Increase in plasma homocysteine levels induced by drug treatments in neurologic patients

Antonio Siniscalchi, Franco Mancuso, Luca Gallelli, Guido Ferreri Ibbadu, Nicola Biagio Mercuri, Giovambattista De Sarro

Research output: Contribution to journalArticlepeer-review


Homocysteine (Hcy) is a thyol amino acid resulting from de-methylation of methionine, an essential amino acid derived from dietary proteins. It is metabolized through two pathways: re-methylation and transsulfuration, which use as cofactors folate, vitamin B6 and vitamin B12. Hyperhomocysteinemia has been identified as a risk factor for cerebrovascular disease, dementia, impaired cognitive function and depression. Several drugs may interfere with metabolic pathways of Hcy, leading to an alteration of plasma Hcy levels. Lipid-lowering agents, used to reduce the risk of cerebral venous thrombosis or occlusive vascular disease in patients with high levels of plasmatic lipids, can increase plasma Hcy levels. Hyperhomocysteinemia has been also documented in Parkinson disease patients treated with levodopa and in epileptic patients after chronic treatment with antiepileptic drugs. In contrast, vitamins supplementations may be warranted in patients treated with lipid-lowering agents, levodopa and antiepileptic drugs in order to maintain normal plasma Hcy values. In contrast, higher doses of vitamins can induce dysfunctions in central and peripheral nervous system; therefore excessive supplements should be avoided.

Original languageEnglish
Pages (from-to)367-375
Number of pages9
JournalPharmacological Research
Issue number5
Publication statusPublished - Nov 2005


  • Cardiovascular effects
  • Homocysteine
  • Hyperhomocysteinemia
  • Neurological drugs
  • Vitamin supplementation

ASJC Scopus subject areas

  • Pharmacology


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