Iodine-131 given for therapeutic purposes modulates differently interferon-γ-inducible α-chemokine CXCL10 serum levels in patients with active Graves' disease or toxic nodular goiter

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.