1. Painless (silent) thyroiditis (subacute lymphocytic thyroiditis): Autoimmune, painless, chronic thyroiditis, which is considered to be a variant of Hashimoto thyroiditis. It is characterized by a 4-phase course that includes a transient phase of thyrotoxicosis with low iodine uptake (phase 1) followed by a transient euthyroid phase (phase 2), a hypothyroid phase (phase 3), and subsequent return to the euthyroid status (phase 4). A small painless goiter is observed; the course is otherwise similar to that of subacute thyroiditis (see below). The disease occurs spontaneously or within 1 year of childbirth (or miscarriage); in the latter case, it is referred to as postpartum thyroiditis. In the thyrotoxicosis phase administer a beta-blocker or, in severe cases, a glucocorticoid. This condition is usually self-limiting in patients who develop permanent hypothyroidism start levothyroxine (L-T4) replacement therapy (see Hypothyroidism).
2. Riedel thyroiditis: Very rare fibrosing thyroiditis, which gradually involves the whole thyroid gland and other tissues of the neck (the thyroid gland is very hard on palpation). Patients may develop dyspnea, recurrent laryngeal nerve palsy, Horner syndrome, or hypoparathyroidism. Fine-needle biopsy (FNB) does not yield diagnostic samples. Total thyroidectomy is practically impossible; the tracheal compression can be reduced by wedge resection of the thyroid isthmus. Treatment with glucocorticoids is sometimes effective.
3. Chronic interferon alpha–induced thyroiditis: In persons with a genetic predisposition, interferon alpha induces the production of autoantibodies, including antithyroid antibodies, thus increasing the risk of developing subacute lymphocytic thyroiditis, chronic autoimmune thyroiditis, or (rarely) Graves disease. Thyroiditis is not fully reversible.
4. Chronic amiodarone-induced thyroiditis: The drug causes hypothyroidism or (less frequently) thyrotoxicosis (amiodarone-induced thyrotoxicosis [AIT]; see Thyrotoxicosis and Hyperthyroidism). Thyroid function (thyroid-stimulating hormone [TSH] levels) should be measured before starting treatment, after 3 to 4 months, and then yearly. Type 1 AIT is caused by excess iodine, coming from the amiodarone molecule, which is used as a substrate for the synthesis of thyroid hormones (increased production of thyroid hormones in patients with subclinical disorders or in genetically predisposed persons). Type 2 AIT is a chronic thyroiditis causing destruction of the previously structurally intact thyroid gland and release of excess thyroid hormones to the circulation (the production of thyroid hormones is not increased).
Diagnosis: Signs and symptoms of hyperthyroidism may be subtle; exacerbation of preexisting arrhythmia may be the only sign (in such patients it is necessary to assess thyroid-stimulating hormone levels).
Differential diagnosis and treatment: see Table 6.7-3. Treatment may be prolonged and difficult; it may require discontinuation of amiodarone. In patients with mixed features of type 1 and type 2 AIT or without clear diagnosis, combined treatment is recommended: start therapy with an antithyroid drug and prednisone in patients in whom thyrotoxicosis-related symptoms do not improve. When amiodarone is used for non–life-threatening arrhythmias, cardiology consultation is suggested to consider the possibility of drug discontinuation.