title: Reduction of lipoprotein(a) by LDL-apheresis using a dextran sulfate cellulose column in patients with familial hypercholesterolemia.
abstract: Lipoprotein(a) (Lp(a)) was eliminated by LDL-apheresis using a dextran sulfate cellulose column in 3 homozygous and 10 heterozygous familial hypercholesterolemic patients. Immediately after LDL-apheresis by the LA-15 system (continuous LDL apheresis), there were significant reductions in Lp(a) concentrations (28.6 +/- 11.8 mg/dl (mean +/- S.E.) to 9.6 +/- 5.6 mg/dl (P < 0.01)), and in LDL-cholesterol concentrations (156 +/- 32 mg/dl to 48 +/- 18 mg/dl (P < 0.01)). Immediately following LDL-apheresis, Lp(a) and LDL-cholesterol were reduced by 67.4% +/- 11.6% and 68.3% +/- 11.8%, respectively. The removal of Lp(a) paralleled that of LDL-cholesterol. The reduced levels of Lp(a) nearly returned to baseline within 7 days. In 6 of the heterozygous FH patients the rates of recovery of LDL cholesterol and Lp(a) were calculated, according to Apstein's equation after discontinuing lipid altering drug treatment for 4 weeks. Mean constant k values of LDL cholesterol and Lp(a) were 0.354 (range: 0.136-0.752) and 0.427 (range 0.112-0.933), respectively. The average concentration during the 7 days following LDL-apheresis was calculated. Average reductions were 28% in LDL cholesterol and 18% in Lp(a). Pravastatin treatment, which continued for 4 weeks, significantly decreased LDL cholesterol (P < 0.01); however, before LDL-apheresis pravastatin treatment significantly increased Lp(a) levels (P < 0.05) in a small number (n = 6) of the FH patients, who had been regularly treated with LDL-apheresis. These results suggest that LDL-apheresis using the dextran sulfate cellulose column is an effective treatment to reduce levels of serum Lp(a) and LDL proportionally. This therapy may be of value in the prevention and regression of coronary artery disease in FH patients.
authors.affiliation: 2nd Department of Internal Medicine, School of Medicine, University of Kanazawa, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Koizumi
authors.forename: I
authors.initials: I
authors.lastname: Koizumi
authors.forename: Y
authors.initials: Y
authors.lastname: Uno
authors.forename: A
authors.initials: A
authors.lastname: Inazu
authors.forename: K
authors.initials: K
authors.lastname: Kajinami
authors.forename: T
authors.initials: T
authors.lastname: Haraki
authors.forename: K
authors.initials: K
authors.lastname: Yagi
authors.forename: N
authors.initials: N
authors.lastname: Kamon
authors.forename: S
authors.initials: S
authors.lastname: Miyamoto
authors.forename: T
authors.initials: T
authors.lastname: Takegoshi
mesh_terms: D000293:Adolescent; D000328:Adult; D001055:Apolipoproteins B / Q000097:blood; D001781:Blood Component Removal / Q000295:instrumentation; D002482:Cellulose; D008078:Cholesterol, LDL / Q000097:blood; D016264:Dextran Sulfate; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000188:drug therapy / Q000628:therapy*; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D017035:Pravastatin / Q000627:therapeutic use
chemical_list: D001055:Apolipoproteins B; D008078:Cholesterol, LDL; D017270:Lipoprotein(a); D002482:Cellulose; D016264:Dextran Sulfate; D017035:Pravastatin