title: The effect of atorvastatin treatment on lipid profile and adhesion molecule levels in hypercholesterolemic patients: relation to low-density lipoprotein receptor gene polymorphism.
abstract: Inflammation has been indicated to play a major role in the development of atherosclerosis. The beneficial effect of statins has been suggested to be related to their anti-inflammatory properties. We have studied plasma levels of soluble adhesion molecules in patients with hypercholesterolemia before and after 3 months of treatment with atorvastatin and evaluated possible relations to the mutations in low-density lipoprotein receptor (LDLR) gene. In patients with no LDLR gene polymorphism (group A), lower baseline levels of total cholesterol and LDL cholesterol were found than in patients with LDLR gene polymorphism (group B). The soluble adhesion molecules sICAM-1, sE-selectin and sP-selectin, but not sVCAM-1 and sL-selectin, were higher in group B than in group A. sICAM-1 levels decreased in group A by 7% (p = 0.007) and in group B by 21% (p = 0.039), whereas levels of sVCAM-1 decreased in group A by 12% (p = 0.001) and in group B patients by 19% (p = 0.039). Atorvastatin did not change sE-selectin nor sP-selectin levels in group A. However, in group B, the treatment reduced E-selectin and sP-selectin levels by 39% (p = 0.007) and 24% (p = 0.007), respectively. Atorvastatin attenuates the inflammatory reaction in hypercholesterolemic patients, but in patients with LDLR gene polymorphism, this effect is more profound.
authors: Poznań Medical University, Cardiac and Rehabilitation Hospital Kowanowko, Poznań, Poland.
authors: Andrzej
authors: A
authors: Bolewski
authors: Janusz
authors: J
authors: Lipiecki
authors: Robert
authors: R
authors: Plewa
authors: Pawel
authors: P
authors: Burchardt
authors: Tomasz
authors: T
authors: Siminiak
mesh_terms: D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D019040:E-Selectin / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy* / Q000235:genetics*; D018836:Inflammation Mediators / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011336:Probability; D011446:Prospective Studies; D011758:Pyrroles / Q000008:administration & dosage*; D011973:Receptors, LDL / Q000235:genetics* / Q000378:metabolism; D012016:Reference Values; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019040:E-Selectin; D006538:Heptanoic Acids; D018836:Inflammation Mediators; D011758:Pyrroles; D011973:Receptors, LDL; D018799:Intercellular Adhesion Molecule-1; D000069059:Atorvastatin