R. Wu et al., Antibodies to platelet-activating factor are associated with borderline hypertension, early atherosclerosis and the metabolic syndrome, J INTERN M, 246(4), 1999, pp. 389-397
Citations number
49
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Objective. Platelet-activating factor (PAF) is a phospholipid inflammatory
mediator which is synthesized by a variety of cells, including monocytes an
d endothelial cells, and PAF can be retained in activated endothelial cell
membranes. Furthermore, PAF-like lipids are produced in other phospholipid
membranes as in oxidized LDL. Atherosclerosis is a chronic inflammation in
the artery wall, but little is known about the role of immune reactions in
the early stages of development of cardiovascular disease. In the present s
tudy we investigated if there are antibodies to PAF (aPAF) that may play a
role in borderline hypertension and early atherosclerosis.
Design. Seventy-three men with borderline hypertension (BHT) and 73 age-mat
ched normotensive (NT) men (diastolic blood pressure 85-94 and <80 mmHg, re
spectively) were recruited from a population screening programme. Antibody
levels were determined by use of ELISA. Carotid intima-media (IM)- thicknes
s and atherosclerosis was determined by B-mode ultrasonography.
Results. BHT men had 49.3% higher aPAF levels of IgG class than NT controls
(P = 0.0007). Antibodies to the biologically inactive lysoPAF did not diff
er between BHT and NT group, aPAF levels were associated with LM-thickness
in the left (P = 0.02) and right (P = 0.009) carotid artery. Furthermore, a
PAF levels were enhanced in individuals with the metabolic syndrome (n = 44
) as compared to those without (n = 102; P = 0.009), and also significantly
associated with insulin levels (P = 0.02) and insulin resistance (P = 0.02
).
Conclusions. aPAF antibodies may reflect early vascular changes and thus se
rve as novel markers for disease, and they may also be pathogenic, by elici
ting an inflammatory reaction in the vascular wall.