Comparative Teratogenicity of Cortisone and Phenytoin in Mice

McDevitt, Joseph M.; Gautieri, Ronald F.; Mann, David E.

doi:10.1002/jps.2600700614

Cited by 24 publications

(8 citation statements)

References 18 publications

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“…It is thought that this agent has a high likelihood of causing congenital malformation based primarily on experimental studies. 1,5,7,11,13,16,20 However, despite numerous reports, the concentration at which PTH could become harmful has not yet been clarified.…”

Section: Discussionmentioning

confidence: 96%

“…McDavitt and colleagues suggested that PTH may produce palatal anomalies, similar to those produced by cortisone, in mouse fetuses. 7 Gupta et al proposed that PTH executes its teratogenic effect by inhibiting prostaglandin production. 21 However, the mechanism of its teratogenic effect remains uncertain, as does the concentration necessary to induce teratogenicity.…”

Section: Discussionmentioning

confidence: 99%

“…The teratogenic effects of PTH and carbamazepine are still poorly understood. [1][2][3][4][5][6][7][8][9][10][11][12][13] However, a woman with epilepsy who uses anti-epileptic medication during the early stages of pregnancy faces a high risk of teratogenicity.…”

Section: Introductionmentioning

confidence: 99%

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Effect of sodium phenytoin concentration on neural tube development in the early stages of chicken embryo development

Temız

Demirel

et al. 2009

Journal of Clinical Neuroscience

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Effect of sodium phenytoin concentration on neural tube development in the early stages of chicken embryo development

Temız

Demirel

et al. 2009

Journal of Clinical Neuroscience

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“…This basic spectrum of birth defects was confirmed and expanded upon by subsequent investigations into the teratogenicity of PHT to include tracheoesophageal fistulas, cutaneous hemorrhages and NTDs. The differences in the observed pattern of malformations were generally attributable to the differences in species or strain of the experimental animals, route of administration and dosages used in the various studies [Finnell et al, 1993;Fritz et al, 1976;McDevitt et al, 1981;Paulson et al, 1979].…”

Section: Antiepileptic Drugsmentioning

confidence: 99%

Antiepileptic Drugs and Pregnancy Outcomes

Wlodarczyk

Palacios

George³

et al. 2012

Obstetrical &Amp; Gynecological Survey

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The treatment of epilepsy in women of reproductive age remains a clinical challenge. While most women with epilepsy require anticonvulsant drugs for adequate control of their seizures, the teratogenicity associated with some antiepileptic drugs is a risk that needs to be carefully addressed. Antiepileptic medications are also used to treat an ever broadening range of medical conditions such as bipolar disorder, migraine prophylaxis, cancer and neuropathic pain. Despite the fact that the majority of pregnancies of women with epilepsy who are receiving pharmacological treatment are normal, studies have demonstrated that the risk of having a pregnancy complicated by a major congenital malformation is doubled when comparing the risk of untreated pregnancies. Furthermore, when antiepileptic drugs (AEDs) are used in polytherapy regimens, the risk is tripled, especially when valproic acid (VPA) is included. However, it should be noted that the risks are specific for each anticonvulsant drug. Some investigations have suggested that the risk of teratogenicity is increased in a dose-dependent manner. More recent studies have reported that in utero exposure to AEDs can have detrimental effects on the cognitive functions and language skills in later stages of life. In fact, the FDA just issued a safety announcement on the impact of VPA on cognition (Safety Announcement 6-30-2011). The purpose of this document is to review the most commonly used compounds in the treatment of women with epilepsy, and to provide information on the latest experimental and human epidemiological studies of the effects of antiepileptic drugs in the exposed embryos.

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“…When given in vivo with cortisone, DPH does not increase the frequency of cleft palate (20), and a probit analysis of cleft palate produced by DPH and cortisone indicates an identical mechanism (21). Both drugs delay shelf elevation from a vertical to a horizontal position (22).…”

mentioning

confidence: 97%

Inhibition of Programmed Cell Death in Mouse Embryonic Palate in Vitro by Cortisol and Phenytoin: Receptor Involvement and Requirement of Protein Synthesis

Goldman

Baker

Piddington

et al. 1983

Experimental Biology and Medicine

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In an in vitro model cortisol and phenytoin inhibit the precisely timed process of palatal development, the lysosomally mediated cell death of the medial edge palatal epithelium. This inhibition of programmed cell death of the palatal midline epithelium by each drug is virtually completely blocked by the antiglucocorticoid, cortexolone, whose blocking action results from competitive binding of the glucocorticoid receptor site. The inhibition produced by each of these drugs is prevented by the protein synthesis blocker, cycloheximide. Thus, blockade of programmed cell death by each of these drugs involves the glucocorticoid receptor site and requires protein synthesis. 239

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Comparative Teratogenicity of Cortisone and Phenytoin in Mice

Cited by 24 publications

References 18 publications

Effect of sodium phenytoin concentration on neural tube development in the early stages of chicken embryo development

Effect of sodium phenytoin concentration on neural tube development in the early stages of chicken embryo development

Antiepileptic Drugs and Pregnancy Outcomes

Inhibition of Programmed Cell Death in Mouse Embryonic Palate in Vitro by Cortisol and Phenytoin: Receptor Involvement and Requirement of Protein Synthesis

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