Approach

The diagnosis of painless thyroiditis can be established based on history, clinical features, thyroid function tests, and radioiodine uptake. It generally has a triphasic course, characterized by a thyrotoxic phase, which usually lasts about 2 to 3 months but is occasionally more prolonged, followed by a hypothyroid phase of usually up to several months.[1][2][3][4] However, either phase may be associated with minimal symptoms or pass unnoticed. This is usually followed by restoration of normal thyroid function, the final phase.[1]

History

A history should be taken to assess for the following:[5]

  • Recent pregnancy (including miscarriage and medical abortion)

  • Underlying autoimmune disorders such as type 1 diabetes

  • Treatment with immunomodulatory drugs such as interferon alfa, tyrosine kinase inhibitors (e.g., sunitinib), and monoclonal antibodies (e.g., alemtuzumab, ipilimumab, nivolumab).

    • Note that alemtuzumab-related thyroid dysfunction typically presents 16 to 23 months after the last alemtuzumab treatment for multiple sclerosis, but later cases have been reported.[8]

  • Treatment with lithium (a mood stabilizer used to treat psychiatric conditions such as bipolar disorder and depression)[6]

  • Treatment with amiodarone (an antiarrhythmic medication used to treat heart rhythm disorders such as atrial fibrillation)[14][15]

  • Radiation therapy

All of these factors increase risk for thyroid dysfunction and painless thyroiditis.

Clinical presentation

Screening for symptoms should be tailored to the two main clinical phases of the disorder. Some symptoms (excessive fatigue and poor concentration) may be observed in both phases.

Initial thyrotoxic (hyperthyroid) phase (2 to 3 months):

  • Excessive fatigue

  • Palpitations

  • Tremulousness

  • Increased appetite with weight loss

  • Poor concentration

  • Heat intolerance.

Hypothyroid phase (several months):

  • Excessive fatigue

  • Bloating

  • Muscle cramps

  • Weight gain

  • Poor concentration

  • Cold intolerance.

On exam, a small, nontender goiter is a characteristic finding. Absence of a painful or tender thyroid gland is a key differential from other forms of thyroiditis (e.g., subacute, suppurative).

Investigations

Thyroid function tests are ordered either for symptoms of hyper- or hypothyroidism or as a screening test - for example, for the evaluation of fatigue.[4][21]​​ During the thyrotoxic phase thyroid-stimulating hormone (TSH) is likely to be suppressed, and free T3/T4 elevated, whereas in the hypothyroid phase TSH is elevated. Do not order more laboratory tests until TSH is confirmed as abnormal.[22]​ In practice, thyrotoxicosis often evolves spontaneously to euthyroidism or hypothyroidism during the time between the first serum TSH test and a specialist reviewing the patient. Therefore, if the serum TSH is repeated by the specialist, this can confirm the diagnosis of thyroiditis without the need for scans.

Radioiodine uptake of <1% is the key test to distinguish from other forms of thyrotoxicosis.[2][3][4] Imaging with technetium-99m pertechnetate can be performed when radioiodine is unavailable. Assessing TSH-receptor antibodies (TRAb) and the ratio of total T3/T4 also helps to differentiate Graves disease and toxic nodular goiter from painless thyroiditis.[23] The presence of TRAb is highly suggestive of Graves disease, but may be positive in Hashitoxicosis, a variant of Graves disease characterized by spontaneous episodes of hyper- and hypothyroidism. 

During the postpartum period, when radioisotope imaging may be contraindicated due to breastfeeding, postpartum thyroiditis was differentiated from Graves hyperthyroidism by several additional factors in one study: thyrotoxicosis up to 3 months postpartum was thyroiditis, while thyrotoxicosis later than 6.5 months postpartum was Graves disease; color-flow Doppler ultrasound was low in thyroiditis and elevated in most patients with Graves hyperthyroidism; and thyrotropin receptor antibodies were positive in Graves disease.[24]

Thyroid biopsy is seldom necessary but reveals lymphocytic infiltrate if conducted in the hyperthyroid phase. Inflammatory markers (erythrocyte sedimentation rate, c-reactive protein) are not elevated, in contrast to subacute and suppurative thyroiditis. See Subacute granulomatous thyroiditis for more information.

In some cases of suspected thyroiditis (provided patients are minimally or not symptomatic during the thyrotoxic phase and not at risk of complications such as atrial fibrillations), additional investigations may be omitted and an expectant approach pursued for 1 to 2 months with monitoring of thyroid function.

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