Hashimoto's thyroiditis (HT) is part of the spectrum of autoimmune thyroid diseases. Clinical manifestations of HT are variable and commonly include diffuse or nodular goiter with euthyroidism, subclinical hypothyroidism and permanent hypothyroidism. Uncommonly, HT causes acute destruction of thyroid tissue and release of stored thyroid hormones, causing transient thyrotoxicosis (hashitoxicosis). The contribution of methods and techniques of nuclear medicine to diagnosis and differential diagnosis of HT is indisputable. In HT patients with overt hypothyroidism L-thyroxine (L-T(4)) should be given in the usual replacement doses, but in HT patients with a large goiter and normal or elevated serum thyroid-stimulating hormone (TSH), L-T(4) may be given in doses sufficient to suppress serum TSH. Symptomatic patients with hashitoxicosis and low 24-hour thyroid radioactive iodine ((123)I or (123)I) uptake (RIU) may be treated with beta-blockers (as propranolol) and sodium ipodate or iopanoic acid (iodinated contrast agents) that block the peripheral conversion of T(4) to T(3). Recent clinical studies have documented the suppressive effect of selenium treatment on serum anti-thyroid peroxidase concentrations in patients with HT.