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Nutrients 2019, 11(2), 363; https://doi.org/10.3390/nu11020363

Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis

1
Medical Department, Divisions of Hepatology, Gastroenterology, Oncology, Hematologyand Diabetes, Ruppiner Kliniken, Brandenburg Medical School, 16816 Neuruppin, Germany
2
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Medical Department, Division of Hepatology and Gastroenterology (including Metabolic Diseases), Campus Virchow Klinikum, 13353 Berlin, Germany
3
Institute for Food Toxicology and Analytical Chemistry, University of Veterinary Medicine Hannover, 30173 Hannover, Germany
4
Chair of Food Chemistry, Faculty of Mathematics and Natural Sciences, University of Wuppertal, 42119 Wuppertal, Germany
v
Contributed equally
*
Author to whom correspondence should be addressed.
Received: 26 October 2018 / Revised: 2 February 2019 / Accepted: 5 February 2019 / Published: 9 February 2019
PDF [660 KB, uploaded 9 February 2019]

Abstract

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.
Keywords: lipid apheresis; hyperlipoproteinaemia; gas chromatography; oxylipins; lipid mediators; omega-3 polyunsaturated fatty acids, eicosapentaenoic acid; docosahexaenoic acid; lipidomics; LC-MS/MS; n-3 PUFA; n-6 PUFA. lipid apheresis; hyperlipoproteinaemia; gas chromatography; oxylipins; lipid mediators; omega-3 polyunsaturated fatty acids, eicosapentaenoic acid; docosahexaenoic acid; lipidomics; LC-MS/MS; n-3 PUFA; n-6 PUFA.
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Weylandt, K.-H.; Schmöcker, C.; Ostermann, A.I.; Kutzner, L.; Willenberg, I.; Kiesler, S.; Steinhagen-Thiessen, E.; Schebb, N.H.; Kassner, U. Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis. Nutrients 2019, 11, 363.

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