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Increased serum CXCL10 in Graves’ disease or autoimmune thyroiditis is not associated with hyper- or hypothyroidism per se, but is specifically sustained by the autoimmune, inflammatory process

Metabolism Unit, Department of Internal Medicine and CNR Institute of Clinical Physiology, University of Pisa-School of Medicine, Via Roma, 67, I-56100, Pisa, Italy, ¹ Department of Clinical and Experimental Medicine and Surgery ‘F. Magrassi-A. Lanzara’, Second University of Naples, Naples, Italy, ² Department of Clinical Pathophysiology, Endocrinology Unit, University of Florence, Florence, Italy and ³ Regional Center of Nuclear Medicine, University of Pisa Medical School, Pisa, Italy

(Correspondence should be addressed to A Antonelli; Email: a.antonelli{at}med.unipi.it)

Objective: Serum CXCL10 (an interferon--inducible chemokine) levels (sCXCL10) are increased in several autoimmune conditions, including Graves’ disease (GD) and autoimmune thyroiditis (AT). Longitudinal assessment of sCXCL10 in autoimmune hypo- or hyperthyroidism has not yet been performed.

Design and methods: We longitudinally assayed sCXCL10 in the following groups:

1. thirty-three GD and 11 toxic nodular goiter (TNG) patients when hyperthyroid (Hyper) and when reaching euthyroidism (Eu) with methimazole therapy (MMI)
   
2. sixty-six AT (33 hypothyroid (Hypo) and 33 Eu) patients, basally and after reaching EU (for Hypo) with levothyroxine (L-T₄) therapy
   
3. twenty-two patients with thyroid cancer (CA) under L-T₄-suppressive treatment, of whom 11 were re-evaluated after L-T₄ withdrawal for diagnostic WBS, and 11 after recombinant TSH (rhTSH) administration
   
4. thirty-three healthy controls.
   

Results: At initial evaluation, Hyper GD and AT (Hypo significantly higher than Eu) showed significantly higher mean sCXCL10 than all other groups. MMI treatment led to a significant decrease in sCXCL10 only in GD (not in TNG), while restoration of Eu, in Hypo AT, by L-T₄ was not accompanied by significant sCXCL10 change. CA showed sCXCL10 comparable to controls, and both Hypo after L-T₄ withdrawal and rhTSH injection had no effect on sCXCL10.

Conclusions: Treatment of Hyper leads to a significant decrease in sCXCL10 only in GD, and this probably depends upon the MMI immunomodulatory effect. L-T₄ correction of Hypo is not accompanied by significant modification of sCXCL10 in AT. Increased sCXCL10 is not associated with Hyper or Hypo per se, but is specifically sustained by the autoimmune inflammatory event occurring in both GD and AT.

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