Abstract

I read with great interest the recent article by Mazur et al.1Mazur P. Kozynacka A. Durajski L. Głowacki R. Pfitzner R. Fijorek K. et al.Nɛ-homocysteinyl-lysine isopeptide is associated with progression of peripheral artery disease in patients treated with folic acid.Eur J Vasc Endovasc Surg. 2012; 43: 588-593Google Scholar A number of vitamin deficiencies besides vitamin B12 deficiency may contribute to PAD. Vitamin D deficiency is an independent risk factor for the development and progression of PAD. Individuals with lower serum vitamin D are more prone to develop PAD. Similarly, one third of the increased risk of PAD in Afro-American populations in comparison to Caucasian populations is explained by the lower vitamin D status observed in Afro-American populations. Not surprisingly, secondary hyperparathyroidism is relatively more common in patients with PAD. Higher amputation rates have been noticed in individuals with lower serum vitamin D in the scenario of underlying PAD.2Gaddipati V.C. Bailey B.A. Kuriacose R. Copeland R.J. Manning T. Peiris A.N. The relationship of vitamin D status to cardiovascular risk factors and amputation risk in veterans with peripheral arterial disease.J Am Med Dir Assoc. 2011; 12: 58-61Google Scholar Nearly 14% of patients with PAD demonstrate vitamin C levels less than 11.4 μmol/l.3Langlois M. Duprez D. Delanghe J. De Buyzere M. Clement D.L. Serum vitamin C concentration is low in peripheral arterial disease and is associated with inflammation and severity of atherosclerosis.Circulation. 2001; 103: 1863-1868Google Scholar In fact, a shorter absolute claudication distance is seen in those with low l-ascorbic acid concentration and underlying PAD. The above examples clearly illustrate the importance of vitamin supplementation in patients with PAD and the need to increase awareness about this amongst physicians as well as patients. None declared. Re: ‘Vitamin D Deficiency and PAD: A Close and Often Overlooked Relationship’: Vitamins and Homocysteine MetabolismEuropean Journal of Vascular and Endovascular SurgeryVol. 45Issue 2PreviewWe thank Dr. Kapoor for his interest in our recent article1 and comments on potential links between vitamin D and peripheral artery disease (PAD). Metabolism of homocysteine (Hcy), derived from dietary methionine (Met), is regulated by transsulfuration to cysteine, catalyzed by vitamin B6 dependent cystathionine β-synthase (CBS), and remethylation to Met, catalyzed by vitamin B12 and 5,10-methylenetetrahydrofolate dependent Met synthase (MS).2 Deficiency in vitamin B12, vitamin B6 or folate is associated with increased plasma total Hcy (tHcy), but it is still unknown to what extent reduced vitamin cofactors alter Nɛ–homocysteinyl–lysine (Nɛ–Hcy–Lys), a degradation product of homocysteinylated proteins. Full-Text PDF Open Archive

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