title: Iodine-131 given for therapeutic purposes modulates differently interferon-gamma-inducible alpha-chemokine CXCL10 serum levels in patients with active Graves' disease or toxic nodular goiter.
abstract: BACKGROUND
  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.
authors.affiliation: Metabolism Unit, Department of Medicine, Regional Center of Nuclear Medicine, University of Pisa Medical School, Via Roma, 67, I-56100 Pisa, Italy. a.antonelli@med.unipi.it
authors.forename: Alessandro
authors.initials: A
authors.lastname: Antonelli
authors.forename: Mario
authors.initials: M
authors.lastname: Rotondi
authors.forename: Poupak
authors.initials: P
authors.lastname: Fallahi
authors.forename: Mariano
authors.initials: M
authors.lastname: Grosso
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Boni
authors.forename: Silvia Martina
authors.initials: SM
authors.lastname: Ferrari
authors.forename: Paola
authors.initials: P
authors.lastname: Romagnani
authors.forename: Mario
authors.initials: M
authors.lastname: Serio
authors.forename: Giuliano
authors.initials: G
authors.lastname: Mariani
authors.forename: Ele
authors.initials: E
authors.lastname: Ferrannini
mesh_terms: D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood*; D005260:Female; D006044:Goiter, Nodular / Q000097:blood / Q000532:radiotherapy*; D006111:Graves Disease / Q000097:blood / Q000532:radiotherapy*; D006801:Humans; D007371:Interferon-gamma / Q000502:physiology* / Q000528:radiation effects; D007457:Iodine Radioisotopes / Q000493:pharmacokinetics / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D007457:Iodine Radioisotopes; D014284:Triiodothyronine; D007371:Interferon-gamma; D013972:Thyrotropin; D013974:Thyroxine