Triglyceride-rich proteins (TRL) consist of a great variety of lipoproteins differing in size, density, and apolipoprotein content. Based on their size and ability to enter the arterial wall, certain TRLs are considered atherogenic while others are not. Remnant lipoproteins, which are considered atherogenic, consist of partially catabolized intestinal chylomicrons or hepatic very low density lipoproteins (VLDLs) that are reduced in size, partially depleted of triglycerides, and enriched with cholesteryl esters. Remnant lipoproteins are also referred to as intermediate density lipoproteins (IDLs) based on how they separate on ultracentrifugation; IDLs are lipoproteins with a density that falls between low density lipoproteins (LDLs) and VLDLs.
Measurement of IDLs has been technically difficult and largely confined to a research setting because IDLs vary in size and contain varying proportions of triglycerides and cholesterol, with no available direct method of testing. However, recently, an immunoseparation assay has received approval from the U.S. Food and Drug Administration (FDA) for the direct measurement of IDL. Measurement of IDLs has been investigated in 2 settings:
- As a tool for risk assessment for coronary heart disease
IDLs are considered atherogenic, and a variety of studies have suggested that IDL are associated with an increase in coronary heart disease risk; e.g., elevated IDLs may be a predictor of progression of coronary atherosclerosis and coronary events. Elevated IDLs may also be associated with a high triglyceride level (from 200-499 mg/dL), which is also a cardiac risk factor.
- As a technique to diagnose type III hyperlipoproteinemia (also called dysbetalipoproteinemia)
Type III hyperlipoproteinemia is an uncommon familial disorder characterized by tuboeruptive and pathognomonic planar xanthomas and a marked predisposition to severe premature atherosclerosis. The disorder is characterized by elevated plasma cholesterol and trigylceride levels, both typically greater than 300 mg/dL. The hyperlipidemia is caused by the accumulation of remnant lipoproteins. Receptor-binding defective forms of apolipoprotein E are typically found. Apo E mediates binding of remnant lipoproteins to their hepatic receptors, and, therefore, when dysfunctional apo E is present, these remnants accumulate in the plasma. Diagnosis of this abnormality is usually based on apo E pheno- or genotyping.