title: Decreased number of circulating endothelial progenitor cells in patients with Graves' hyperthyroidism.
abstract: OBJECTIVE
  A relevant biological role of circulating endothelial progenitor cells (EPC) was recently demonstrated. EPC are generated in the bone marrow, and interact with damaged endothelium, restoring the integrity of the monolayer. Therefore, aim of the present study was to evaluate EPC in the blood of patients with untreated Graves' hyperthyroidism (GD), in whom an increased oxidative stress was observed.
  
  
  METHODS
  Twenty-three patients with untreated active GD and 18 matched normal controls (NC) were included in the study. Circulating EPC were isolated from peripheral blood. Mononuclear cells were cultured with endothelial basal medium supplemented with EGM SingleQuots, and were identified by positive double staining after 7 days in culture. Circulating levels of C reactive protein, total antioxidant power, interleukin (IL)-6, IL- 18, monocyte chemoattractant protein-1, tumor necrosis facotr- α, soluble vascular cell adhesion molecule (VCAM) and intracellular adhesion molecule were evaluated by enzymelinked immunosorbent assay kit. EPC number was also evaluated in a subgroup of GD patients after restoration of euthyroidism.
  
  
  RESULTS
  Systolic blood pressure resulted increased in GD patients compared with control subjects whereas diastolic blood pressure was not significantly different. Patients with GD showed an increase in circulating levels of IL-18 and VCAM-1 and a reduction of total antioxidant power (p<0.05) compared to NC. Moreover, a reduced number of EPC was observed in patients with GD compared to NC (p<0.05) which turned to NC values after restoring euthyroidism.
  
  
  CONCLUSIONS
  Patients with GD showed a reduction in the physiological protective mechanisms against endothelial damage, probably induced by increased inflammation and oxidative stress.
authors.affiliation: Clinica Medica, Department of Medical and Surgical Sciences, University of Brescia, Spedali Civili, 25100 Brescia, Italy.
authors.forename: C
authors.initials: C
authors.lastname: De Ciuceis
authors.forename: A
authors.initials: A
authors.lastname: Pilu
authors.forename: C
authors.initials: C
authors.lastname: Cappelli
authors.forename: E
authors.initials: E
authors.lastname: Porteri
authors.forename: F
authors.initials: F
authors.lastname: Zani
authors.forename: A
authors.initials: A
authors.lastname: Santoro
authors.forename: E
authors.initials: E
authors.lastname: Gandossi
authors.forename: G E M
authors.initials: GE
authors.lastname: Boari
authors.forename: N
authors.initials: N
authors.lastname: Rizzardi
authors.forename: M
authors.initials: M
authors.lastname: Castellano
authors.forename: D
authors.initials: D
authors.lastname: Rizzoni
authors.forename: E
authors.initials: E
authors.lastname: Agabiti Rosei
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000097:blood; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D005260:Female; D006111:Graves Disease / Q000097:blood* / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D020382:Interleukin-18 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D018932:Chemokine CCL2; D020382:Interleukin-18; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1