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1
Question:

A 34-year-old woman comes to the office due to an uncomfortable sensation of rapid heartbeat for the past few weeks.  She has had no chest pain or shortness of breath.  The patient reports that her anxiety level has been high recently due to stress at work, and she has lost close to 2 kg (4.4 lb) during this time.  Her last menstrual period was 5 days ago.  Medical history is unremarkable, and the patient takes no medications.  On examination, the thyroid gland is diffusely enlarged and nontender.  Laboratory results are as follows:

Complete blood count
Hemoglobin12.9 g/dL
Hematocrit39%
Platelets200,000/mm3
Leukocytes8,500/mm3
Serum chemistry
Sodium139 mEq/L
Potassium4.2 mEq/L
Chloride100 mEq/L
Bicarbonate25 mEq/L
Blood urea nitrogen10 mg/dL
Creatinine1.0 mg/dL
Calcium9.1 mg/dL
Glucose102 mg/dL
TSH <0.001 µU/mL
Free T4  4.6 ng/dL (normal: 0.9-2.4 ng/dL)

ECG shows sinus tachycardia at 120/min.  Radioactive iodine uptake is <5%, and serum titers of anti–thyroid peroxidase antibodies are elevated.  Which of the following is the most appropriate next step in management of this patient?

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Explanation:

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This patient has primary hyperthyroidism (elevated free T4, suppressed TSH) with signs of thyrotoxicosis (eg, anxiety, weight loss, tachycardia).  Primary hyperthyroidism can result from:

  • overproduction of thyroid hormone (eg, Graves disease, toxic nodular goiter).
  • release of preformed hormone (eg, painless thyroiditis, subacute thyroiditis).

These etiologies can be distinguished with radioactive iodine uptake (RAIU) scintigraphy, which measures uptake and organification of iodine in the thyroid gland.  Uptake is increased in thyrotoxicosis caused by thyroid hormone overproduction (eg, Graves disease) and is low or undetectable in thyrotoxicosis caused by release of preformed hormone.  In this patient, the low RAIU and nontender goiter are most consistent with painless (silent) thyroiditis.

Painless thyroiditis is associated with thyroid peroxidase autoantibodies and is considered a variant of chronic lymphocytic (Hashimoto) thyroiditis.  (Postpartum thyroiditis is also similar but by definition occurs within <12 months following childbirth.)  Following a self-limited hyperthyroid phase, patients often enter a hypothyroid phase, which may persist or progress to a euthyroid state.  Painless thyroiditis does not require specific antithyroid therapy; however, patients with signs of adrenergic overstimulation (eg, palpitations, tachycardia, tremulousness) should be treated with a beta blocker (eg, propranolol) rather than only observation and monitoring (Choice C).

(Choice A)  Levothyroxine is required for patients who develop significant hypothyroidism, but it would not be appropriate now in this patient with overt hyperthyroidism.

(Choices B and F)  Methimazole decreases thyroid hormone production; RAI causes radiation-induced destruction of thyroid follicular cells.  These treatments are used for thyrotoxicosis due to thyroid hormone overproduction but are not helpful for patients with excess release of preformed hormone, as in painless thyroiditis.

(Choice D)  Prednisone is used to treat thyroid pain refractory to nonsteroidal anti-inflammatory drugs in patients with subacute (de Quervain) thyroiditis.  Although subacute thyroiditis is also associated with low RAIU, it presents with a painful, tender goiter and is typically preceded by an upper respiratory tract infection.  This patient has a nontender goiter, which is more consistent with painless thyroiditis.

Educational objective:
Painless thyroiditis is a variant of chronic lymphocytic (Hashimoto) thyroiditis characterized by a self-limited hyperthyroid phase due to release of preformed thyroid hormone, followed by a hypothyroid phase or return to a euthyroid state.  It does not require specific antithyroid therapy, but patients with hyperadrenergic symptoms (eg, palpitations, tremulousness) should be treated with a beta blocker and receive monitoring of thyroid function.