A 29-year-old woman with type 1 diabetes mellitus comes to the office due to increasing fatigue and irritability. The symptoms started 2 weeks after the patient developed an upper respiratory infection. The cough and rhinorrhea have improved, but she continues to have fatigue and has lost 7 kg (15.43 lb) over the past month. The patient had an uncomplicated delivery 2 months ago and is exclusively formula-feeding her infant. Blood pressure is 148/72 mm Hg, pulse is 98/min, and respirations are 16/min. BMI is 26 kg/m². The thyroid is symmetrically enlarged and nontender. Cardiopulmonary examination is unremarkable. The abdomen is soft and nontender. A hand tremor is present. TSH level is low, and free T3 and T4 levels are high. There is low uptake on a radioactive iodine uptake scan. Which of the following is the most likely cause of this patient's symptoms?
RAIU findings in thyrotoxicosis | |
Normal or increased |
|
Decreased |
|
RAIU = radioactive iodine uptake. | |
This patient has clinical features (eg, fatigue, weight loss, tremor) and laboratory findings (ie, decreased TSH, elevated T4 and T3) consistent with hyperthyroidism (ie, thyrotoxicosis). The most common causes of hyperthyroidism are Graves disease and painless autoimmune thyroiditis (a variant of Hashimoto thyroiditis), which both can cause a painless, symmetrically enlarged thyroid. Patients with another autoimmune disease (eg, type 1 diabetes mellitus) are at increased risk for both disorders.
These disorders can be differentiated by a radioactive iodine uptake scan, which shows metabolic activity in the thyroid.
In Graves disease, the thyroid is stimulated by autoantibodies to increase tissue metabolic activity, causing increased thyroid hormone synthesis (as evidenced by increased uptake of radioactive iodine) and increased release of thyroid hormone (Choice B).
In contrast, in painless autoimmune thyroiditis, the thyroid tissue is destroyed, leading to increased release of preformed thyroid hormone and resulting hyperthyroidism. The destroyed thyroid cells are unable to synthesize thyroid hormone, as evidenced by low radioactive iodine uptake.
A form of painless autoimmune thyroiditis is postpartum thyroiditis, which can occur within 12 months of delivery. Patients with postpartum thyroiditis can have a variable disease course (based on the amount of thyroid destruction and recovery), including being hyperthyroid only (as in this patient), hypothyroid only, or hyperthyroid then hypothyroid. The diagnosis can be confirmed with a positive thyroid peroxidase antibody assay. Most patients eventually return to a euthyroid state and do not require treatment.
(Choice A) Exogenous thyroid ingestion suppresses thyroid hormone production, thereby causing decreased TSH levels and low radioiodine uptake. However, these patients typically have an atrophic, not enlarged, thyroid.
(Choice C) Nonthyroidal illness (ie, euthyroid sick syndrome) is an abnormal pattern of thyroid markers seen in patients with severe, acute illness. T3 is typically low and free T4 and TSH are normal to low.
(Choice E) Subacute granulomatous thyroiditis (ie, de Quervain thyroiditis) can cause hyperthyroidism and often presents after an upper respiratory infection. However, patients typically have fever and a severely painful, tender goiter, making this diagnosis unlikely.
Educational objective:
Postpartum thyroiditis, a form of painless autoimmune thyroiditis occurring within 12 months of delivery, can present with signs of hyperthyroidism (eg, weight loss, tremor, elevated T4 and T3 levels) and low uptake on a radioactive iodine uptake scan.