Test ID: LMPP    
Lipoprotein Metabolism Profile

Diagnosing dyslipoproteinemia

Quantitation of cholesterol and triglycerides in very-low-density lipoprotein (VLDL), LDL, HDL, and chylomicrons

Identification of LpX

Classifying hyperlipoproteinemias (lipoprotein phenotyping)

Evaluating patients with abnormal lipid values (cholesterol, triglyceride, HDL, LDL)

Quantifying lipoprotein a (Lp[a]) cholesterol

Lipoprotein metabolism profile analysis adds practical information about the etiology of cholesterol and/or triglyceride elevation. In some patients, increased serum lipids reflects elevated levels of intermediate-density lipoprotein (IDL), very-low-density lipoprotein (VLDL), lipoprotein a (Lp[a]), or even the abnormal lipoprotein complex-LpX. These elevations can be indicative of a genetic deficiency in lipid metabolism or transport, nephrotic syndrome, endocrine dysfunction or even cholestasis. Identification of the lipoprotein associated with lipid elevation is achieved using the gold-standard methods, which include ultracentrifugation, selective precipitation, electrophoresis, and direct measurement of cholesterol and triglycerides in isolated lipoprotein fractions. Proper characterization of a patient’s dyslipidemic phenotype aids clinical decisions and guides appropriate therapy.

Classifying the hyperlipoproteinemias into phenotypes places disorders that affect plasma lipid and lipoprotein concentrations into convenient groups for evaluation and treatment. A clear distinction must be made between primary (inherited) and secondary (liver disease, alcoholism, metabolic diseases) causes of dyslipoproteinemia. Lipoprotein profiling will identify the presence of Lp(a) and LpX and distinguish between the following dyslipidemias:

-Exogenous hyperlipemia (Type I)

-Familial Hypercholesterolemia (Type IIa)

-Familial Combined Hyperlipidemia (Type IIb)

-Familial dysbetalipoproteinemia (Type III)

-Endogenous hyperlipemia (Type IV)

-Mixed hyperlipemia (Type V)

Reference values have not been established for patients that are <2 years of age.

*National Cholesterol Education Program (NCEP)

**Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents

***National Lipid Association

For discussion of primary disorders associated with dyslipidemias see Lipids and Lipoproteins in Blood Plasma (Serum) in Special Instructions.

For discussion of Lp(a), see LPAWS / Lipoprotein (a) Cholesterol, Serum.

Reference values are based on fasting collections; it is essential that the patient fasts 12 to 14 hours before the test.

Result can be falsely decreased in patients with elevated levels of N-acetyl-p-benzoquinone imine (NAPQI)-a metabolite of acetaminophen), N-acetylcysteine (NAC), and metamizole.

1. Schriver CR, Beaudet AL, Sly WS, Valle D: Lipoprotein and lipid disorders. In The Metabolic Basis of Inherited Disease. Sixth edition. Edited by JB Stanbury, JB Wyngaarden, DS Frederickson. New York, McGraw-Hill Book Company, 1989, pp 1129-1302

2. Grinstead GF, Ellefson RD: Heterogeneity of lipoprotein Lp(a) and apolipoprotein(a). Clin Chem 1988;34:1036-1040

3. Jacobson TA, Ito MK, Maki KC, et al: National Lipid Association recommendations for patient-centered management of dyslipidemia: Part 1-executive summary. J Clin Lipidol 2014 Sep-Oct;8(5):473-488

4. Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report. Pediatrics 2011 Dec;128 Suppl 5:S213-S256

5. Contois JH, McConnell JP, Sethi AA, et al: Apolipoprotein B and Cardiovascular Disease Risk: Position Statement from the AACC Lipoproteins and Vascular Diseases Division Working Group on Best Practices. Clinical Chemistry 2009:55:3:407-419

• Lipids and Lipoproteins in Blood Plasma (Serum)