Second trimester serum predictors of congenital heart defects in pregnancies without chromosomal or neural tube defects

2011 ◽  
Vol 31 (5) ◽  
pp. 466-472 ◽  
Author(s):  
Laura Jelliffe-Pawlowski ◽  
Rebecca Baer ◽  
Anita J. Moon-Grady ◽  
Robert J. Currier
Keyword(s):  
Congenital Heart Defects ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Second Trimester

Hyperglycemia-induced oxidative-stress, apoptosis, and embryopathy

2010 ◽  
Vol 01 (04) ◽  
pp. 309-324 ◽  
Author(s):  
Robert Miller
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Congenital Heart Defects ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Congenital Malformations ◽  
Congenital Heart ◽  
Pediatric Patients ◽  
Heart Defects ◽  
Developmental Problems

AbstractAs the incidence of both type-1 and type-2 diabetes increases, more diabetes-related complications are being observed in pediatric patients. However, some diabetes-related issues in pediatric patients may be a carry-over or consequence of gestational or fetal diabetes. Elevated maternal glucose levels have been associated with increased incidence of spontaneous abortions, perinatal mortality, stillbirths, and congenital malformations. A few of these congenital malformations (embryopathy) in both humans and animals include skin discoloration; webbed toes; cleft lips and palates; congenital heart defects; and neural tube defects. While neural tube defects and congenital heart defects are the most frequent consequence of embryonic / fetal hyperglycemia, hyperglycemia-induced hepatic and renal developmental problems are also known. Hyperglycemia-induced embryopathy has been associated with reduced cell proliferation, oxidative-stress, increased rates of lipid peroxidation coupled with increased homocysteine levels, and apoptosis. Consequently, this review discusses embryonic hyperglycemia-induced reduced embryo viability, increased rates of oxidative-stress, increased lipid peroxidation rates coupled with elevated homocysteine levels, and increased apoptosis rates.

Sacral Meningocele with Conotruncal Heart Defects: A Possible Autosomal Recessive Trait

PEDIATRICS ◽  
1984 ◽  
Vol 74 (3) ◽  
pp. 395-398
Author(s):  
Boris G. Kousseff
Keyword(s):  
Congenital Heart Defects ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Neural Tube Defect ◽  
Congenital Heart ◽  
Autosomal Recessive ◽  
Heart Defects ◽  
Recurrence Risk ◽  
Type I ◽  
Conotruncal Heart Defects

Three of four siblings had sacral meningocele with subsequent development of hydrocephaly; two died during the neonatal period due to conotruncal heart defects (transposition of the great vessels and truncus arteriosus type I, respectively). An in utero diagnosis of open neural tube defect was made on the third sibling; persistent slightly elevated α-fetoprotein levels in amniotic fluid and increased number of rapidly adhering cells in short term amniotic cell culture were found. The unique combination of sacral meningocele and conotruncal malformations in this sibship suggests a new autosomal recessive condition. It also emphasizes the heterogeneity of both the open neural tube defects and congenital heart defects. Awareness of this variant is necessary in regard to the 25% recurrence risk instead of the 3% to 5% recurrence risk given for both congenital heart defects and open neural tube defects as isolated anomalies. The difficult prenatal diagnosis for the small neural tube defect should be appreciated.

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