Estimating LDL Apob: Infomania Or Clinical Advance?(Editorial) (Clinical Report‪)‬

Epidemiological and clinical studies have consistently demonstrated that increased concentrations of LDL cholesterol in plasma are associated with increased risk of atherosclerotic cardiovascular disease (CVD). [1] The reference method for LDL cholesterol is [beta]-quantification, a method developed by the CDC that requires ultracentrifugation and is accordingly labor intensive, time consuming, and expensive. Thus, in routine clinical laboratory practice, LDL cholesterol is estimated by the Friedewald formula (1). This equation requires the measurement of total cholesterol, HDL cholesterol, and triglycerides, together with a calculation factor that estimates the concentration of cholesterol in very-low-density lipoprotein (VLDL). However, this formula is not valid for nonfasting patients, when plasma triglyceride concentrations are [greater than or equal to] 4.5 mmol/L (400 mg/dL), in familial dysbetalipoproteinemia, or when there is abnormal VLDL composition. Direct measures of LDL cholesterol are available, but they are not standardized and are expensive. Apolipoprotein B (apoB), a large amphipathic glycoprotein, plays a central role in human lipoprotein metabolism (2). The APOB gene is located on chromosome 2 and produces, via a unique mRNA editing process, two forms of apoB in circulating lipoproteins, apoB-48 and apoB-100 (3). ApoB-48 is the truncated form of apoB-100 consisting of the N-terminal 48% of full-length apoB-100. ApoB-48 is synthesized in the intestine and is essential for the formation and secretion of chylomicrons. ApoB-100 is synthesized in the liver and is an essential structural and functional component of VLDL and its metabolic products, intermediate-density lipoprotein (IDL) and LDL, being the ligand for the LDL receptor.