title: [Serum lipoprotein (a) levels during treatment with LDL apheresis for homozygous familial hypercholesterolemia].
abstract: BACKGROUND
  Due to the double atherogenic and antifibrinolytic action of lipoprotein (a) (Lp [a]) and its predictive value of cardiovascular disease in hypercholesterolemic patients, we document in the present work the changes in Lp (a) levels of a patient with homozygous familial hypercholesterolemia after one year of LDL-apheresis treatment.
  
  
  METHODS
  A child with LDL-receptor deficiency under weekly LDL-apheresis treatment with dextran-sulfate columns. Serum samples were taken in basal conditions (pre-apheresis) and post-apheresis, as well as from the perfusion system to evaluate the lipoprotein retention capacity of the columns. Samples were processed for Lp (a) determination by ELISA with polyclonal antibodies.
  
  
  RESULTS
  When the treatment was initiated, the patient's Lp (a) serum levels were very high (997 mg/l), and they reduced progressively with the apheresis sessions. After one year of treatment, maximum Lp (a) concentration is only slightly higher than 400 mg/l, whereas minimum Lp (a) concentration is lower than 50 mg/l. Dextran-sulfate columns in the apheresis system retain every lipoprotein containing apo B, including LDL and Lp (a), with high affinity and high capacity in such a way that the treatment of three-fold the plasma volume of the patient results in an 85% decrease of Lp (a) levels. After each LDL-apheresis treatment, there is a progressive increase in Lp (a) concentration. The analysis of these data allowed the estimation of the fractional catabolic rate of Lp (a) in the patient, which was 0.08 pools/day. Simultaneous treatment with lovastatin (20 mg/day) did not alter this parameter or Lp (a) serum concentration.
  
  
  CONCLUSIONS
  After one year of weekly LDL-apheresis treatment, the patient's average Lp (a) serum concentration is lower than 300 mg/l, which is below the risk threshold level. Therefore, apheresis with dextran-sulfate columns is a very effective treatment for the reduction of both LDL and Lp (a) serum concentrations in homozygous familial hypercholesterolemia.
authors.affiliation: Servicio de Bioquímica-Investigación, Hospital Ramón y Cajal, Universidad de Alcalá de Henares, Madrid.
authors.forename: M A
authors.initials: MA
authors.lastname: Lasunción
authors.forename: J L
authors.initials: JL
authors.lastname: Teruel
authors.forename: J J
authors.initials: JJ
authors.lastname: Alvarez
authors.forename: D
authors.initials: D
authors.lastname: Gómez-Coronado
authors.forename: J
authors.initials: J
authors.lastname: Ortuño
authors.forename: E
authors.initials: E
authors.lastname: Herrera
mesh_terms: D001781:Blood Component Removal; D002648:Child; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000628:therapy*; D017270:Lipoprotein(a) / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male
chemical_list: D017270:Lipoprotein(a); D008077:Lipoproteins, LDL
vernacular_title: Lipoproteína (a) en suero durante el tratamiento con aféresis de LDL en la hipercolesterolemia familiar homocigótica.