title: Intravenous prostaglandin E1 reduces monocyte chemoattractant protein-1 levels in peripheral arterial obstructive disease.
abstract: OBJECTIVE
  Blood monocytes are the precursors of the lipid-laden foam cells that are the hallmark of early atherosclerotic lesions, and monocyte chemoattractant protein-1 (MCP-1) plays important roles in their recruitment to the vessel wall. In this study, we measured serum levels of MCP-1 in patients with peripheral arterial obstructive disease (PAOD) and investigated whether intravenous prostaglandin E1 (PGE1) treatment, which produces clinical benefits in PAOD, might decrease such levels.
  
  
  METHODS
  Eight patients with PAOD at Fontaine stage II to IV were treated with a daily intravenous infusion of 10 microg of PGE1 for 7 consecutive days. Blood samples before and after 7-day PGE1 treatment were used for assays of MCP-1, interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), von Willebrand factor (vWF), and endothelin-1 (ET-1).
  
  
  RESULTS
  Serum MCP-1 levels in patients with PAOD were significantly higher than those in healthy control subjects (263.8 +/- 52.8 vs 136.5 +/- 15.0 pg/mL, P =.002). PGE1 administration for 7 days resulted in a significant decrease in the MCP-1 level, from 263.8 +/- 52.8 to 196.1 +/- 25.5 pg/mL (P =.02), whereas levels of IL-6, hs-CRP, and ET-1 and the activity of vWF were not affected.
  
  
  CONCLUSIONS
  Serum MCP-1 levels were elevated in patients with PAOD, indicating the involvement of activation of monocytes in the pathogenesis of this disorder. Parenteral administration of PGE1 appeared to decrease circulating MCP-1 levels, which might lead to the suppression of the development of atherosclerotic lesions in patients with PAOD.
authors.affiliation: Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
authors.forename: Keiji
authors.initials: K
authors.lastname: Matsui
authors.forename: Uichi
authors.initials: U
authors.lastname: Ikeda
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Murakami
authors.forename: Toru
authors.initials: T
authors.lastname: Yoshioka
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Shimada
mesh_terms: D000328:Adult; D000368:Aged; D000527:Alprostadil / Q000008:administration & dosage / Q000627:therapeutic use*; D001157:Arterial Occlusive Diseases / Q000097:blood* / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood*; D019332:Endothelin-1 / Q000097:blood; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D007275:Injections, Intravenous; D015850:Interleukin-6 / Q000097:blood; D007383:Intermittent Claudication / Q000097:blood / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D016491:Peripheral Vascular Diseases / Q000097:blood* / Q000188:drug therapy; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D019332:Endothelin-1; D005343:Fibrinolytic Agents; D015850:Interleukin-6; D014665:Vasodilator Agents; D014841:von Willebrand Factor; D002097:C-Reactive Protein; D000527:Alprostadil