CONTEXT: The mechanism of activation of the immune system after iodine-131 (131I) treatment of hyperthyroidism is still not fully clarified. Serum levels of CXCL10, a prototype of the CXC family of chemokines, are increased in several endocrine autoimmune conditions, and this chemokine plays a role at least in the initial phases of thyroid autoimmune disease and in Graves' disease (GD). OBJECTIVE, DESIGN, AND PATIENTS: The aim of the present study was to measure the serum CXCL10 levels in 20 patients with GD and 10 patients with toxic nodular goiter (TNG) before and 6 months after 131I treatment, when patients had achieved euthyroidism. Forty healthy subjects and 40 patients with autoimmune thyroiditis served as control groups. RESULTS: Before 131I, mean CXCL10 was significantly higher in patients with GD and thyroiditis than controls or those with TNG. Serum CXCL10 levels significantly decreased in GD patients 6 months after 131I treatment, whereas they remained within normal limits in TNG patients after restoration of euthyroidism by 131I. CONCLUSIONS: In conclusion, our results demonstrate that high serum CXCL10 levels are associated with the hyperthyroid phase in GD but not TNG, providing further evidence for a minimal role of hyperthyroidism per se in determining high CXCL10 levels and showing a strong association with the autoimmune process. The reduction of CXCL10 levels after 131I treatment in GD only shows that the thyroid gland itself is the main source of circulating CXCL10.
CONTEXT: The mechanism of activation of the immune system after iodine-131 (131I) treatment of hyperthyroidism is still not fully clarified. Serum levels of CXCL10, a prototype of the CXC family of chemokines, are increased in several endocrine autoimmune conditions, and this chemokine plays a role at least in the initial phases of thyroid autoimmune disease and in Graves' disease (GD). OBJECTIVE, DESIGN, AND PATIENTS: The aim of the present study was to measure the serum CXCL10 levels in 20 patients with GD and 10 patients with toxic nodular goiter (TNG) before and 6 months after 131I treatment, when patients had achieved euthyroidism. Forty healthy subjects and 40 patients with autoimmune thyroiditis served as control groups. RESULTS: Before 131I, mean CXCL10 was significantly higher in patients with GD and thyroiditis than controls or those with TNG. Serum CXCL10 levels significantly decreased in GDpatients 6 months after 131I treatment, whereas they remained within normal limits in TNGpatients after restoration of euthyroidism by 131I. CONCLUSIONS: In conclusion, our results demonstrate that high serum CXCL10 levels are associated with the hyperthyroid phase in GD but not TNG, providing further evidence for a minimal role of hyperthyroidism per se in determining high CXCL10 levels and showing a strong association with the autoimmune process. The reduction of CXCL10 levels after 131I treatment in GD only shows that the thyroid gland itself is the main source of circulating CXCL10.