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International Journal of Vascular Medicine
Volume 2012 (2012), Article ID 968761, 7 pages
Clinical Study

Benfotiamine Counteracts Smoking-Induced Vascular Dysfunction in Healthy Smokers

1Diabetes Center, Heart and Diabetes Center NRW Bad Oeynhausen, Ruhr University of Bochum, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
2Profil Institute for Metabolic Research, Hellersbergstrasse 9, 41460 Neuss, Germany
3Institute for Laboratory and Transfusion Medicine, Heart and Diabetes Center NRW, Bad Oeynhausen, Ruhr University of Bochum, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
4Center for Diabetes, Nutrition and Metabolic Diseases, “Iuliu Hatieganu” University, Str. Clinicilor nr. 2, 400006 Cluj-Napoca, Romania

Received 13 February 2012; Revised 22 August 2012; Accepted 5 September 2012

Academic Editor: Tomoki Hashimoto

Copyright © 2012 Alin Stirban et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Smoking induces endothelial dysfunction (ED) mainly by exacerbating oxidative stress (OS) and inflammation. Benfotiamine, a thiamine prodrug with high bioavailability, prevents nicotine-induced vascular dysfunction in rats. It remained unknown whether this effect also occurs in humans. Methods. Therefore, 20 healthy volunteers (mean age: 38 years) were investigated twice, 7–10 days apart in a randomized, cross-over, and investigator-blinded design. Vascular function was assessed by flow-mediated vasodilatation (FMD) of the brachial artery and by measurements of the soluble vascular cell adhesion molecule (sVCAM)-1. Investigations were performed after an overnight fast as well as 20 minutes after one cigarette smoking. On another day, the same procedure was applied following a 3-day oral therapy with benfotiamine (1050 mg/day). Ten patients were randomized to start with smoking alone, and ten started with benfotiamine. Results. Results are expressed as (mean ± SEM). Smoking acutely induced a decrease in FMD by 50% ( versus baseline) an effect significantly reduced by benfotiamine treatment to 25%§ ( versus baseline, § versus smoking alone). Smoking-induced elevation in sVCAM-1 was also prevented by benfotiamine. The endothelium-independent vasodilatation remained unaltered between days. Conclusion. In healthy volunteers, smoking blunts vascular function mirrored by a decrease in FMD and an increase in sVCAM-1. Short-term treatment with benfotiamine significantly reduces these effects, showing protective vascular properties.