<abstract xmlns="http://www.w3.org/1999/xhtml"><bold>Background</bold>: there is an overt bias between cardiovascular morbidity and mortality in male and female patients. Research of the past decades postulated that this difference could be due to the lipid-lowering effect of male sexual-steroids, that show decreased values in cardiovascular disease.<bold>Methods</bold>: the aim of our study was to determine total serum testosterone and dehydroepiandrosterone sulfate (DHEA-S) on a peripheral arterial disease patient’s cohort (n=35), in comparison with a healthy control group, (n=23) and to establish correlations with other biological risk factors like serum lipids, C-reactive protein, plasma fibrinogen, and the ankle-brachial pressure index.<bold>Results</bold>: our results showed that total serum testosterone and DHEA-S were significantly decreased in PAD patients in comparison to the control group. We could not observe any significant correlation with the presence of critical ischemia, the levels of total cholesterol, HDL-cholesterol, triglycerides, lipoprotein (a), C-reactive protein or plasma fibrinogen.<bold>Conclusion</bold>: these results express that low androgen levels could be implicated in the pathogenesis of peripheral arterial disease, but testosterone and DHEA-S are not markers of disease severity. The elucidation of their exact role needs larger, population-based studies.</abstract>

Background: there is an overt bias between cardiovascular morbidity and mortality in male and female patients. Research of the past decades postulated that this difference could be due to the lipid-lowering effect of male sexual-steroids, that show decreased values in cardiovascular disease.Methods: the aim of our study was to determine total serum testosterone and dehydroepiandrosterone sulfate (DHEA-S) on a peripheral arterial disease patient’s cohort (n=35), in comparison with a healthy control group, (n=23) and to establish correlations with other biological risk factors like serum lipids, C-reactive protein, plasma fibrinogen, and the ankle-brachial pressure index.Results: our results showed that total serum testosterone and DHEA-S were significantly decreased in PAD patients in comparison to the control group. We could not observe any significant correlation with the presence of critical ischemia, the levels of total cholesterol, HDL-cholesterol, triglycerides, lipoprotein (a), C-reactive protein or plasma fibrinogen.Conclusion: these results express that low androgen levels could be implicated in the pathogenesis of peripheral arterial disease, but testosterone and DHEA-S are not markers of disease severity. The elucidation of their exact role needs larger, population-based studies.

Correlations of Endogenous Testosterone and DHEA-S in Peripheral Arterial Disease

University of Medicine and Pharmacy Tirgu Mures, Romania

Acta Marisiensis - Seria Medica

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Background: there is an overt bias between cardiovascular morbidity and mortality in male and female patients. Research of the past decades postulated that...

Correlations of Endogenous Testosterone and DHEA-S in Peripheral Arterial Disease

Published Online: May 20, 2016

Page range: 217 - 220

Received: Jan 19, 2016

Accepted: Mar 23, 2016

DOI: https://doi.org/10.1515/amma-2016-0021

Keywords
testosterone, DHEA-S, serum lipids, peripheral arterial disease

© 2016 Nagy Elod et al., published by De Gruyter Open

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Correlations of Endogenous Testosterone and DHEA-S in Peripheral Arterial Disease

Published Online: May 20, 2016

Page range: 217 - 220

Received: Jan 19, 2016

Accepted: Mar 23, 2016

DOI: https://doi.org/10.1515/amma-2016-0021

Keywordstestosterone, DHEA-S, serum lipids, peripheral arterial disease

© 2016 Nagy Elod et al., published by De Gruyter Open

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Keywords
testosterone, DHEA-S, serum lipids, peripheral arterial disease