PMID- 12595852
OWN - NLM
STAT- MEDLINE
DCOM- 20030318
LR  - 20151119
IS  - 1097-6744 (Electronic)
IS  - 0002-8703 (Linking)
VI  - 145
IP  - 2
DP  - 2003 Feb
TI  - Intravenous prostaglandin E1 reduces monocyte chemoattractant protein-1 levels in 
      peripheral arterial obstructive disease.
PG  - 330-3
AB  - OBJECTIVES: 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.
FAU - Matsui, Keiji
AU  - Matsui K
AD  - Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
FAU - Ikeda, Uichi
AU  - Ikeda U
FAU - Murakami, Yoshiaki
AU  - Murakami Y
FAU - Yoshioka, Toru
AU  - Yoshioka T
FAU - Shimada, Kazuyuki
AU  - Shimada K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am Heart J
JT  - American heart journal
JID - 0370465
RN  - 0 (Biomarkers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Endothelin-1)
RN  - 0 (Fibrinolytic Agents)
RN  - 0 (Interleukin-6)
RN  - 0 (Vasodilator Agents)
RN  - 0 (von Willebrand Factor)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - F5TD010360 (Alprostadil)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Alprostadil/administration & dosage/*therapeutic use
MH  - Arterial Occlusive Diseases/*blood/drug therapy
MH  - Biomarkers/blood
MH  - C-Reactive Protein/analysis
MH  - Case-Control Studies
MH  - Chemokine CCL2/*blood
MH  - Endothelin-1/blood
MH  - Female
MH  - Fibrinolytic Agents/administration & dosage/*therapeutic use
MH  - Humans
MH  - Injections, Intravenous
MH  - Interleukin-6/blood
MH  - Intermittent Claudication/blood/drug therapy
MH  - Male
MH  - Middle Aged
MH  - Peripheral Vascular Diseases/*blood/drug therapy
MH  - Vasodilator Agents/administration & dosage/*therapeutic use
MH  - von Willebrand Factor/analysis
EDAT- 2003/02/22 04:00
MHDA- 2003/03/19 04:00
CRDT- 2003/02/22 04:00
PHST- 2003/02/22 04:00 [pubmed]
PHST- 2003/03/19 04:00 [medline]
PHST- 2003/02/22 04:00 [entrez]
AID - S0002870302948350 [pii]
AID - 10.1067/mhj.2003.145 [doi]
PST - ppublish
SO  - Am Heart J. 2003 Feb;145(2):330-3. doi: 10.1067/mhj.2003.145.