title: Tissue and serum angiogenic activity is associated with low prevalence of ischemic complications in patients with giant-cell arteritis.
abstract: BACKGROUND
  Vascular inflammatory lesions from patients with giant-cell arteritis show a remarkable amount of neovascularization, but its clinical implications have never been investigated.
  
  
  RESULTS
  To assess the clinical relevance of neovascularization in giant-cell arteritis, angiogenesis was measured in temporal artery sections from 31 patients with biopsy-proven giant-cell arteritis by staining endothelial cells with Ulex europaeus lectin. Angiogenesis was highly variable among these patients. Patients without ischemic complications had higher tissue angiogenesis scores than patients with ischemic events (5.69+/-0.6 versus 2.91+/-0.6, P=0.003). Angiogenesis was also more prominent in patients with a strong acute phase response (score: 5.31+/-0.6) compared with those with a weak systemic inflammatory reaction (2.30+/-0.44; P=0.0007). Serum angiogenic activity was studied in an additional series of 38 biopsy-proven patients. Sera from patients without ischemic events tended to be more active in stimulating human umbilical vein endothelial cell growth (optical density x1000, 270+/-15 versus 192+/-14, P=0.065) and differentiation into capillary-like structures (107+/-5 versus 84+/-8 relative units, P=0.0058) than patients with ischemic complications. Sera from patients without ischemic events had more in vivo full angiogenic activity tested in the chick chorioallantoic membrane than sera from patients with ischemic complications.
  
  
  CONCLUSIONS
  Inflammation-induced angiogenic activity may play a compensatory role for ischemia in patients with giant-cell arteritis.
authors.affiliation: Vasculitis Research Unit, Department of Internal Medicine, Hospital Clínic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain. mccid@clinic.ub.es
authors.forename: Maria C
authors.initials: MC
authors.lastname: Cid
authors.forename: José
authors.initials: J
authors.lastname: Hernández-Rodríguez
authors.forename: María-José
authors.initials: MJ
authors.lastname: Esteban
authors.forename: Mireia
authors.initials: M
authors.lastname: Cebrián
authors.forename: Yong Song
authors.initials: YS
authors.lastname: Gho
authors.forename: Carme
authors.initials: C
authors.lastname: Font
authors.forename: Alvaro
authors.initials: A
authors.lastname: Urbano-Márquez
authors.forename: Josep M
authors.initials: JM
authors.lastname: Grau
authors.forename: Hynda K
authors.initials: HK
authors.lastname: Kleinman
mesh_terms: D000210:Acute-Phase Reaction / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology; D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001681:Biological Assay; D001706:Biopsy; D001798:Blood Proteins / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D002642:Chick Embryo; D002823:Chorion / Q000098:blood supply / Q000166:cytology / Q000187:drug effects; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects; D005260:Female; D013700:Giant Cell Arteritis / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007511:Ischemia / Q000175:diagnosis* / Q000209:etiology; D037102:Lectins; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D018919:Neovascularization, Physiologic / Q000187:drug effects; D037121:Plant Lectins; D011446:Prospective Studies; D012016:Reference Values; D013699:Temporal Arteries / Q000473:pathology; D014651:Vasa Vasorum / Q000473:pathology
chemical_list: D001798:Blood Proteins; D037102:Lectins; D037121:Plant Lectins; C036850:Ulex europaeus lectins