Effect of LDL-apheresis on the soluble form of Activated Leukocyte Cell Adhesion Molecule (ALCAM)

Introduction/Background: Cardiovascular disease is the major cause of death in patients with diabetes and atherosclerosis is exacerbated under diabetes. Atherosclerosis is an inflammatory disorder in which several converging immune responses induce lipid accumulation in macrophages. Activated leukocyte cell adhesion molecule (ALCAM) functions as a pattern recognition receptor and its soluble form sALCAM is involved in ALCAM-dependent and -independent immune mechanisms. The aim of this study was to investigate the role of aggressive removal of low density lipoprotein-cholesterol (LDL-C) and lipoprotein(a) (Lp [a]) by LDL-apheresis (LA) on sALCAM and to evaluate its association with serum markers of inflammation.

Material and methods: A total of thirteen patients with familial hypercholesterolemia (FH) and severe atherosclerosis refractory to medication and diet were treated additionally with LA every 1 – 2 week for 3 months. Whole blood samples were taken before and after LA treatment and serum concentration of total cholesterol, LDL-C, HDL-C, non-fasting triglycerides, Lp(a), hsCRP and sALCAM were measured.

Results: The concentration of lipoprotein profile parameters decreased after LA as expected. The concentration of sALCAM and hsCRP decreased significantly after LA by 16% and 50% respectively (105.3 ± 7.7 vs. 88.2 ± 6.4 ng/ml, P < 0.005 for sALCAM and 9.0 ± 1.3 vs. 4.5 ± 0.6 mg/l, P < 0.0001 for hsCRP). No correlation was found between the decrease of sALCAM and the decrease of hsCRP.

Conclusions: In patients with severe hypercholesterolemia and advanced atherosclerosis, serum concentration of sALCAM and hsCRP decreased significantly by chronic LA treatment. sALCAM might be a novel marker of immune responses in atherosclerosis which can be significantly lowered by chronic LA.