Approach

Treatment is focused on providing pain relief and treating any manifestations of hyper- or hypothyroidism that may be present. Not all patients require treatment, as symptoms may be mild and/or subsiding by the time the diagnosis is made.

Hyperthyroid (thyrotoxic) phase

Treatment is supportive. Symptoms are due to the release of preformed thyroid hormone, and antithyroid drugs that inhibit new hormone synthesis are ineffective.

Non-steroidal anti-inflammatory drugs (NSAIDs) are used in the management of thyroid pain.[4]​ In most patients, the symptoms of hyperthyroidism are mild and do not require treatment. However, if thyrotoxic symptoms (e.g., tachycardia, anxiety, and/or tremor) are troublesome, patients can benefit from treatment with a beta-blocker or calcium-channel blocker.[4][28]​​ Beta-blockers are recommended for the management of sinus tachycardia in thyrotoxic patients.[4]​ Calcium-channel blockers can be used in the thyrotoxic phase when beta-blockers are contraindicated (e.g., in patients with bronchospasm and asthma) or not tolerated, but are associated with increased risk for hypotension.[4]

Severe pain or pain unresponsive to analgesics

Thyroid pain that is severe, unresponsive to NSAIDs, or prevents patients from swallowing or sleeping, may be treated with corticosteroids (e.g., prednisolone).[4][22]​​[28][50]​​​ If pain does not respond to corticosteroids in 1-2 days, the diagnosis should be reconsidered.

A relatively high dose of prednisolone is usually required for 1-2 weeks, followed by taper over 2-4 weeks (or longer, depending on clinical course.[4]​ ​Some data suggest that lower doses of corticosteroid may be effective for pain control.[51][52][53]​​​​ Corticosteroid treatment may be associated with reduced incidence of permanent hypothyroidism compared with treatment with an NSAID.[54][55]​​​​ Note, however, that if corticosteroids are stopped too early, the pain may return.[56]​

Patients with severe symptoms of thyrotoxicosis

Inhibiting the conversion of thyroxine (T4) to triiodothyronine T3 may benefit patients with severe symptoms of thyrotoxicosis (because T3 is 20-50 times more bioactive than T4). Conversion of T4 to T3 can be reduced by a high level of iodine, usually achieved by giving a saturated solution of potassium iodide, along with high doses of corticosteroids.[57]

Hypothyroid phase

The treatment is supportive in mild cases (i.e., thyroid-stimulating hormone [TSH] <10-15 mIU/L). Generally, patients with this degree of hypothyroidism do not require thyroid hormone therapy with levothyroxine, unless the patient is actively trying to conceive or is already pregnant.[58]​ Thyroid function (TSH and free thyroxine level) is checked every 4-6 weeks, when symptoms can also be assessed. Levothyroxine should be considered if, with subsequent testing, the TSH level increases.

A low to moderate dose of levothyroxine can be given for up to several months for a patient:

  • Adversely affected by hypothyroidism, or

  • With hypothyroidism that is moderate to severe biochemically (TSH >15 IU/L), and/or accompanied by fatigue that interferes with daily activities

Thyroid function (TSH and free thyroxine level) should be checked every 4-6 weeks during treatment with levothyroxine, and the dose adjusted to maintain a normal TSH level. Treatment should be withdrawn after 3-6 months to determine if endogenous function has returned to normal.[4]​ Most patients (85% to 90%) return to normal thyroid function and will not need long-term levothyroxine.[2]​ If raised, levothyroxine may be restarted in a patient with permanent hypothyroidism subsequent to subacute thyroiditis.[1][2][22]

Patients who have moderate deficiency (i.e., TSH >15 IU/L) should be treated with levothyroxine to normalise the TSH.

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