title: Homocysteine levels in patients treated with lipid apheresis: effect of a vitamin therapy.
abstract: BACKGROUND
  Patients treated with lipid apheresis already suffer from familial hypercholesterolemia and severe coronary heart disease: any additional risk factor is dangerous for these patients. Hyperhomocysteinemia has been recognized as an independent risk factor for atherosclerotic disease. We checked the frequency of hyperhomocysteinemia in lipid apheresis patients and measured the effect of a vitamin therapy.
  
  
  METHODS
  Sixteen heterozygous patients (10 males, 6 females) were studied, who were being treated by three different apheresis procedures. Homocysteine was measured using an enzyme conversion immunoassay. Cystathionine and methylmalonic acid were assessed by gas chromatography/mass spectrometry. Serum levels of folic acid, vitamin B12, and vitamin B6 were also determined. The patients received a vitamin therapy (3 mg folate, 60 microg cyanocobalamine, 10 mg pyridoxine hydrochloride daily) for 12 weeks.
  
  
  RESULTS
  In 9 out of 16 patients, plasma homocysteine levels were found to be elevated (> 12 micromol L(-1)). Cystathionine concentrations were also increased, especially in those patients with elevated homocysteine. Methylmalonic acid levels were not elevated. Serum folic acid, vitamin B6, and vitamin B12 concentrations were initially in the normal range and not correlated to plasma homocysteine. The vitamin therapy reduced the plasma homocysteine concentrations in all patients significantly by 33%. Among those patients with elevated homocysteine levels, the optimal range < 12 micromol L(-1) for homocysteine was rarely reached.
  
  
  CONCLUSIONS
  In patients treated with lipid apheresis, a hyperhomocysteinemia can be frequently seen. The constellation of both elevated homocysteine and cystathionine levels points to the existence of tissue vitamin deficiencies, folate and vitamin B-6, which were improved by vitamin supplements. Because methylmalonic acid was mostly normal, a vitamin B-12 deficiency was not proven.
authors.affiliation: Institut und Poliklinik für Klinische Stoffwechselforschung, Universitätsklinikum Dresden, Dresden, Germany. julius@rcs.urz.tu-dresden.de
authors.forename: U
authors.initials: U
authors.lastname: Julius
authors.forename: J
authors.initials: J
authors.lastname: Pietzsch
authors.forename: S
authors.initials: S
authors.lastname: Gromeier
authors.forename: H
authors.initials: H
authors.lastname: Schorr
authors.forename: W
authors.initials: W
authors.lastname: Herrmann
mesh_terms: D000328:Adult; D003540:Cystathionine / Q000097:blood; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage / Q000032:analysis / Q000097:blood / Q000627:therapeutic use*; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000188:drug therapy* / Q000209:etiology; D006938:Hyperlipoproteinemia Type II / Q000097:blood* / Q000150:complications / Q000628:therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D014805:Vitamin B 12 / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*; D025101:Vitamin B 6 / Q000008:administration & dosage / Q000097:blood / Q000627:therapeutic use*
chemical_list: D008055:Lipids; D006710:Homocysteine; D003540:Cystathionine; D025101:Vitamin B 6; D005492:Folic Acid; D014805:Vitamin B 12