Patients with ischemic optical neuropathy may also benefit from LDL apheresis, and in such a population E-selectin, VCAM-1 and ICAM-1 were significantly reduced with a correlation to clinical improvement [85]. In type 2 diabetic patients with end-stage renal disease and peripheral artery disease who were in haemodialysis, LDL apheresis significantly lowered E-Selectin, but not VCAM-1 and ICAM-1 [86]. Consistently, current data indicate that LDL apheresis reduces the expression of adhesion molecules, although with differences between https://www.selleckchem.com/products/ch5424802.html the columns and patient populations tested. The consequences of these findings depend on whether the reduction is purely related to

adsorption to the column, or whether they reflect reduced endothelial cell activation, the latter being of potentially more benefit than the former. The high-density lipoprotein (HDL) molecule is highly complex and consists of lipids and selleck kinase inhibitor several apolipoproteins, among others apolipoprotein-A-1, apolipoprotein-A-2, apolipoprotein-E and apolipoprotein-M [87]. Levels of HDL cholesterol

are closely linked to prognosis in CAD [88, 89]. HDL itself is considered anti-inflammatory [90]. Recent research has demonstrated that the vasoprotective effects of HDL are mediated through apolipoprotein-M and sphingosine-1-phosphate [91]. Sphingosine-1-phosphate exerts its vasoprotective effects through nitric oxide and prostacyclin [92], while apolipoprotein-M seems to increase the antioxidant effect of HDL [93]. It is well known that Urease LDL apheresis lowers HDL cholesterol [94]. Our group also noted a decrease in HDL cholesterol of 12-20% depending on the type of LDL apheresis column [46]. Imminently, this seems like

an unwanted effect of the treatment. The reverse cholesterol transport and anti-inflammatory effects of HDL are thought to be protective for atherosclerosis [82]. However, in the presence of systemic inflammation, the HDL particles can become proinflammatory [95]. Opole et al. [96] showed a reduction in inflammatory HDL cholesterol (cell culture model) during LDL apheresis in parallel with reduction in serum HDL. Moriarty et al. [97] have later demonstrated a reduction in the proinflammatory, HDL-bound apolipoprotein-E (ApoE) during LDL apheresis in heFH. ApoE levels are increased in the FH population [98]. Orsoni et al. [99] confirmed the reduction in ApoE during LDL apheresis in FH and also demonstrated that most of the reduction in HDL was owing to reduction in HDL2 rich in ApoE. The same group has recently reported that LDL apheresis in FH also inhibits the reverse cholesterol pathway [100]. In summary, HDL cholesterol is anti-inflammatory and protects against atherosclerosis owing to complex interactions. Several studies have pointed out that LDL apheresis in addition to lowering LDL cholesterol also lowers HDL cholesterol.