Association Between Maternal Intake of Diazepam and Oral Clefts

Saxén, Irma; Saxén, Lauri

doi:10.1016/s0140-6736(75)90567-x

Cited by 149 publications

(35 citation statements)

References 3 publications

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“…However, recall bias may explain the association with diazepam and other drugs found in this study, as it has been reported recently that mothers of malformed children tend to report more accurately exposure to certain drugs and exposure to other factors than do mothers of reference children (26). Therefore, although an association between exposure to diazepam during pregnancy and certain congenital malformations has been reported (27)(28)(29)(30)(31)(32)(33), our findings can hardly be regarded as supportive of this possibility if we consider that the association was present for a heterogeneous group of congenital anomalies and that recall bias could not be excluded.…”

Section: Discussionmentioning

confidence: 71%

Birth defects among children born to a population occupationally exposed to pesticides in Colombia.

Restrepo¹,

Muñóz²,

Day³

et al. 1990

Scand J Work Environ Health

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Section: Discussionmentioning

confidence: 71%

Birth defects among children born to a population occupationally exposed to pesticides in Colombia.

Restrepo¹,

Muñóz²,

Day³

et al. 1990

Scand J Work Environ Health

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“…The induction of cleft palate both by loss-of-function mutations and by an enhancement of function by benzodiazepines suggests that a process during palatogenesis requires a specific range of GABA signaling for normal development. In humans, a link between benzodiazepine use during pregnancy and craniofacial defects has been reported (23)(24)(25) but is controversial (26). The highly penetrant cleft palate phenotype seen in our mice and in the GABA A receptor knockout indicates that the role of benzodiazepines in human craniofacial defects should be carefully reexamined given the widespread use of these drugs.…”

Section: Resultsmentioning

confidence: 95%

Cleft palate in mice with a targeted mutation in the γ-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67

Condie

Bain

Gottlieb

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

137

103

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The functions of neurotransmitters in fetal development are poorly understood. Genetic observations have suggested a role for the inhibitory amino acid neurotransmitter ␥-aminobutyric acid (GABA) in the normal development of the mouse palate. Mice homozygous for mutations in the ␤-3 GABA A receptor subunit develop a cleft secondary palate. GABA, the ligand for this receptor, is synthesized by the enzyme glutamic acid decarboxylase. We have disrupted one of the two mouse Gad genes by gene targeting and also find defects in the formation of the palate. The striking similarity in phenotype between the receptor and ligand mutations clearly demonstrates a role for GABA signaling in normal palate development.

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“…A higher teratogenic risk of diazepam was reported in pregnant women with psychiatric diseases [57][58][59][60] but not in non-psychiatric pregnant women [39,[61][62][63]. The previously mentioned 1,044 pregnant women who attempted suicide during pregnancy, 112 used very large doses of diazepam (25-800 mg) and 37 women attempted suicide between the 4th and 12th gestation week, but a higher rate of CAs was not detected [64].…”

Section: Discussionmentioning

confidence: 99%

Critical Evaluation of Antiepileptic Drugs in Epileptic Pregnant Women - Hungarian Experiences

Czeizel¹,

Bánhidy²

2011

Open Drug Saf J

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Abstract:The prevalence of epilepsy is 0.3-0.6% in pregnant women and the higher rate of structural birth defects, i.e. congenital abnormalities (CAs) was recognized in their children. There are four aims of this review based on the population-based large data set of the Hungarian Case-Control Surveillance of Congenital Abnormalities (HCCSCA), 1980-1996 with the good validity of CA-diagnoses. (I) Most studies on the teratogenic/fetotoxic effects of antiepileptic drugs (AED) had too small samples therefore underpowered, thus the evaluation the findings of different studies together are appropriate to draw significant conclusions, therefore the data of HCCSCA are presented here. Of 22,843 cases with CA, 95 (0.42%), while of 38,151 controls without CA, 90 (0.24 %) had mothers with medically recorded epilepsy (OR with 95% CI: 1.8, 1.3-2.4) and AED in the prenatal maternity logbook. (II) Hungary had different spectrum of AED as in Western countries, thus the teratogenic potential of some less-known AED (e.g. sultiame) can be evaluated. (III) The efficacy of recent special medical care of epileptic pregnant women introduced in 1990 is worth checking. There was no significant increase in the proportion of monotherapy but the rate of total CAs decreased by 20% in the 1990s compared to the 1980s. (IV) Folic acid may reduce the teratogenic potential of some AED, nevertheless this analysis revealed that folic acid was used less frequently by epileptic pregnant women than by non-epileptic pregnant women. Thus an international consensus statement is an urgent task in this topic.

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Association Between Maternal Intake of Diazepam and Oral Clefts

Cited by 149 publications

References 3 publications

Birth defects among children born to a population occupationally exposed to pesticides in Colombia.

Birth defects among children born to a population occupationally exposed to pesticides in Colombia.

Cleft palate in mice with a targeted mutation in the γ-aminobutyric acid-producing enzyme glutamic acid decarboxylase 67

Critical Evaluation of Antiepileptic Drugs in Epileptic Pregnant Women - Hungarian Experiences

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