while the Free T3 level remains high due to the exogenous intake.

Step-by-Step Solution

1
Evaluate the clinical presentation.
The patient has classic signs of thyrotoxicosis, including tachycardia, weight loss, tremor, and diaphoresis, along with a nonpalpable thyroid gland.
Establishing the clinical state (hyperthyroid vs. hypothyroid) is essential before interpreting the lab values.
2
Interpret the thyroid function tests.
TSH is suppressed, confirming the thyrotoxic state. Free T3 is markedly elevated, but Free T4 is abnormally low.
This specific dissociation (low T4 with high T3) narrows down the differential diagnosis significantly.
3
Correlate lab findings with pathophysiology to determine the underlying cause.
The combination of thyrotoxicosis, suppressed TSH, high Free T3, low Free T4, and a nonpalpable thyroid gland exclusively points to exogenous triiodothyronine (T3) use.
Exogenous T3 suppresses TSH. The lack of TSH stimulation leads to thyroid follicular atrophy (nonpalpable gland) and ceased endogenous T4 production. Since the body does not convert T3 back into T4, serum T4 levels drop while T3 remains high due to the supplements.

Key Concept

Diagnosis of factitious thyrotoxicosis due to exogenous liothyronine (T3) ingestion.

Alternative Method

When evaluating thyrotoxicosis without a palpable goiter, one can categorize by T4 levels: if T4 is high, consider thyroiditis or exogenous T4 (differentiate via thyroglobulin). If T4 is low but T3 is high, it is almost exclusively exogenous T3.
Estimated Time:1m 15s
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