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LDL Cholesterol Direct

LDL Cholesterol Direct
Low Density Lipoproteins (LDL) play a key role in causing and influencing the progression of atherosclerosis and coronary sclerosis in particular. The LDLs are derived from VLDLs (Very Low Density Lipoproteins) rich in trigiycerides by the action of various lipolytic enzymes and are synthe-sized in the liver. The elimination of LDL from plasma takes place mainly by liver parenchymal cells via specific LDL receptors. Elevated LDL concentrations in blood and an increase in their residence time coupled with an increase in the biological modification rate results in the destruction of the endothelial function and a higher LDL-cholesterol uptake in the monocyte/macrophage system as well as by smooth muscle cells in vessel walls. The majority of cholesterol stored in atherosclerotic plaques originates from LDL. The LDL-cholesterol value is the most powerful clinical predictor among all of the single parameters with respect to coronary atherosclerosis. Therefore, therapies focusing on lipid reduction primarily target the reduction of LDL-cholesterol which is then expressed in an improvement of the endothelial function, prevention of atherosclerosis and reducing its progression as well as preventing plaque rupture.

Various methods are available for the determination of LDL-cholesterol such as ultracentrifugation as the reference method, lipoprotein electrophoresis and precipitation methods. In the precipitation methods apolipoprotein-B-containing LDL-cholesterol is, for example, precipitated using either polyvinyl sulfate, dextran sulfate or polycyclic anions. The LDL-cholesterol content is usually calculated from the difference between total cholesterol and cholesterol in the remainder (VLDL- and HDL-cholesterol) in the supernate after precipitation with polyvinyl sulfate and dextran sulfate. Lipid Research Clinics recommend a combination of ultracentrifugation and precipitation methods using polyanions in the presence of divalent cations. The precipitation methods are however time-consuming, cannot be automated and are susceptible to inter-ference by hyperlipidemic serum, particularly at high concentrations of free fatty acids. A more recent method is based on the determination of LDL-cholesterol after the sample is subjected to immunoadsorption and centrifugation.
The calculation of the LDL-cholesterol concentration according to Friedewald's formula is commonly practised. The formula is based on 2 cholesterol determinations, 1 triglyceride determination as well as precipitation of the HDL particles and presumes that a direct relationship exists between VLDL-cholesterol and triglycerides in fasting blood samples. Even in the presence of small amounts of chylomicrons or abnormal lipoproteins, the formula gives rise to falsely low LDL-chol-esterol values. For this reason a great need exists for a simple and reliable method for the determination of LDL-cholesterol without any preparatory steps or calculation.

Intended use
Homogeneous enzymatic assay for the direct quantitative determination of LDL-cholesterol in human serum and plasma

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