Maternal Epilepsy and Abnormalities of the Fetus and Newborn

Livingston, Samuel; Berman, Wulfred; Pauli, Lydia L.

doi:10.1016/s0140-6736(73)91006-4

Cited by 10 publications

(2 citation statements)

References 2 publications

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“…Similar developmental toxicities have been demonstrated in a range of animal species including the rat (Rowland et al ; Finnell and Dansky ; Beekhuijzen et al, ). However, some human studies have cast doubt on the association between DPH exposure and teratologic risk (Livingston et al, ; Meyer, ; Goujard et al, ; Shepard and Lemire, ). Additionally, no obvious teratogenic effects were found in monkeys even at a maternotoxic and embryo‐lethal doses (Hendrie et al, ; Phillips and Lockard, ).…”

Section: Discussionmentioning

confidence: 99%

“…Meyer (1973) studied retrospectively 199 children born from mothers treated with antiepileptics and could not demonstrate teratogenic action. Livingston et al (1973) and Goujard et al (1974) also reported negative findings. Hanson (1986) reviewed the clinical effects and stated that not more than 5 to 10% of exposed infants develop hydantoin syndrome and that subtle changes can be found in 30%.…”

Section: Introductionmentioning

confidence: 93%

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Dose–Response Effects of Diphenylhydantoin on Pregnant Dams and Embryo‐Fetal Development in Rats

Kim

Lee

Baek

et al. 2012

Birth Defects Research Pt B

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Despite the widespread use of diphenylhydantoin (DPH), there is a lack of reliable information on the teratogenic effects, correlation with maternal and developmental toxicity, and dose-response relationship of DPH. This study investigated the dose-response effects of DPH on pregnant dams and embryo-fetal development as well as the relationship between maternal and developmental toxicity. DPH was orally administered to pregnant rats from gestational days 6 through 15 at 0, 50, 150, and 300 mg/kg/day. At 300 mg/kg, maternal toxicity including increased clinical signs, suppressed body weight, decreased food intake, and increased weights of adrenal glands, liver, kidneys, and brain were observed in dams. Developmental toxicity, including a decrease in fetal and placental weights, increased incidence of morphological alterations, and a delay in fetal ossification delay also occurred. At 150 mg/kg, maternal toxicity manifested as an increased incidence of clinical signs, reduced body weight gain and food intake, and increased weights of adrenal glands and brain. Only minimal developmental toxicity, including decreased placental weight and an increased incidence of visceral and skeletal variations, was observed. No treatment-related maternal or developmental effects were observed at 50 mg/kg. These results show that DPH is minimally embryotoxic at a minimal maternotoxic dose (150 mg/kg/day) but is embryotoxic and teratogenic at an overt maternotoxic dose (300 mg/kg/day). Under these experimental conditions, the no-observed-adverse-effect level of DPH for pregnant dams and embryo-fetal development is considered to be 50 mg/kg/day. These data indicate that DPH is not a selective developmental toxicant in the rat.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 93%

Dose–Response Effects of Diphenylhydantoin on Pregnant Dams and Embryo‐Fetal Development in Rats

Kim

Lee

Baek

et al. 2012

Birth Defects Research Pt B

View full text Add to dashboard Cite

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The Pregnant Epileptic

Montouris¹

1979

Arch Neurol

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The Fetal Trimethadione Syndrome

Feldman

Weaver²,

Lovrien

1977

Am J Dis Child

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We describe a family in which seven pregnancies resulted in four infants who died and in three abortions. During these pregnancies the mother took trimethadione (Tridione), as well as other anticonvulsants. Two normal children were born after treatment with all medications were stopped. There have now been 53 reported pregnancies in which the fetuses were exposed to trimethadione or paramethadione; 48 (87%) resulted in fetal loss or a child born with congenital malformations. The most common defects include malformed ears, cleft palate, cardiac defects, urogenital malformations, and skeletal abnormalities. Delayed mental and physical development were also seen. These findings constitute a clinical entity termed the fetal trimethadione syndrome. The malformation rate is believed to be due to the teratogenic effects of trimethadione. Physicians need to be aware of the danger of trimethadione and related drugs during pregnancy and should withhold these medications during this period.

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Maternal Epilepsy and Abnormalities of the Fetus and Newborn

Cited by 10 publications

References 2 publications

Dose–Response Effects of Diphenylhydantoin on Pregnant Dams and Embryo‐Fetal Development in Rats

Dose–Response Effects of Diphenylhydantoin on Pregnant Dams and Embryo‐Fetal Development in Rats

The Pregnant Epileptic

The Fetal Trimethadione Syndrome

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