Homocysteine (HCY), folate (FA) and vitamin B-12 (B12) in patients receiving an anticonvulsant

Academic Article

Abstract

  • To test a hypothesis that the treatment with anticonvulsant increases plasma HCY secondary to FA deficiency, we measured plasma HCY, folate (PFA) and B12 (PB12), and red-cell folate (RFA) levels in a total of 54 patients with epilepsy (mean 39 years; 28 females and 26 males). For a mean duration of 68 months with a minimum of 3 months, they received mono-anticonvulsant therapy including: phenytoin (P, n=18); lamotrigine (L, n=6); carbamazepine (C, n= 18); and valproate (V, n= 12). Creatinine levels were measured in 41 patients, and all were normal. None of the patients took vitamin supplements. Concentrations of HCY and vitamins (mean ± SD) in each therapy group P L C V HCY (μmol/L) 11.6 ± 9.6 10.0 ± 7.5 11.7 ± 4.5 8.7 ± 2.7 PFA (nmol/L) 7.6 ± 5.9 21.6 ± 14.4* 9.8 ± 7.0 13.3 ± 6.1 RFA (nmol/L) 749 ± 561 1038 ± 471 866 ± 354 943 ± 271 PB12 (pmol/L) 328 ± 125 243 ± 70 327 ± 136 665 ± 325** FA in the L group and PB12 in the V group were significantly higher than the other groups (* p < 0.05, ** p < 0.01); however, there was no difference in HCY among all groups. There were significant negative correlations between HCY and PFA (p < 0.02) and between HCY and PB12 (p < 0.03) in only the C group, indicating HCY may be regulated by unknown factors in addition to FA or B12 nutriture in other groups. Of 54 patients, 7(13%) had their HCY more than 15 μmol/L (24.2 ± 10.1) with a low mean PFA (5.7 ± 3.7). Although anticonvulsant therapy alone does not appear to increase HCY in all patients, it may be preferable to monitor vitamin nutriture among patients with epilepsy.
  • Published In

  • The FASEB Journal  Journal
  • Author List

  • Johnston KE; Tamura T; Vaughn WH; Faught E
  • Volume

  • 11
  • Issue

  • 3