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Valproic acid effect on neural tube defects is not prevented by concomitant folic acid supplementation: Early chick
Insights
Folic acid (FA) may not fully protect against valproic acid (VA)-induced neural tube defects (NTDs) in chick embryos. While FA reduced NTDs, the protective effect did not reach statistical significance in this animal model study.
Area of Science:
- Developmental biology
- Teratology
- Pharmacology
Background:
- Neural tube defects (NTDs) are common congenital malformations.
- Folic acid (FA) supplementation reduces NTD risk during pregnancy.
- Valproic acid (VA), an antiepileptic drug, is associated with increased NTD risk.
Purpose of the Study:
- To investigate the dose-response relationship between valproic acid (VA) and NTDs in an early chick embryo model.
- To determine the protective effect of folic acid (FA) against VA-induced NTDs.
Main Methods:
- Fertile leghorn chicken eggs were divided into six groups (n=20 each): control, FA only, low-dose VA, high-dose VA, low-dose VA + FA, and high-dose VA + FA.
- Eggs were incubated for 24 hours, injected with respective solutions, and examined at 72 hours of incubation.
Main Results:
- No NTDs were observed in the control or FA-only groups.
- High-dose VA significantly increased NTDs compared to low-dose VA (p=0.018).
- A significant difference in NTDs was also observed between low-dose and high-dose VA when combined with FA (p=0.031).
Conclusions:
- Concomitant folic acid administration showed a trend towards decreasing NTDs but did not reach statistical significance.
- Further experimental and clinical studies are needed to elucidate the mechanism of FA in potentially inhibiting antiepileptic drug-induced teratogenicity.
Background:
Neural tube defect is one of the most prevalent congenital malformations and it involves a variety of malformations ranging from anencephaly to spina bifida. Folic acid supplementation during pregnancy is known to reduce risk of neural tube defects. Antiepileptic drugs have been associated with neural tube defects, one of which is valproic acid. Protective effect of folic acid on congenital malformations in patients using valproic acid or other antiepileptic medicines during pregnancy has not clearly been delineated uniformly in previous clinical series. In this experimental animal study of early chick embryo model, we would like to determine if there is any dose-response relationship between VA and NTDs and if there is any protective effect of FA on this relationship in early chick embryo period.
Methods:
One hundred twenty-two fertile leghorn type chicken eggs were used in this study. Six groups, each of which composed of 20 fertilized eggs, were categorized as: group A-control, group B- folic acid, group C-low-dose valproic acid, group D-high-dose valproic acid, group E-low-dose valproic acid + folic acid, group F-high-dose valproic acid + folic acid. Eggs were hatched for 24 h and injected with destined solutions and hatched till 72th hour.
Results:
No neural tube defect was observed in group A and B. High dose valproic acid led to significantly higher number of embryos with neural tube defects compared to low-dose valproic acid (p = 0.018). This significant difference was also present between low-dose and high dose valproic acid combined with folic acid (p = 0.031). When effect of folic acid was evaluated no significant difference observed between groups.
Conclusions:
Even though number of embryos with neural tube defects decreased with concomitant folic acid administration, this difference could not reach a statistical level. More experimental animal and large-scaled prospective clinical studies are in need to detect folic acid mechanism in inhibiting antiepileptic drugs, if any present.
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