title: Endothelial dysfunction in Graves' disease.
abstract: OBJECTIVE
  Graves' disease (GD) is an organ-specific autoimmune thyroid disease, characterized by hyperthyroidism due to excessive production of thyroid hormone induced by thyrotropin receptor-specific stimulatory autoantibodies. In this study, we determined serum levels of the soluble forms of ICAM-1, VCAM-1, vWF, IL-6, IL-12, IL-18, fibrinogen and CRP in patients with subclinical (SH) and overt hyperthyroidism (OH) caused by GD to elucidate a possible role of those parameters as markers of endothelium dysfunction (ED).
  
  
  METHODS
  The study included 96 patients: 52 with GD and 44 euthyroid controls, divided into 3 groups according to their thyroid function tests: SH, OH and controls (CG).
  
  
  RESULTS
  The values of IL-6, IL-12 and IL-18 were significantly higher in GD than in CG patients (p < 0.0001, p < 0.0001; p < 0.00001, respectively). Significant difference of sVCAM-1 values were found in the patients with GD compared to CG (p < 0.0001). Patients with GD had significantly higher levels of PAI-1 (p < 0.00001), vWF (p < 0.0001), fibrinogen (p < 0.0001) in comparison to CG. In patients with OH, we observed statistically higher values of fibrinogen compared to SH group (p < 0.05). There were no significant differences in serum concentration of other study parameters in patients with SH compared to the OH.
  
  
  CONCLUSIONS
  ED occurs during subclinical and overt hyperthyroidism causing decreased fibrinolytic activity, hypercoagulability and increased levels of IL-6, Il-12 and IL-18. These results support the notion that serum cytokines could be used as a marker of GD activity. Results of this study support the opinion that GD might require treatment as early as in the phase of SH.
authors.affiliation: Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, Bialystok, Poland. annapoplawskakita@op.pl
authors.forename: A
authors.initials: A
authors.lastname: Popławska-Kita
authors.forename: M
authors.initials: M
authors.lastname: Szelachowska
authors.forename: A
authors.initials: A
authors.lastname: Modzelewska
authors.forename: K
authors.initials: K
authors.lastname: Siewko
authors.forename: J
authors.initials: J
authors.lastname: Dzięcioł
authors.forename: P A
authors.initials: PA
authors.lastname: Klimiuk
authors.forename: M
authors.initials: M
authors.lastname: Górska
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood*; D001777:Blood Coagulation; D002097:C-Reactive Protein / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis; D006111:Graves Disease / Q000097:blood* / Q000150:complications; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood* / Q000209:etiology; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D018664:Interleukin-12 / Q000097:blood; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D013960:Thyroid Function Tests; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D020382:Interleukin-18; D015850:Interleukin-6; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1; D018664:Interleukin-12; D005340:Fibrinogen; D002097:C-Reactive Protein