title: Elevated plasma levels of vascular endothelial growth factor and plasminogen activator inhibitor-1 decrease during improvement of psoriasis.
abstract: OBJECTIVE
  An evaluation of angiogenesis related molecules during open treatment of psoriasis.
  
  
  METHODS
  Plasma samples and skin biopsies from 16 patients with psoriasis and plasma samples from 13 healthy controls.
  
  
  METHODS
  Ranitidine 300 mg orally twice daily for 6 months.
  
  
  METHODS
  Vascular endothelial growth factor (VEGF) and plasminogen activator inhibitor-1 (PAI-1) were determined by ELISA methods in plasma collected from the patients before treatment and after 1, 3 and 6 months. Vessel counts were performed in biopsies from affected skin areas taken before treatment and after 3 and 6 months. The results were compared to simultaneous PASI scores.
  
  
  RESULTS
  Pre-treatment plasma levels of VEGF and PAI-1 were significantly elevated in patients compared with levels in healthy persons (p = 0.02 and p = 0.04, respectively). The plasma levels decreased significantly during treatment (p = 0.03 and p = 0.01, respectively), and the decrease in combined levels correlated with the decrease in PASI score. However, the vessel density in affected skin did not change during treatment.
  
  
  CONCLUSIONS
  Increased pre-treatment levels of VEGF and PAI-1 and decrease during improvement of the disease suggest that the two molecules may play a role in pathogenesis of psoriasis.
authors.affiliation: Department of Surgical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Hvidovre Denmark. h.j.nielsen@ofir.dk
authors.forename: H J
authors.initials: HJ
authors.lastname: Nielsen
authors.forename: I J
authors.initials: IJ
authors.lastname: Christensen
authors.forename: M N
authors.initials: MN
authors.lastname: Svendsen
authors.forename: U
authors.initials: U
authors.lastname: Hansen
authors.forename: K
authors.initials: K
authors.lastname: Werther
authors.forename: N
authors.initials: N
authors.lastname: Brünner
authors.forename: L J
authors.initials: LJ
authors.lastname: Petersen
authors.forename: J K
authors.initials: JK
authors.lastname: Kristensen
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D016228:Endothelial Growth Factors / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008222:Lymphokines / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011565:Psoriasis / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology; D011899:Ranitidine / Q000627:therapeutic use; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012867:Skin / Q000098:blood supply / Q000737:chemistry; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D006635:Histamine H2 Antagonists; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D017395:Plasminogen Activator Inhibitor 1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D011899:Ranitidine