Maternal Global Methylation Status and Risk of Congenital Heart Diseases

• DOI: 10.1097/aog.0b013e31817dd058
• Publication Date: 2010-11-30T12:46:33Z
• Authors: Lydi M. J. W. van...; Robert de Jonge; Willem A. Helbing; Bertrand D. van Z...; Jaap Ottenkamp; Eric A. P. Steegers; Rėgine P. M. Stee...
• Keywords: Adult; Heart Defects, Congenital; 0301 basic medicine; S-Adenosylmethionine; Hyperhomocysteinemia; Pregnancy Outcome; Infant; Heart; Methylation; S-Adenosylhomocysteine; EMC MGC-02-52-01-A; 3. Good health; Pregnancy Complications; 03 medical and health sciences; Pregnancy; Risk Factors; Case-Control Studies; Prenatal Exposure Delayed Effects; Linear Models; Humans; Female; Down Syndrome; Child; Biomarkers

To investigate whether the association between maternal methylation status as reflected by low S-adenosylmethionine and high S-adenosylhomocysteine, is detrimental for cardiogenesis congenital heart disease (CHD) in offspring.As part of a case-control study western Netherlands, we evaluated 231 mothers children with CHD 315 control nonmalformed children. The total case group was analyzed stratified into isolated (n=180) nonisolated CHDs (n=51). latter subgroup further subdivided Nonsyndromic (n=20), Down Syndrome (n=19), Other Syndromes (n=12). A multivariable general linear model used to test differences groups controls. All analyses were adjusted current B vitamin supplement use.Plasma homocysteine significantly different (median, range 10.3, 4.0-43.8, P=.026) cases (11.1, 5.5-43.8, P=.006) compared controls (10.0, 5.3-42.0). presented higher S-adenosylhomocysteine levels lower S-adenosylmethionine/S-adenosylhomocysteine ratio than controls.Maternal hyperhomocysteinemia, not hypomethylation, risk factor having child CHD. Maternal however, seems be associated offspring syndrome.