Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.

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The object was to carry out a prospective study of the changes in serum thyroid hormones and thyroglobulin (Tg) following resection of nontoxic goiter and to investigate if there was a correlation to the pattern of relapse. A group of 39 consecutive patients, mainly with nodular, nontoxic goiter, were studied for 13 years following thyroidectomy. No thyroid hormone replacement therapy was given after surgery. The preoperative serum Tg level was elevated. After operation the mean serum Tg declined to a nadir of 43 micrograms/L at 1 year and subsequently increased to 90 micrograms/L at 10 years, with large individual differences. In 19 patients the serum Tg increased, in 1 it decreased, and in 19 no significant alteration was observed. Serum free thyroxine and triiodothyronine indices decreased following resection but achieved normal levels within 6 to 12 months. Serum thyroid-stimulating hormone increased after resection, with a peak level 1 month after surgery, but it returned to normal levels at 1 year and remained stable for the rest of the period. At 13 years after resection the thyroid volume was determined by ultrasonography in 30 of the patients. In 10 patients the thyroid volume was enlarged (>/= 28 ml). In this group a rise of average serum Tg after resection [DeltaTg(10-1 year)] of 133 micrograms/L was observed, compared to 26 micrograms/L in the 20 patients without sonographic relapse (volume < 28 ml). A positive correlation was demonstrated between serum DeltaTg(10-1 year) postsurgically and thyroid volume 13 years after surgery. However, an overlap was observed between the groups with and without ultrasonographic relapse, probably in part due to large differences in the Tg synthesis activity of different follicle cell clones. It is concluded that repeated serum Tg determinations may provide biochemical evidence of increased growth activity of thyroid remnants monitored after goiter resection.