|Values are valid only on day of printing.|
Lysophosphatidylcholine (LPC), also referred to as lysolecithin, is the most abundant lysophospholipid in blood. LPCs may originate from the enzyme lecithin cholesterol acyltransferase (LCAT), by hepatic secretion or via phospholipase A2 activity. The framework of LPC species includes a glycerol frame, one fatty acid, and phosphocholine. The primary fatty acid species LPC associates with in plasma include palmitic acid (16:0) and stearic acid (18:0).(1) The 16:0 LPCs are enriched in HDL whereas the 18:0 forms are predominantly associated with the apolipoprotein-B-containing lipoproteins very-low-density lipoprotein (VDRL) and low-density lipoprotein (LDL). This association may reflect distinct metabolic pathways for individual LPC species.(2)
LPC is a major component of oxidized LDL which is thought to promote atherogenesis by increasing the chemotactic activity of monocytes, inducing adhesion molecules on endothelial cells and accumulating in ischemic myocardium.(3,4) Plasma LPC concentrations may be increased in individuals with various types of cancer and in non-insulin-dependent diabetes mellitus. Decreased concentrations of LPC may be seen in patients with hypoalphalipoproteinemia or acquired diseases such as renal failure.(5) Low LPC concentrations alone are not specific for LCAT deficiency. The LCATD / Lecithin Cholesterol Acyltransferase Deficiency Profile should be ordered if LCAT deficiency is suspected. Results of this profile only give a phenotypic interpretation and molecular testing is recommended for confirmation of LCAT deficiency.
LPC is also a source of lysophosphatidic acid (LPA) which is formed from LPC via hydrolysis. LPA has significant biological activities related to smooth muscle contraction, tumor cell invasion, and cell proliferation.
A screening aid in patients presenting with decreased high density lipid (HDL) cholesterol, to investigate potential hypoalphalipoproteinemia phenotypes prior to confirmatory molecular testing
Decreased concentrations of 16:0 lysophosphatidylcholine (LPC) and 18:0 LPC may suggest lecithin cholesterol acyltransferase deficiency. Results must be interpreted in the context of the patient’s clinical presentation.
No significant cautionary statements
> or =16 years: > or =62 mcmol/L
> or =16 years: > or =20 mcmol/L
Reference values have not been established for patients that are <16 years of age.
1. Croset M, Brossard N, Polette A, Lagarde M. Characterization of plasma unsaturated lysophosphatidylcholines in human and rat. Biochem J 2000; 345:61–67
2. Kontush A, Lhomme M, Chapman MJ. Unravelling the complexities of the HDL lipidome. J Lipid Res 2013 Nov;54(11):2950-2963
3. Quinn MT, Parthasarathy S, Steinberg D. Lysophosphatidylcholine: a chemotactic factor for human monocytes and its potential role in atherogenesis. Proc Natl Acad Sci USA 1988;85:2805–2809
4. Kume N, Cybulsky MI, Gimbrone MA. Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces mononuclear leukocyte adhesion molecules in cultured human and rabbit arterial endothelial cells. J Clin Invest 1992; 90:1138-1144
5. Santamarina-Fojo S, Hoeg JM, Assman G, Brewer HB Jr: Lecithin cholesterol acyltransferase deficiency and fish eye disease. In The Metabolic and Molecular Basis of Inherited Disease. Eighth edition. Edited by C Scriver, A Beaudet, W Sly, et al. New York, McGraw-Hill Book Company, 2001, pp 2817-2833