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Double filtration plasmapheresis maintains normal adhesion molecule levels
S Yamane1, T Matsugane, K Motohashi
1Tokatsu Clinic Hospital, Matsudo, Chiba, Japan.
Summary
Double filtration plasmapheresis (DFPP) treatment in familial hypercholesterolemia patients did not significantly alter levels of soluble intercellular adhesion molecule-1 (sICAM-1) or soluble vascular cell adhesion molecule-1 (sVCAM-1). DFPP may prevent atherosclerosis progression by removing endothelial-damaging substances.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Medical Technology
Background:
- Elevated plasma levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and von Willebrand factor (vWF) are associated with peripheral vascular disease, ischemic heart disease, and atherosclerosis progression.
- These molecules, along with thrombomodulin (TM), serve as indicators of endothelial damage.
Purpose of the Study:
- To evaluate the impact of long-term double filtration plasmapheresis (DFPP) on plasma levels of vWF, sICAM-1, sVCAM-1, and TM in patients with familial hypercholesterolemia (FH).
- To assess whether DFPP treatment affects endothelial integrity.
Main Methods:
- Plasma levels of vWF, sICAM-1, sVCAM-1, and TM were measured in 4 FH patients before and after DFPP treatment administered at 2-week intervals over 3 years.
- Comparison of pre- and post-treatment values was performed.
Main Results:
- While plasma vWF activity significantly decreased post-DFPP (158% to 45%), plasma TM levels showed no significant change (3.0 FU/ml to 3.4 FU/ml).
- Average sICAM-1 levels decreased slightly from 221 ng/ml to 197 ng/ml, and sVCAM-1 levels decreased from 601 ng/ml to 486 ng/ml, but these changes were not statistically significant.
- Pre-treatment sICAM-1 and sVCAM-1 levels in FH patients with ischemic heart disease were elevated compared to normal values.
Conclusions:
- Long-term DFPP treatment in FH patients does not appear to cause endothelial damage.
- DFPP may potentially inhibit atherosclerosis progression by removing substances that stimulate sICAM-1 and sVCAM-1 production.