title: Increase of interferon-gamma-inducible CXC chemokine CXCL10 serum levels in patients with active Graves' disease, and modulation by methimazole therapy.
abstract: BACKGROUND
  CXCL10 plays an important role in the initial phases of Graves' disease (GD) and autoimmune thyroiditis (AT); however, until now, CXCL10 serum levels (sCXCL10) in patients with GD have never been evaluated in relation to thyroid function and treatment.
  
  
  OBJECTIVE
  To evaluate sCXCL10 in GD.
  
  
  METHODS
  Cross-sectional.
  
  
  METHODS
  One hundred and three GD, 164 AT, 20 nontoxic multinodular goitre (NTMNG), 16 toxic nodular goitre (TNG) patients and 70 healthy controls (age- and sex-matched).
  
  
  METHODS
  We measured sCXCL10 in patients and controls, to relate this parameter to the clinical phenotype.
  
  
  RESULTS
  Mean sCXCL10 in GD and AT patients were comparable (122+/-81 and 133+/-102 pg/ml) and significantly higher (P<0.01) than in controls or NTMNG patients (73+/- 32 and 76+/- 25 pg/ml, respectively). Hyperthyroid GD had significantly higher sCXCL10 than euthyroid or hypothyroid GD (145+/- 92, 107+/- 56 and 105+/- 46 pg/ml, respectively; P=0.01). GD patients with untreated hyperthyroidism had higher sCXCL10 than hyperthyroid or euthyroid GD patients under methimazole (MMI) treatment (166+/-125, 124+/- 41 and 94+/- 35 pg/ml, respectively; P=0.006). Comparable sCXCL10 levels were observed in newly diagnosed untreated hyperthyroid GD patients with respect to untreated patients with relapse of hyperthyroidism after a previous MMI course (176+/-125, 155+/- 97 pg/ml, respectively). GD had similar sCXCL10 to AT and higher than TNG patients or controls (all age- and sex-matched) (144+/- 81, 149+/- 114, 101+/- 27 and 86+/- 44 pg/ml, respectively; P=0.02).
  
  
  CONCLUSIONS
  sCXCL10 is associated with the active phase of GD in both newly diagnosed and relapsing hyperthyroid patients. The reduction in sCXCL10 in treated patients with GD may be related to the immunomodulatory effects of MMI.
authors.affiliation: Metabolism Unit, Department of Medicine and CNR Institute of Clinical Physiology, University of Pisa School of Medicine, Pisa, Italy. a.antoinelli@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: Paola
authors.initials: P
authors.lastname: Romagnani
authors.forename: Silvia Martina
authors.initials: SM
authors.lastname: Ferrari
authors.forename: Lucio
authors.initials: L
authors.lastname: Barani
authors.forename: Ele
authors.initials: E
authors.lastname: Ferrannini
authors.forename: Mario
authors.initials: M
authors.lastname: Serio
mesh_terms: D000328:Adult; D000906:Antibodies / Q000097:blood; D013956:Antithyroid Agents / Q000627:therapeutic use*; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood*; D003430:Cross-Sectional Studies; D005260:Female; D006044:Goiter, Nodular / Q000097:blood / Q000188:drug therapy / Q000276:immunology; D006111:Graves Disease / Q000097:blood / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology*; D008297:Male; D008713:Methimazole / Q000627:therapeutic use*; D008875:Middle Aged; D010641:Phenotype; D011989:Receptors, Thyrotropin / Q000276:immunology; D013961:Thyroid Gland / Q000503:physiopathology; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000188:drug therapy / Q000276:immunology; D013972:Thyrotropin / Q000097:blood; D016896:Treatment Outcome; D014284:Triiodothyronine / Q000097:blood
chemical_list: D000906:Antibodies; D013956:Antithyroid Agents; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D011989:Receptors, Thyrotropin; D014284:Triiodothyronine; D008713:Methimazole; D007371:Interferon-gamma; D013972:Thyrotropin