OBJECTIVE: Our purpose was to study maternal blood and amniotic fluid concentrations of homocysteine and relevant vitamins in relation to neural tube defects. STUDY DESIGN: Concentrations of total homocysteine, folate, and vitamins B12 and B6 were measured in maternal blood and amniotic fluid of 27 women carrying a fetus with a neural tube defect and 31 control women carrying a healthy fetus. RESULTS: The mean total homocysteine concentration in amniotic fluid of the study group was significantly higher than that of the control group. The mean concentrations of total homocysteine in blood and the vitamins folate, B12, and B6 in, respectively, blood and amniotic fluid were not significantly different between the groups. The mean concentrations of homocysteine and vitamin B6 were significantly lower in amniotic fluid than in blood in both groups, whereas vitamin B12 in amniotic fluid was higher than in blood. CONCLUSION: These results support the hypothesis that at least the cause of a subset of neural tube defects could reside in a primary or secondary maternal or fetal derangement of homocysteine metabolism.
OBJECTIVE: Our purpose was to study maternal blood and amniotic fluid concentrations of homocysteine and relevant vitamins in relation to neural tube defects. STUDY DESIGN: Concentrations of total homocysteine, folate, and vitamins B12 and B6 were measured in maternal blood and amniotic fluid of 27 women carrying a fetus with a neural tube defect and 31 control women carrying a healthy fetus. RESULTS: The mean total homocysteine concentration in amniotic fluid of the study group was significantly higher than that of the control group. The mean concentrations of total homocysteine in blood and the vitamins folate, B12, and B6 in, respectively, blood and amniotic fluid were not significantly different between the groups. The mean concentrations of homocysteine and vitamin B6 were significantly lower in amniotic fluid than in blood in both groups, whereas vitamin B12 in amniotic fluid was higher than in blood. CONCLUSION: These results support the hypothesis that at least the cause of a subset of neural tube defects could reside in a primary or secondary maternal or fetal derangement of homocysteine metabolism.
Authors: Kerina J Denny; Christina F Kelly; Vinod Kumar; Katey L Witham; Robert M Cabrera; Richard H Finnell; Stephen M Taylor; Angela Jeanes; Trent M Woodruff Journal: Birth Defects Res A Clin Mol Teratol Date: 2016-02-22
Authors: D A Swanson; M L Liu; P J Baker; L Garrett; M Stitzel; J Wu; M Harris; R Banerjee; B Shane; L C Brody Journal: Mol Cell Biol Date: 2001-02 Impact factor: 4.272
Authors: Marie Sutton; James L Mills; Anne M Molloy; James F Troendle; Lawrence C Brody; Mary Conley; Robert Mc Donnell; John M Scott; Peadar N Kirke Journal: Birth Defects Res A Clin Mol Teratol Date: 2011-05-17
Authors: Lynda Knott; Tom Hartridge; Nathan L Brown; Jason P Mansell; Jonathon R Sandy Journal: In Vitro Cell Dev Biol Anim Date: 2003 Jan-Feb Impact factor: 2.416
Authors: Carla A Martinez; Hope Northrup; Jone-Ing Lin; Alanna C Morrison; Jack M Fletcher; Gayle H Tyerman; Kit Sing Au Journal: Am J Obstet Gynecol Date: 2009-08-15 Impact factor: 8.661