title: Atorvastatin in low-density lipoprotein apheresis-treated patients with homozygous and heterozygous familial hypercholesterolemia.
abstract: To further reduce low-density lipoprotein-cholesterol (LDL-C), atorvastatin treatment was investigated in patients with homozygous (n = 4) and heterozygous (n = 10) familial hypercholesterolemia (FH) undergoing LDL-apheresis. After a wash-out period of 4 weeks, atorvastatin therapy was administered in escalating doses (10 up to 80 mg/d). LDL-apheresis was performed at weekly intervals during the entire study period. The LDL-C concentration decreased from 240 +/- 35 mg/dL after the wash-out period to 206 +/- 63 mg/dL during treatment with 10 mg atorvastatin. Four weeks of treatment with 80 mg atorvastatin resulted in an additional 24% (P <.05) reduction in LDL-C. LDL-C increased from 28.8 +/- 14.2 mg/dL immediately after apheresis to 156.6 +/- 25.5 mg/dL at day 7. LDL-C values remained below the recommended target range for an extended duration of 48 hours in atorvastatin-treated patients, but not in those without concomitant lipid-lowering drug therapy. The levels of high-density lipoprotein-cholesterol (HDL-C) and plasma fibrinogen were unchanged during the entire study period. No adverse events were observed with atorvastatin treatment. Finally, high-dose atorvastatin therapy resulted in a 40% reduction in LDL-apheresis sessions in these patients. Our results show that LDL-C reduction by atorvastatin is a safe and effective therapy in LDL-apheresis patients with severe heterozygous or homozygous FH.
authors.affiliation: Division of Nephrology and Dialysis, Department of Medicine III, University Hospital, Vienna, Austria.
authors.forename: Andreas
authors.initials: A
authors.lastname: Goldammer
authors.forename: Stefanie
authors.initials: S
authors.lastname: Wiltschnig
authors.forename: Gottfried
authors.initials: G
authors.lastname: Heinz
authors.forename: Martin
authors.initials: M
authors.lastname: Jansen
authors.forename: Thomas
authors.initials: T
authors.lastname: Stulnig
authors.forename: Walter H
authors.initials: WH
authors.lastname: Hörl
authors.forename: Kurt
authors.initials: K
authors.lastname: Derfler
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D000069059:Atorvastatin; D001781:Blood Component Removal; D008078:Cholesterol, LDL / Q000097:blood / Q000302:isolation & purification*; D003362:Cost-Benefit Analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006538:Heptanoic Acids / Q000009:adverse effects / Q000627:therapeutic use*; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000188:drug therapy* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011758:Pyrroles / Q000009:adverse effects / Q000627:therapeutic use*; D014280:Triglycerides / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D014280:Triglycerides; D005340:Fibrinogen; D000069059:Atorvastatin