title: Treatment of hyperhomocysteinaemia in haemodialysis patients at high cardiovascular risk.
abstract: OBJECTIVE
  Cardiovascular disease (CVD) is the main cause of death among haemodialysis (HD) patients. Emerging cardiovascular risk factors such as oxidative stress and chronic inflammation are involved in these patients together with traditional risk factors. Here we investigate the effects of a short-term folate treatment on some markers of chronic inflammation in two groups of HD patients with and without vascular occlusive disease (VOD).
  
  
  METHODS
  Homocysteine (HCy), C-reactive protein (CRP), Folate, fibrinogen and alpha1 acid glycoprotein (alpha1AGP) were dosed before and after a 3-month course of high-dose folate (25 mg intravenous calcium laevofolinate pentahydride once weekly) and again after a one-month washout in 15 HD patients with established VOD (group A) and in 15 comparable HD patients with no diagnosis of VOD (group B).
  
  
  RESULTS
  Baseline HCy and CRP were significantly elevated in patients of both groups A and B compared to normal values. Folate treatment significantly reduced HCy in patients of both groups A and B and alpha1AGP only in patients of group A, while the other markers were not modified. After the one-month washout a significant raise of CRP could be observed in patients of group A; again, the other markers were not modified.
  
  
  CONCLUSIONS
  Our results suggest that significant reduction of serum HCy can be achieved in both patients with or without VOD after administration of high-dose folic acid. Hence, folic acid supply is useful in the treatment of hyperhomocysteinemia in HD patients, although it is not sufficient to modify their chronic inflammatory status.
authors.affiliation: Chair of Nephrology, Department of Internal Medicine, Tor Vergata University, Rome, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Manca di Villahermosa
authors.forename: M
authors.initials: M
authors.lastname: Tedesco
authors.forename: M
authors.initials: M
authors.lastname: Lonzi
authors.forename: F R
authors.initials: FR
authors.lastname: Della Rovere
authors.forename: M
authors.initials: M
authors.lastname: De Francesco
authors.forename: A
authors.initials: A
authors.lastname: Noce
authors.forename: G
authors.initials: G
authors.lastname: Colarieti
authors.forename: G
authors.initials: G
authors.lastname: Chamoun
authors.forename: E
authors.initials: E
authors.lastname: Moscaritolo
authors.forename: E
authors.initials: E
authors.lastname: Bernabei
authors.forename: E
authors.initials: E
authors.lastname: Athanasopoulou
authors.forename: G
authors.initials: G
authors.lastname: Di Giandomenico
authors.forename: M
authors.initials: M
authors.lastname: Taccone-Gallucci
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D005492:Folic Acid / Q000627:therapeutic use*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis; D012307:Risk Factors; D014652:Vascular Diseases / Q000150:complications; D014803:Vitamin B Complex / Q000627:therapeutic use*
chemical_list: D014803:Vitamin B Complex; D005492:Folic Acid