Low phospholipid transfer protein (PLTP) is a risk factor for peripheral atherosclerosis.
OBJECTIVE
Phospholipid transfer protein (PLTP) facilitates cholesterol efflux from cells, intravascular HDL remodelling and transfer of vitamin E and endotoxin. In humans, the relationship of PLTP to atherosclerosis is unknown. However, strong coronary risk factors like obesity, diabetes, cigarette smoking and inflammation increase circulating levels of active PLTP. The aim of the present, cross-sectional study was to analyze the relationship of PLTP to peripheral arterial disease, a marker of generalized atherosclerosis, independently of potentially confounding factors like obesity, diabetes and smoking.


METHODS
We performed a case control study in 153 patients with symptomatic peripheral arterial disease (PAD) and 208 controls free of vascular disease. Smokers and patients with diabetes mellitus were excluded. A lipoprotein-independent assay was used for measurement of circulating bioactive PLTP and an ELISA utilizing a monoclonal antibody was used to analyze PLTP mass.


RESULTS
PLTP activity was significantly decreased in patients with PAD 5.5 (4.6-6.4)(median (25th-75th percentile)) versus 5.9 (5.1-6.9) micromol/mL/h in controls (p=0.001). In contrast, PLTP mass was similar in patients with PAD 8.5 microg/mL (7.3-9.5) and in controls 8.3 microg/mL (6.9-9.7) (p=0.665). Multivariate logistic regression analysis revealed that PLTP activity is independently associated with the presence of PAD. PLTP activity was similar in patients with and without lipid-lowering drugs (p=0.396).


CONCLUSIONS
Our results show that in non-diabetic, non-smoking subjects low rather than high PLTP activity is a marker for the presence of peripheral arterial disease and that distribution of PLTP between high-activity and low-activity forms may be compromised in atherosclerosis.
Schgoer
Wilfried
W
Department of Internal Medicine, Medical University Innsbruck, Austria.
Mueller
Thomas
T
Department of Laboratory Medicine, Konventhospital Barmherzige Brueder, Linz, Austria.
Jauhiainen
Matti
M
Department of Molecular Medicine, National Public Health Institute, Biomedicum, Helsinki, Finland.
Wehinger
Andreas
A
Department of Internal Medicine, Medical University Innsbruck, Austria; Department of Internal Medicine, Landeskrankenhaus Bregenz, Austria.
Gander
Roland
R
Department of Internal Medicine, Medical University Innsbruck, Austria.
Tancevski
Ivan
I
Department of Internal Medicine, Medical University Innsbruck, Austria.
Salzmann
Karin
K
Department of Internal Medicine, Medical University Innsbruck, Austria.
Eller
Philipp
P
Department of Internal Medicine, Medical University Innsbruck, Austria.
Ritsch
Andreas
A
Department of Internal Medicine, Medical University Innsbruck, Austria.
Haltmayer
Meinhard
M
Department of Laboratory Medicine, Konventhospital Barmherzige Brueder, Linz, Austria.
Ehnholm
Christian
C
Department of Molecular Medicine, National Public Health Institute, Biomedicum, Helsinki, Finland.
Patsch
Josef R
JR
Department of Internal Medicine, Medical University Innsbruck, Austria.
Foeger
Bernhard
B
Department of Internal Medicine, Medical University Innsbruck, Austria; Department of Internal Medicine, Landeskrankenhaus Bregenz, Austria. Electronic address: bernhard.foeger@lkhb.at.
D000368:Aged; D050197:Atherosclerosis / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D016491:Peripheral Vascular Diseases / Q000378:metabolism*; D049294:Phospholipid Transfer Proteins / Q000097:blood / Q000378:metabolism*
D015415:Biomarkers; C493430:PLTP protein, human; D049294:Phospholipid Transfer Proteins