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Difficulty: HardEndocrinology and Metabolism

Complaints of a racing heart, persistent heat intolerance, and frequent loose stools have brought a 31-year-old medical assistant to the clinic. She reports unintentionally losing 44 kg (8.88.8 lb) over the past month. She denies any neck pain, dysphagia, or recent viral illnesses. Her past medical history is unremarkable, and she denies taking any prescribed medications or over-the-counter supplements. Vital signs show a blood pressure of 138/78138/78 mm Hg and a regular pulse of 112112/min. Physical examination reveals an anxious-appearing woman with a fine, symmetric resting tremor in her outstretched fingers. The neck is supple, and the thyroid gland is not palpable. No proptosis or localized pretibial edema is noted.

Laboratory studies yield the following results:
- Thyroid-stimulating hormone (TSH): 0.020.02 μ\mu U/mL (Normal: 0.4−4.20.4-4.2 μ\mu U/mL)
- Free T4: 3.43.4 ng/dL (Normal: 0.8−1.80.8-1.8 ng/dL)
- Free T3: 6.26.2 pg/mL (Normal: 2.3−4.22.3-4.2 pg/mL)

A 24-hour radioactive iodine uptake scan demonstrates an uptake of 1%1\% (Normal: 15%−30%15\%-30\%).

Which of the following laboratory findings is most likely present in this patient?

  1. A
    Markedly elevated erythrocyte sedimentation rate
  2. B
    Elevated thyroid-stimulating immunoglobulin
  3. Decreased serum thyroglobulin concentrationAnswer
  4. D
    Elevated thyroid peroxidase antibodies
  5. E
    Markedly elevated serum thyroglobulin concentration

Answer

Decreased serum thyroglobulin concentration
This patient is experiencing thyrotoxicosis, as evidenced by her suppressed TSH and elevated free T4 and T3 levels. The critical branch point in her workup is the severely decreased 2424-hour radioactive iodine uptake (RAIU). A low RAIU indicates that the thyroid gland is not actively synthesizing hormone. The differential diagnosis for thyrotoxicosis with a low RAIU includes subacute (de Quervain) thyroiditis, painless (silent) thyroiditis, iodine-induced thyrotoxicosis, struma ovarii, and factitious (exogenous) thyrotoxicosis.

Subacute thyroiditis is ruled out by the absence of an exquisitely tender goiter and viral prodrome. Painless thyroiditis typically presents with a non-tender but palpable goiter. This patient's completely non-palpable thyroid gland and her access to medications as a medical assistant strongly point toward factitious thyrotoxicosis (surreptitious ingestion of thyroid hormone). In factitious thyrotoxicosis, the exogenous hormone suppresses TSH secretion, which in turn halts the endogenous production of both thyroid hormones and thyroglobulin. Consequently, serum thyroglobulin levels will be characteristically decreased. In contrast, all endogenous causes of low-uptake thyrotoxicosis (subacute thyroiditis, painless thyroiditis, struma ovarii) result in elevated serum thyroglobulin due to the destruction of thyroid follicles or ectopic production.

Step-by-Step Solution

1
Interpret the initial thyroid function tests and clinical presentation.
The patient has overt, TSH-suppressed thyrotoxicosis with a normal physical examination (no goiter, no exophthalmos).
To establish the baseline biochemical state and correlate it with the absence of typical autoimmune physical findings.
2
Analyze the radioactive iodine uptake (RAIU) scan results.
The RAIU is severely decreased (1%1\%).
To differentiate true hyperthyroidism (high uptake, indicating overproduction) from destructive or exogenous causes of thyrotoxicosis (low uptake).
3
Formulate a differential diagnosis for low-uptake thyrotoxicosis and match it to the patient's presentation.
The differential includes subacute thyroiditis (painful goiter), painless thyroiditis (non-tender goiter), struma ovarii (pelvic mass), and factitious thyrotoxicosis. The lack of neck pain, absence of a palpable goiter, and her profession (medical assistant) point to factitious (exogenous) thyrotoxicosis.
To systematically rule out competing etiologies based on key negative clinical findings.
4
Determine the confirmatory laboratory test pattern for the suspected diagnosis.
Exogenous intake of thyroid hormone suppresses TSH, which halts endogenous synthesis of thyroglobulin. Therefore, the serum thyroglobulin concentration will be decreased.
To definitively confirm factitious thyrotoxicosis and rule out endogenous destructive processes.

Key Concept

The measurement of serum thyroglobulin is the crucial next step in differentiating factitious (exogenous) thyrotoxicosis (low thyroglobulin) from endogenous destructive thyroiditides (elevated thyroglobulin) in patients presenting with thyrotoxicosis and a low radioactive iodine uptake.
Estimated Time:1m 30s
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Topics

Endocrinology and Metabolism

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