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Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis

Lipoprotein apheresis reliably reduces low-density lipoprotein (LDL) cholesterol in patients with atherosclerotic disease and therapy-refractory hypercholesterolemia or elevated lipoprotein (a) (Lp(a)). Besides lowering lipoproteins and triglycerides, apheresis also decreases levels of essential ome...

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Autores principales: Weylandt, Karsten-H., Schmöcker, Christoph, Ostermann, Annika I., Kutzner, Laura, Willenberg, Ina, Kiesler, Stefanie, Steinhagen-Thiessen, Elisabeth, Schebb, Nils Helge, Kassner, Ursula
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412478/
https://www.ncbi.nlm.nih.gov/pubmed/30744123
http://dx.doi.org/10.3390/nu11020363
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author Weylandt, Karsten-H.
Schmöcker, Christoph
Ostermann, Annika I.
Kutzner, Laura
Willenberg, Ina
Kiesler, Stefanie
Steinhagen-Thiessen, Elisabeth
Schebb, Nils Helge
Kassner, Ursula
author_facet Weylandt, Karsten-H.
Schmöcker, Christoph
Ostermann, Annika I.
Kutzner, Laura
Willenberg, Ina
Kiesler, Stefanie
Steinhagen-Thiessen, Elisabeth
Schebb, Nils Helge
Kassner, Ursula
author_sort Weylandt, Karsten-H.
collection PubMed
description Lipoprotein apheresis reliably reduces low-density lipoprotein (LDL) cholesterol in patients with atherosclerotic disease and therapy-refractory hypercholesterolemia or elevated lipoprotein (a) (Lp(a)). Besides lowering lipoproteins and triglycerides, apheresis also decreases levels of essential omega-6 and omega-3 polyunsaturated fatty acids (n-6 and n-3 PUFAs) in blood plasma. In contrast, heparin-induced extracorporeal low-density lipoprotein precipitation (HELP) lipid apheresis might increase the formation of potentially pro-inflammatory and pro-thrombotic lipid mediators derived from n-6 and n-3 PUFAs. The study presented here analyzed lipid mediator profiles in the plasma of patients with hyperlipidemia treated by one of three different apheresis methods, either HELP, direct absorption (DA), or membrane filtration (MDF), in a direct pre- and post-apheresis comparison. Using gas chromatography and liquid chromatography tandem mass spectrometry (LC-MS/MS) we were able to analyze fatty acid composition and the formation of lipid mediators called oxylipins. Our data illustrate—particularly in HELP-treated patients—significant decreases of essential omega-6 and omega-3 polyunsaturated fatty acids in blood plasma but significant increases of PUFA-derived lipoxygenase-, as well as cyclooxygenase- and cytochrome P450-derived lipid mediators. Given that n-3 PUFAs in particular are presumed to be cardioprotective and n-3 PUFA-derived lipid mediators might limit inflammatory reactions, these data indicate that n-3 PUFA supplementation in the context of lipid apheresis treatment might have additional benefits through apheresis-triggered protective n-3 PUFA-derived lipid mediators.
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spelling pubmed-64124782019-03-29 Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis Weylandt, Karsten-H. Schmöcker, Christoph Ostermann, Annika I. Kutzner, Laura Willenberg, Ina Kiesler, Stefanie Steinhagen-Thiessen, Elisabeth Schebb, Nils Helge Kassner, Ursula Nutrients Article Lipoprotein apheresis reliably reduces low-density lipoprotein (LDL) cholesterol in patients with atherosclerotic disease and therapy-refractory hypercholesterolemia or elevated lipoprotein (a) (Lp(a)). Besides lowering lipoproteins and triglycerides, apheresis also decreases levels of essential omega-6 and omega-3 polyunsaturated fatty acids (n-6 and n-3 PUFAs) in blood plasma. In contrast, heparin-induced extracorporeal low-density lipoprotein precipitation (HELP) lipid apheresis might increase the formation of potentially pro-inflammatory and pro-thrombotic lipid mediators derived from n-6 and n-3 PUFAs. The study presented here analyzed lipid mediator profiles in the plasma of patients with hyperlipidemia treated by one of three different apheresis methods, either HELP, direct absorption (DA), or membrane filtration (MDF), in a direct pre- and post-apheresis comparison. Using gas chromatography and liquid chromatography tandem mass spectrometry (LC-MS/MS) we were able to analyze fatty acid composition and the formation of lipid mediators called oxylipins. Our data illustrate—particularly in HELP-treated patients—significant decreases of essential omega-6 and omega-3 polyunsaturated fatty acids in blood plasma but significant increases of PUFA-derived lipoxygenase-, as well as cyclooxygenase- and cytochrome P450-derived lipid mediators. Given that n-3 PUFAs in particular are presumed to be cardioprotective and n-3 PUFA-derived lipid mediators might limit inflammatory reactions, these data indicate that n-3 PUFA supplementation in the context of lipid apheresis treatment might have additional benefits through apheresis-triggered protective n-3 PUFA-derived lipid mediators. MDPI 2019-02-09 /pmc/articles/PMC6412478/ /pubmed/30744123 http://dx.doi.org/10.3390/nu11020363 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Weylandt, Karsten-H.
Schmöcker, Christoph
Ostermann, Annika I.
Kutzner, Laura
Willenberg, Ina
Kiesler, Stefanie
Steinhagen-Thiessen, Elisabeth
Schebb, Nils Helge
Kassner, Ursula
Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title_full Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title_fullStr Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title_full_unstemmed Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title_short Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
title_sort activation of lipid mediator formation due to lipoprotein apheresis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412478/
https://www.ncbi.nlm.nih.gov/pubmed/30744123
http://dx.doi.org/10.3390/nu11020363
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