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BioMed Research International
Volume 2017 (2017), Article ID 7404397, 5 pages
Research Article

Abnormal Biomarkers of Homocysteine Metabolism in Neonates with Conotruncal Heart Defects

Department of Neonatology, School of Medicine in Katowice, Medical University of Silesia, Katowice, Poland

Correspondence should be addressed to Piotr Surmiak; moc.liamg@kaimrus.kertoip

Received 25 January 2017; Revised 4 May 2017; Accepted 28 June 2017; Published 27 July 2017

Academic Editor: Betti Giusti

Copyright © 2017 Piotr Surmiak 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.


Objectives. The etiology of conotruncal heart defects (CHD) remains unknown; however relation between homocysteine, folate levels, and congenital heart disease was found. With this perspective in mind, the aim of the study was to investigate biomarkers of homosyteine metabolism pathway in mothers and their neonates with CHD. Material and Methods. Forty-three pairs of mothers and their neonates with CHD and forty pairs of mothers and neonates with nonconotruncal heart defects (non-CHD) were enrolled. The control group (CG) consisted of fifty-nine pairs of mothers and their healthy neonates. For estimating the plasma total homocysteine (tHcy), serum folates, and cobalamin levels, mothers’ venous blood samples and umbilical cord blood were taken in all groups. Results. We observed higher tHcy levels in newborns with CHD in comparison to their mothers and to neonates with non-CHD. Cobalamin levels were significantly lower in neonates with CHD compared to other children. Folates and cobalamin levels were lower in CHD mothers compared to their children. Conclusions. Elevated homocysteine levels in neonates with CHD and folate metabolism disturbances in their mothers were noticed. The observed differences in homocysteine and cobalamin levels between neonates with CHD suggest the influence of various agents disturbing homocysteine metabolic pathways.