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Published on: October 12, 2017
Activation of Lipid Mediator Formation Due to Lipoprotein Apheresis
Karsten-H Weylandt1,2, Christoph Schmöcker3, Annika I Ostermann4
1Medical Department, Divisions of Hepatology, Gastroenterology, Oncology, Hematologyand Diabetes, Ruppiner Kliniken, Brandenburg Medical School, 16816 Neuruppin, Germany. karsten.weylandt@charite.de.
Insights
Lipid apheresis lowers cholesterol but reduces essential fatty acids. Certain methods, like HELP apheresis, increase pro-inflammatory lipid mediators, suggesting omega-3 fatty acid supplementation may offer cardioprotective benefits.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Lipid Metabolism
Background:
- Lipoprotein apheresis effectively lowers LDL cholesterol in patients with atherosclerotic disease and hypercholesterolemia.
- Apheresis treatments can decrease levels of essential omega-6 and omega-3 polyunsaturated fatty acids (PUFAs).
- Heparin-induced extracorporeal LDL precipitation (HELP) apheresis may promote pro-inflammatory lipid mediators derived from PUFAs.
Purpose of the Study:
- To analyze lipid mediator profiles in hyperlipidemia patients undergoing different apheresis methods.
- To compare pre- and post-apheresis changes in fatty acid composition and oxylipin formation.
- To investigate the impact of HELP, direct absorption (DA), and membrane filtration (MDF) apheresis on lipid mediators.
Main Methods:
- Analysis of plasma lipid mediator profiles using gas chromatography and liquid chromatography tandem mass spectrometry (LC-MS/MS).
- Direct pre- and post-apheresis comparison of patients treated with HELP, DA, or MDF apheresis.
- Quantification of fatty acid composition and oxylipin levels.
Main Results:
- Significant decreases in omega-6 and omega-3 PUFAs were observed, particularly in HELP-treated patients.
- Significant increases in PUFA-derived lipoxygenase-, cyclooxygenase-, and cytochrome P450-derived lipid mediators were noted.
- HELP apheresis showed a distinct impact on lipid mediator profiles compared to DA and MDF.
Conclusions:
- Lipid apheresis, especially HELP, alters essential PUFA levels and increases potentially pro-inflammatory lipid mediators.
- Omega-3 PUFAs are considered cardioprotective, and their derived mediators may reduce inflammation.
- Omega-3 PUFA supplementation during apheresis could enhance cardioprotective effects via apheresis-triggered mediators.
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.
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