The effects of three different LDL-apheresis methods on the plasma concentrations of E-selectin, VCAM-1, and ICAM-1
✍ Scribed by Klaus Empen; Carsten Otto; Uli C. Brödl; Klaus G. Parhofer
- Book ID
- 102299063
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 114 KB
- Volume
- 17
- Category
- Article
- ISSN
- 0733-2459
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✦ Synopsis
Abstract
Plasma concentrations of cellular adhesion molecules are associated with atherosclerotic diseases and major cardiovascular risk factors. It was shown that LDL‐apheresis with dextran sulfate lowers the levels of E‐selectin and ICAM‐1 in patients with familial hypercholesterolemia. The effects of different LDL‐apheresis methods have not been studied yet. Cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, fibrinogen, and the adhesion molecules E‐selectin, VCAM‐1, and ICAM‐1 were measured in 20 patients with coronary heart disease and severe hyperlipoproteinemia immediately before and after regular LDL‐apheresis. Treatment was performed by different apheresis methods (direct absorption, DA, n = 6; dextran sulfate adsorption, DS, n = 7; heparin precipitation, HP, n = 7). Rebound data of adhesion molecule levels were obtained from 2 patients of each group. Lipids were reduced similarly in all groups. The concentrations of all adhesion molecules were lowered during apheresis. The reduction of E‐selectin (−31 ± 7 vs. −6 ± 5 and −6 ± 5%, respectively, P < 0.001) was most prominent in the patients treated by heparin precipitation. Depending on the method of LDL‐apheresis, the concentrations of VCAM‐1 and E‐selectin in the outlets of the LDL‐apheresis columns were significantly lower compared to the concentration in the inlets. Plasma concentrations of adhesion molecules increased to their pre‐apheresis values within 2 to 4 days following LDL‐apheresis. The reductions of adhesion molecule levels observed during LDL‐apheresis are at least partly due to adsorption to the LDL‐apheresis column. The extent of absorption depends on the principle of extracorporeal LDL elimination. J. Clin. Apheresis 17:38–43, 2002. © 2002 Wiley‐Liss, Inc.