In November 2011, Emily W.Y. Tung and Louise M. Winn of the Department of Pharmacology and Toxicology at Queen’s University in Ontario, Canada published a study titled “Valproic acid-induced DNA damage increases embryonic p27KIP1 and caspase-3 expression: A mechanism for valproic-acid induced neural tube defects” that studied the mechanism by which valproic acid causes neurological birth defects. Valproic acid is the active chemical in antiepileptic drugs Depacon, Depakene, and Depakote.

The abstract of the article begins by stating “Valproic acid (VPA) is a known teratogenic agent that causes neural tube defects.”  Neural tube defects, according to MedlinePlus, a medical encyclopedia curated by the US National Library of Medicine and National Institutes of Health, are described as follows:

“Neural tube defects are birth defects of the brain, spine, or spinal cord. They happen in the first month of pregnancy, often before a woman even knows that she is pregnant. The two most common neural tube defects are spina bifida and anencephaly. In spina bifida, the fetal spinal column doesn’t close completely. There is usually nerve damage that causes at least some paralysis of the legs. In anencephaly, most of the brain and skull do not develop. Babies with anencephaly are either stillborn or die shortly after birth. Another type of defect, Chiari malformation, causes the brain tissue to extend into the spinal canal.”

Tung and Winn write that “[Neural Tube Defects (NTDs)] are one of the more common birth defects seen worldwide, occurring at a rate of 0.5–2 per 1000 pregnancies,” but that “Exposure to VPA during the first trimester of pregnancy results in a 1–2% incidence of NTDs in infants, which is 10–20 times the rate seen in the general population”.  For this reason, these researchers consider valproic acid to be a “model teratogen to study NTDs.”

In their study, this team used rodent models and found that valproic acid during pregnancy caused an increase in production of the protein yH2A.X, used as a marker indicating that the drug had induced “double strand breaks” in the DNA of animals (yH2A.X helps repair broken DNA).  This breaking in DNA limits DNA’s ability to replicate and thus inhibiting normal development.

Sadly, the manufacturer of Depacon, Depakene, and Depakote failed to adequately warn users of the risk for neural tube defects associated with these drugs.  As a result, a number of Depacon / Depakene / Depakote neural tube defects lawsuits have been filed.  If you or a loved one used one of these drugs during pregnancy and your child was born with a neural tube defect, you too may be entitled to significant financial compensation.

For a free, no-obligation consultation, contact our team of Depakote neural tube defects lawyers at the information provided below.  We have the compassion, experience, and resources required to win the justice you deserve.  Call today and see how we can help.

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