PMID- 12756509
OWN - NLM
STAT- MEDLINE
DCOM- 20040115
LR  - 20181130
IS  - 0031-6970 (Print)
IS  - 0031-6970 (Linking)
VI  - 59
IP  - 3
DP  - 2003 Jul
TI  - Effects of atorvastatin, simvastatin, and fenofibrate therapy on monocyte 
      chemoattractant protein-1 secretion in patients with hyperlipidemia.
PG  - 189-93
AB  - OBJECTIVE: Monocytes that migrate into the arterial wall participate in the 
      development and, eventually, rupture of the atherosclerotic plaque. The aim of 
      this study was to evaluate the secretion of monocyte chemoattractant protein-1 
      (MCP-1) by monocytes from hyperlipidemic patients treated with hypolipidemic 
      drugs, namely fenofibrate, simvastatin, or atorvastatin to determine what role is 
      played by these drugs in the development and stabilization of the atherosclerotic 
      plaque. METHODS: Fifty-four hyperlipidemic patients, who did not respond to a 
      low-fat diet, were treated with fenofibrate, simvastatin, or atorvastatin (18 
      patients in each group) for 1 month. The control group included 18 
      normolipidemic, healthy, age-matched participants. Ten hyperlipidemic patients 
      were effectively treated with hypolipidemic diet alone for 1 month. This group 
      was compared with a control group of ten healthy subjects. To accurately evaluate 
      the adhesion molecule levels, we excluded hyperlipidemic patients and control 
      subjects with any inflammatory disease. Before and after treatment, monocytes 
      were isolated from peripheral blood. After stimulation with lipopolysaccharide 
      (LPS), MCP-1 secretion was measured by enzyme-linked immunosorbent assay (ELISA). 
      RESULTS: MCP-1 levels were significantly higher in hyperlipidemic patients than 
      controls: 15.8+/-0.47, 16.7+/-0.23, and 14.9+/-0.45 compared with 12.36+/-0.42 
      ng/ml. Fenofibrate, atorvastatin, and simvastatin significantly decreased MCP-1 
      levels from 15.8+/-0.47 to 8.79+/-0.89, from 16.7+/-0.23 to 7.46+/-0.73, and from 
      14.9+/-0.45 to 10.3+/-0.8 ng/ml, respectively. In the diet-treated group of 
      hyperlipidemic patients, the level of MCP-1 before therapy was significantly 
      higher than in controls (16.89+/-0.31 vs 12.45+/-0.36 ng/ml). The diet therapy 
      caused a significant decrease in levels of MCP-1 to 15.1+/-0.36 ng/ml. There was 
      a correlation between the decreased levels of lipids and the decreased release of 
      MCP-1 in the patients treated with hypolipemic drugs. CONCLUSION: The 
      drug-induced decrease in MCP-1 secretion in hyperlipidemic patients suggests 
      that, apart from acting on lipids, the hypolipidemic drugs studied may directly 
      inhibit the activity of monocytes.
FAU - Kowalski, J
AU  - Kowalski J
AD  - Department of Clinical Pharmacology, Medical University of Silesia, 40-752 
      Katowice, 18 Medykow, Poland. farmklin@infomed.slam.katowice.pl
FAU - Okopien, B
AU  - Okopien B
FAU - Madej, A
AU  - Madej A
FAU - Zielinski, M
AU  - Zielinski M
FAU - Belowski, D
AU  - Belowski D
FAU - Kalina, Z
AU  - Kalina Z
FAU - Herman, Z S
AU  - Herman ZS
LA  - eng
PT  - Clinical Trial
PT  - Controlled Clinical Trial
PT  - Journal Article
DEP - 20030517
PL  - Germany
TA  - Eur J Clin Pharmacol
JT  - European journal of clinical pharmacology
JID - 1256165
RN  - 0 (Chemokine CCL2)
RN  - 0 (Heptanoic Acids)
RN  - 0 (Hypolipidemic Agents)
RN  - 0 (Lipids)
RN  - 0 (Pyrroles)
RN  - A0JWA85V8F (Atorvastatin)
RN  - AGG2FN16EV (Simvastatin)
RN  - U202363UOS (Fenofibrate)
SB  - IM
MH  - Atorvastatin
MH  - Cells, Cultured
MH  - Chemokine CCL2/*blood/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Fenofibrate/*pharmacology/therapeutic use
MH  - Heptanoic Acids/*pharmacology/therapeutic use
MH  - Humans
MH  - Hyperlipidemias/blood/*drug therapy
MH  - Hypolipidemic Agents/*pharmacology/therapeutic use
MH  - Lipids/blood
MH  - Male
MH  - Middle Aged
MH  - Monocytes/drug effects/metabolism
MH  - Pyrroles/*pharmacology/therapeutic use
MH  - Simvastatin/*pharmacology/therapeutic use
EDAT- 2003/05/21 05:00
MHDA- 2004/01/16 05:00
CRDT- 2003/05/21 05:00
PHST- 2002/09/25 00:00 [received]
PHST- 2003/02/03 00:00 [accepted]
PHST- 2003/05/21 05:00 [pubmed]
PHST- 2004/01/16 05:00 [medline]
PHST- 2003/05/21 05:00 [entrez]
AID - 10.1007/s00228-003-0581-7 [doi]
PST - ppublish
SO  - Eur J Clin Pharmacol. 2003 Jul;59(3):189-93. doi: 10.1007/s00228-003-0581-7. Epub 
      2003 May 17.