Abstract
Forty four consecutive subjects aged 29-58 years (21 males and 23 females) with a clinical diagnosis of heterozygous familial hypercholesterolemia period- ically treated every 30 days with LDL-apheresis for statin resistance, were enrolled in this study. A lipid profile was obtained immediately before starting LDL-apheresis, a second profile was obtained within four hours after LDL-apheresis. Chit activity and anti-oxLDL levels were determined with appropriate methods in all patients before and after LDL- apheresis. Total cholesterol, LDL-cholesterol, HDL- cholesterol and triglycerides decreased significantly after LDL-apheresis, while the variations of Chit activity and anti-oxLDL were not significant after LDL-apheresis. The correlation between Chit and total cholesterol was negative (r= -0.44 and -0.50 res- pectively) before and after LDL-apheresis as between Chit and LDL-cholesterol (r= -0.45 and -0.55 respectively). Anti-oxLDL concentration before and after LDL-apheresis positively correlated with Chit activity (r= 0.52 and r = 0.63 respectively), negatively with total cholesterol (r= -0.33 and r = -0.35 res- pectively) and with LDL (r = -0.32 and r = -0.21 respectively). We think that removing LDL with LDL-apheresis the anti-oxLDL/oxLDL ratio could increase and the excess of anti-oxLDL could induce macrophage activation through the surface Fc receptors. Alternatively with high levels of LDL- cholesterol, the deposition of foam cells represent the characteristic evolution of atherosclerosis process. Macrophage activation in the heterozygous familial
Highlights
Familial hypercholesterolemia (FH) is a genetic alteration of lipoprotein metabolism caused by defects in the low density lipoprotein receptor (LDLR) [1]
LDL-apheresis represents an effective therapy in heterozygous FH (heFH) patients, who had no response to highest doses of statin drugs, and could restore the physiological mechanism of antioxLDL/oxidized LDL (oxLDL) immunocomplexes clearance altered by LDLR genetic defect [15]
Chit activity was found elevated before LDL-apheresis, without difference between males (11.94+8.68 nmol/ml/h) and females (12.26+7.70 nmol/ml/h), considering that 7.3±1.9 nmol/ml/h activity was found in healthy control of the same age in our laboratory
Summary
Familial hypercholesterolemia (FH) is a genetic alteration of lipoprotein metabolism caused by defects in the low density lipoprotein receptor (LDLR) [1]. High LDL levels, secondary to the LDLR homozygous defect, are associated to significant increase of oxidized LDL (oxLDL), which removed from circulation lead to massive lipid accumulation, foam cell formation in endothelial wall, often tendom xanthomas (TX) and corneal arcus [2]. FH represent a paradigmatic example of atherosclerosis produced by oxLDL accumulation and a model to study the role of macrophage activation in atherosclerosis process [1]. Generated oxLDL induces an immune response with production of anti-oxLDL antibodies and macrophage cells could remove from circulation immune complexes anti-oxLDL/oxLDL through the Fc receptor for antibodies [4]. Shoji et al 2000 [5] found a inverse correlation among anti-oxLDL and oxLDL in healthy individuals supporting the hypothesis that this mechanism is operating in condition where oxLDL are Published Online November 2009 in SciRes. http://www.scirp.org/journal/jbise
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