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(Circulation Research. 2003;92:1179.)
© 2003 American Heart Association, Inc.

Editorials

Apolipoprotein A-II

Active or Passive Role in Familial Combined Hyperlipidemia

Bradley E. Aouizerat, John P. Kane

From the Department of Physiological Nursing (B.E.A.), School of Nursing, University of California–San Francisco; Cardiovascular Research Institute (J.P.K.), University of California–San Francisco, San Francisco, Calif.

Correspondence to John P. Kane, MD, PhD, Professor of Medicine, Professor of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California–San Francisco, 505 Parnassus Ave, L-1337, San Francisco, CA 94143. E-mail kane@itsa.ucsf.edu

Key Words: apolipoprotein A-II • familial combined hyperlipidemia • hypertriglyceridemia • triglycerides • high-density lipoproteins

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Familial combined hyperlipidemia (FCH) was originally identified as a new phenotype in studies of survivors of myocardial infarctions and their relatives.^1–3 Patients with FCH were found to present with any of three patterns of lipoprotein distribution: elevated plasma levels of very low-density lipoprotein (VLDL) or low-density lipoprotein (LDL) or both. Within kindred, affected individuals often present with different lipoprotein patterns that tend to change over time; most patients manifest the combined pattern at some time.⁴ The phenotype also shares some features with dyslipidemic hypertension⁵ and the metabolic syndrome.⁶ Affected family members tend to display elevated serum apolipoprotein (apo) B levels⁷; in FCH, most studies report an approximate doubling of the secretion rate for apoB-100. The content of intermediate-density lipoproteins (IDL) is usually elevated as well. Of particular interest is the reduced high-density lipoprotein (HDL) cholesterol mass, due in part to the increased movement of cholesteryl esters from HDL particles to triglyceride-rich lipoproteins with increasing plasma triglycerides. This is mediated by cholesteryl ester transfer protein (CETP) and is consistent with a shift of HDL to smaller diameters.

Allayee and colleagues report in this issue of Circulation Research the results of their study of apoA-II levels in families with FCH to determine whether the HDL-associated protein could play a role in the pathogenesis of this common complex lipid disorder.⁸ Their results suggest that plasma apoA-II variation is associated with certain traits that are altered in FCH, providing circumstantial evidence for a potential genetic component for this association. Whereas FCH patients present . . . [Full Text of this Article]

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