Literature DB >> 26011648

Comparison of two low-density lipoprotein apheresis systems in patients with homozygous familial hypercholesterolemia.

Jean-Philippe Drouin-Chartier1, André J Tremblay1, Jean Bergeron2, Maude Pelletier2, Nathalie Laflamme2, Benoît Lamarche1, Patrick Couture1,2.   

Abstract

Low-density lipoprotein (LDL) apheresis (LA) is a reliable method to decrease LDL-C concentrations and remains the gold standard therapy in homozygous familial hypercholesterolemia (HoFH). The objective of this study was to compare the efficacy of two LA systems [heparin-induced extracorporeal LDL precipitation (HELP) vs. dextran sulfate adsorption (DS) on the reduction of lipids, inflammatory markers, and adhesion molecules in a sample of genetically defined HoFH subjects (n = 9)]. Fasting blood samples were collected before and after LA. All subjects served as their own control and were first treated with the HELP system then with DS in this single sequence study. Compared with HELP, DS led to significantly greater reductions in total cholesterol (-63.3% vs. -59.9%; P = 0.05), LDL-C (-70.5% vs. -63.0%; P = 0.02), CRP (-75.3% vs. -48.8%; P < 0.0001), and TNF-α (-23.7% vs. +14.7%; P = 0.003). Reductions in the plasma levels of PCSK9 (-45.3% vs. -63.4%; P = 0.31), lipoprotein (a) (-70.6% vs. -65.0%; P = 0.30), E-selectin (-16.6% vs. -18.3%; P = 0.65), ICAM-1 (-4.0 vs. 5.6%; P = 0.56), and VCAM-1 (8.3% vs. -1.8%; P = 0.08) were not different between the two systems. For the same volume of filtered plasma (3,000 mL), however, HELP led to greater reductions in plasma apoB (-63.1% vs. -58.3%; P = 0.04), HDL-C (-20.6% vs. -6.5%; P = 0.003), and PCSK9 (-63.4% vs. -28.5%; P = 0.02) levels. These results suggest that both LA systems are effective in reducing plasma lipids and inflammatory markers in HoFH. Compared with HELP, greater reductions in lipid levels and inflammatory markers were achieved with DS, most likely because this method allows for a larger plasma volume to be filtered. J. Clin. Apheresis 31:359-367, 2016.
© 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.

Entities:  

Keywords:  apheresis; familial hypercholesterolemia; inflammation; lipoproteins

Mesh:

Substances:

Year:  2015        PMID: 26011648     DOI: 10.1002/jca.21406

Source DB:  PubMed          Journal:  J Clin Apher        ISSN: 0733-2459            Impact factor:   2.821


  4 in total

1.  Plasma PCSK9 correlates with apoB-48-containing triglyceride-rich lipoprotein production in men with insulin resistance.

Authors:  Jean-Philippe Drouin-Chartier; André J Tremblay; Jean-Charles Hogue; Valéry Lemelin; Benoît Lamarche; Patrick Couture
Journal:  J Lipid Res       Date:  2018-06-26       Impact factor: 5.922

Review 2.  Biology of proprotein convertase subtilisin kexin 9: beyond low-density lipoprotein cholesterol lowering.

Authors:  Giuseppe Danilo Norata; Hagai Tavori; Angela Pirillo; Sergio Fazio; Alberico L Catapano
Journal:  Cardiovasc Res       Date:  2016-08-05       Impact factor: 10.787

Review 3.  Current Role of Lipoprotein Apheresis.

Authors:  Gilbert Thompson; Klaus G Parhofer
Journal:  Curr Atheroscler Rep       Date:  2019-05-01       Impact factor: 5.113

Review 4.  Advancements in the Treatment of Homozygous Familial Hypercholesterolemia.

Authors:  Archna Bajaj; Marina Cuchel
Journal:  J Atheroscler Thromb       Date:  2022-04-24       Impact factor: 4.394

  4 in total

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