Vitamin B12 level in peripheral arterial disease

Katalin S. Zsóri, Zoltán Csiki, Éva Katona, Zsuzsnna Bereczky, Amir Houshang Shemirani

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Hyperhomocysteinemia is considered a risk factor for atherosclerosis. Methyltetrahydrofolate reductase (MTHFR) gene mutation and low level of plasma vitamin B12 and folate could take part in the etiology of peripheral arterial disease (PAD). We examined whether plasma vitamin B12 and folate levels and MTHFR-C677T polymorphism are associated with the risk of PAD. The study comprised 293 patients (107 females, 186 males, mean age of 66 ± SEM0.7 years) and 293 sex-matched control subjects (mean age of 62 ± SEM0.8 years). We also determined plasma lipid profile, hs-CRP, creatinine, vitamin B12, folate and total homocysteine (tHcy) for all patients and controls. Odds ratios were non-significant for different genotypes of MTHFR-C677T polymorphism. There was a significant lower level of vitamin B12 in PAD patients. 43 and 25 % of patient and control populations were in the lowest quartile of vitamin B12 (<188 pmol/L), respectively. Plasma level of vitamin B12 in the lowest quartile significantly increased tHcy level in PAD patients, and it was independent of plasma folate level. Low level of plasma vitamin B12 was independently associated with hyperhomocysteinemia in PAD patients. The prevalence of the MTHFR-C677T mutation was not significantly different in patients with PAD compared with controls.

Original languageEnglish
Pages (from-to)77-83
Number of pages7
JournalJournal of Thrombosis and Thrombolysis
Volume36
Issue number1
DOIs
Publication statusPublished - Jul 1 2013

Keywords

  • Folate
  • Methyltetrahydrofolate reductase
  • Peripheral arterial disease
  • Vitamin B

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Vitamin B<sub>12</sub> level in peripheral arterial disease'. Together they form a unique fingerprint.

  • Cite this