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Vitamin B12 level in peripheral arterial disease
Katalin S Zsóri1, Zoltán Csiki, Éva Katona
1Clinical Research Center, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.
Journal of Thrombosis and Thrombolysis
|September 18, 2012
Summary
Low vitamin B12 levels are linked to higher homocysteine in peripheral arterial disease (PAD) patients. MTHFR gene mutations were not significantly associated with PAD risk in this study.
Area of Science:
- Cardiovascular Science
- Nutritional Biochemistry
- Genetics
Background:
- Hyperhomocysteinemia is a known risk factor for atherosclerosis.
- Peripheral arterial disease (PAD) may be influenced by MTHFR gene mutations and low vitamin B12 or folate levels.
Purpose of the Study:
- To investigate the association between plasma vitamin B12, folate levels, MTHFR-C677T polymorphism, and the risk of PAD.
- To determine if these factors are linked to hyperhomocysteinemia in PAD patients.
Main Methods:
- A case-control study involving 293 PAD patients and 293 controls.
- Measurement of plasma lipid profile, hs-CRP, creatinine, vitamin B12, folate, and total homocysteine (tHcy).
- Analysis of MTHFR-C677T polymorphism genotypes.
Main Results:
- No significant association was found between MTHFR-C677T polymorphism genotypes and PAD risk.
- PAD patients exhibited significantly lower plasma vitamin B12 levels compared to controls.
- Low plasma vitamin B12 (<188 pmol/L) was independently associated with hyperhomocysteinemia in PAD patients, irrespective of folate levels.
Conclusions:
- Low plasma vitamin B12 is an independent risk factor for hyperhomocysteinemia in PAD patients.
- MTHFR-C677T gene mutation prevalence did not differ significantly between PAD patients and controls.
- Vitamin B12 deficiency may play a role in the pathophysiology of PAD through elevated homocysteine levels.
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