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Submitted on July 19, 2006
Accepted on January 17, 2007
Metabolism Unit, Department of Medicine, University of Pisa Medical School, Pisa, Italy and Department of Clinical Pathophysiology, Endocrinology Unit, University of Florence, Florence, Italy; Regional Center of Nuclear Medicine, University of Pisa Medical School, Pisa, Italy; CNR Institute of Clinical Physiology, Pisa, Italy
* To whom correspondence should be addressed. E-mail: a.antonelli{at}med.unipi.it.
Context The mechanism of activation of the immune system after 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, Patients Aim of the present study was to measure the serum CXCL10 levels in 20 patients with GD and in 10 patients with TNG (toxic nodular goiter) before and 6 months after 131I treatment, when patients had achieved euthyroidism. Forty healthy subjects and 40 patients with autoimmune thyroiditis (AT) served as control groups.
Results Before 131I, mean CXCL10 was significantly higher in patients with GD and AT than in controls or TNG. Serum CXCL10 levels significantly decreased in GD patients 6 months after 131I treatment, while they remained within normal limits in TNG patients following 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 in 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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