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Iodine-131 Given for Therapeutic Purposes Modulates Differently Interferon--Inducible -Chemokine CXCL10 Serum Levels in Patients with Active Graves’ Disease or Toxic Nodular Goiter

Metabolism Unit (A.A., P.F., S.M.F., E.F.), Department of Medicine, and Regional Center of Nuclear Medicine (M.G., G.M., G.B.), University of Pisa Medical School, I-56100 Pisa, Italy; Department of Clinical Pathophysiology (M.R., P.R., M.S.), Endocrinology Unit, University of Florence, 50139 Florence, Italy; and Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (E.F.), 56126 Pisa, Italy

Address all correspondence and requests for reprints to: Alessandro Antonelli, M.D., Department of Internal Medicine, University of Pisa Medical School, Via Roma, 67, I-56100 Pisa, Italy. E-mail: a.antonelli{at}med.unipi.it.

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.

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