title: Vitamin B-12 metabolism in HIV-infected patients in the age of highly active antiretroviral therapy: role of homocysteine in assessing vitamin B-12 status.
abstract: BACKGROUND
  Before the advent of highly active antiretroviral therapy (HAART), 20% and 10% of HIV-infected patients had low vitamin B-12 and red blood cell folate (RBCF) concentrations, respectively. However, few patients had real vitamin B-12 deficiency.
  
  
  OBJECTIVE
  We evaluated the prevalence of low vitamin B-12 and RBCF concentrations in HIV-infected patients receiving HAART and the usefulness of serum homocysteine (sHcy) for differentiating patients with deficiency from those with harmlessly low vitamin B-12.
  
  
  METHODS
  The prevalence of low vitamin B-12 and RBCF was evaluated in 126 HIV-infected patients receiving HAART. Moreover, sHcy concentrations were evaluated in 40 HIV-infected patients with low vitamin B-12 and in 37 HIV-infected patients with low RBCF and were compared with those in 128 HIV-infected patients with normal vitamin B-12 and RBCF. sHcy was used to monitor treatment with vitamin B-12 and folic acid in 28 patients (24 with low vitamin B-12 and RBCF and 4 with hyperhomocysteinemia but normal vitamin B-12 and RBCF).
  
  
  RESULTS
  The prevalence of low vitamin B-12 was significantly lower in patients receiving HAART than in previously studied patients who did not receive HAART (8.7% compared with 27%). Nine of the 40 patients (22.5%) with low vitamin B-12 (< or = 200 pmol/L) had hyperhomocysteinemia (> 17.5 micromol homocysteine/L). Nineteen (51.4%) of the 37 patients with low RBCF (< or = 580 nmol/L, percentile 10) had hyperhomocysteinemia. Among the 9 patients with an RBCF concentration < or = 450 nmol/L (percentile 2.5), all had hyperhomocysteinemia. The treatment with vitamin B-12 and folic acid normalized sHcy concentrations.
  
  
  CONCLUSIONS
  The prevalence of low vitamin B-12 decreased after the introduction of HAART. The study of sHcy is useful for detecting HIV-infected patients with low vitamin B-12 and real deficiency.
authors.affiliation: Department of Hematology, Hospital de Sant Pau, Barcelona, Spain. aremacha@hsp.santpau.es
authors.forename: Angel F
authors.initials: AF
authors.lastname: Remacha
authors.forename: Josep
authors.initials: J
authors.lastname: Cadafalch
authors.forename: Pilar
authors.initials: P
authors.lastname: Sardà
authors.forename: Montserrat
authors.initials: M
authors.lastname: Barceló
authors.forename: Montserrat
authors.initials: M
authors.lastname: Fuster
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D003937:Diagnosis, Differential; D004912:Erythrocytes / Q000737:chemistry; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage* / Q000097:blood; D005494:Folic Acid Deficiency / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology; D015658:HIV Infections / Q000097:blood* / Q000188:drug therapy; D006710:Homocysteine / Q000097:blood* / Q000502:physiology; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000453:epidemiology; D008297:Male; D015596:Nutrition Assessment; D009752:Nutritional Status; D014805:Vitamin B 12 / Q000008:administration & dosage / Q000097:blood*; D014806:Vitamin B 12 Deficiency / Q000097:blood / Q000175:diagnosis* / Q000453:epidemiology
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D014805:Vitamin B 12