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Статті в журналах з теми "In Utero Drug Exposures"

Автор: Grafiati

Опубліковано: 25 травня 2024

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1

Huestis, Marilyn A., and Robin E. Choo. "Drug abuse’s smallest victims: in utero drug exposure." Forensic Science International 128, no. 1-2 (August 2002): 20–30. http://dx.doi.org/10.1016/s0379-0738(02)00160-3.

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2

Bech, Laura Fuglsang, Christoffer Polcwiartek, Kristian Kragholm, Mikkel Porsborg Andersen, Christopher Rohde, Christian Torp-Pedersen, Jimmi Nielsen, and Søren Hagstrøm. "In utero exposure to antiepileptic drugs is associated with learning disabilities among offspring." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 12 (August 3, 2018): 1324–31. http://dx.doi.org/10.1136/jnnp-2018-318386.

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ObjectivesIn utero exposure to antiepileptic drugs has previously been associated with adverse outcome among offspring, but evidence on longer term milestone development remains limited. We investigated the association between in utero exposure to antiepileptic drugs and learning disabilities in the first year of compulsory education among offspring and assessed which antiepileptic drugs carried the highest risk.MethodsThis population-based case–cohort study used Danish nationwide register data from 2005 to 2008. Cases were offspring exposed to antiepileptic drugs in utero, and controls were unexposed offspring of mothers previously redeeming antiepileptic drug prescriptions. Offspring were followed from birth until the first year of compulsory education from 2011 to 2015. Learning disabilities were defined as mental retardation, specific developmental disorders, autism spectrum disorders, emotional/behavioural disorders or having special educational needs. Logistic regression was used to compute ORs with 95% CIs adjusted for potential confounding.ResultsOf 117 475 incident singleton births, 636 cases and 434 controls were included (median age: 6.1 years, males: 55.7%). Learning disabilities were identified among 7.1% cases compared with 3.7% for controls. During any trimester, the adjusted OR of the association between in utero exposure to antiepileptic drugs and learning disabilities was 2.20 (95% CI 1.16 to 4.17). Among cases not exposed to polytherapy (n=556), in utero exposure to lamotrigine compared with another antiepileptic drug was associated with the lowest adjusted risk (OR 0.42, 95% CI 0.19 to 0.92), and valproate carried a higher risk (OR 4.67, 95% CI 1.73 to 12.59).ConclusionIn utero exposure to antiepileptic drugs was significantly associated with learning disabilities among offspring. Lamotrigine should preferentially be considered over, for example, valproate if clinically feasible.

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3

Wright, Tricia. "Biochemical Screening for in utero Drug Exposure." Drug Metabolism Letters 9, no. 2 (October 27, 2015): 65–71. http://dx.doi.org/10.2174/1872312809666150904182334.

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Mulvihill, A. O., P. D. Cackett, N. D. George, and B. W. Fleck. "Nystagmus secondary to drug exposure in utero." British Journal of Ophthalmology 91, no. 5 (December 13, 2006): 613–15. http://dx.doi.org/10.1136/bjo.2006.105569.

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5

Cackett, Peter D., Nick George, Brian Fleck, and Alan Mulvihill. "Nystagmus Secondary to Drug Exposure In Utero." Journal of American Association for Pediatric Ophthalmology and Strabismus 10, no. 1 (February 2006): 84. http://dx.doi.org/10.1016/j.jaapos.2006.01.138.

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6

Meador, Kimford J. "Effects of in Utero Antiepileptic Drug Exposure." Epilepsy Currents 8, no. 6 (October 6, 2008): 143–47. http://dx.doi.org/10.1111/j.1535-7511.2008.00273.x.

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Recent studies demonstrate an increased teratogenic risk for valproate and a probable increased risk for phenobarbital. Carbamazepine and lamotrigine appear relatively safe; however, results are inconclusive concerning a specific risk for cleft lip/palate for both drugs as well as a dose-dependent effect for malformations associated with lamotrigine. Data regarding teratogenic risks for other antiepileptic drugs are inadequate. Additional studies are needed to delineate further the risks for all antiepileptic drugs and determine the underlying mechanisms.

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7

Schraw, Jeremy M. "Anticancer drug exposure in utero and leukemia." Blood 143, no. 4 (January 25, 2024): 293–94. http://dx.doi.org/10.1182/blood.2023022496.

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8

&NA;. "Long-Term Effects of In Utero Drug Exposure." AJN, American Journal of Nursing 108, no. 5 (May 2008): 21. http://dx.doi.org/10.1097/01.naj.0000317982.71371.39.

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9

Gray, Teresa, and Marilyn Huestis. "Bioanalytical procedures for monitoring in utero drug exposure." Analytical and Bioanalytical Chemistry 388, no. 7 (March 17, 2007): 1455–65. http://dx.doi.org/10.1007/s00216-007-1228-9.

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10

Meador, Kimford. "Anatomical and Behavioral Effects of in Utero Exposure to Antiepileptic Drugs." Epilepsy Currents 5, no. 6 (November 2005): 212–16. http://dx.doi.org/10.1111/j.1535-7511.2005.00067.x.

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Increased Rate of Major Malformations in Offspring Exposed to Valproate during Pregnancy Wyszynski DF, Nambisan M, Surve T, Alsdorf RM, Smith CR, Holmes LB, Antiepileptic Drug Pregnancy Registry Neurology 2005;64:961–965 Purpose To determine the rate of occurrence of major malformations in infants whose mothers had taken the drug valproic acid (VPA) as monotherapy during the first trimester of pregnancy and had enrolled in the North American Antiepileptic Drug Pregnancy Registry. Methods Data were collected from pregnant women throughout the United States and Canada through telephone-based interviews. Each woman was interviewed at enrollment, at 7 months’ gestation, and postpartum. With her written permission, the medical records of each mother and her infant were obtained. The major malformations tabulated were those identified at or before age 5 days. The prevalence of congenital malformations among offspring of monotherapy VPA-exposed women was compared with that among infants of women exposed to all other antiepileptic drugs (internal comparison group) and with that among newborns in the Active Malformations Surveillance Program at Brigham and Women's Hospital (external comparison group). Results Sixteen affected cases were identified among 149 VPA-exposed women (proportion: 10.7%; 95% CI: 6.3 to 16.9%). The prevalence in the internal comparison group was 2.9% (95% CI: 2.0 to 4.1%; odds ratio: 4.0; 95% CI: 2.1 to 7.4; P < 0.001). Assuming a 1.62% prevalence in the external comparison group, the relative risk of having an affected offspring for VPA-exposed women was 7.3 (95% CI: 4.4 to 12.2; P < 0.001). Conclusions Maternal exposure to VPA during the first trimester of pregnancy significantly increased the risk of major malformations. Lamotrigine and the Risk of Malformations in Pregnancy Cunnington M, Tennis P; International Lamotrigine Pregnancy Registry Scientific Advisory Committee Neurology 2005;64(6):955–960 Purpose To report the frequency of major malformations in lamotrigine (LTG)-exposed pregnancies from September 1, 1992, through March 31, 2004, in the International Lamotrigine Pregnancy Registry. Methods Health care professionals throughout the world can voluntarily enroll LTG-exposed pregnancies in this observational study. Only pregnancies with unknown outcomes at the time of enrollment were included in the analysis. The percentage of outcomes with major birth defects was calculated as the total number of outcomes with major birth defects divided by the sum of the number of outcomes with major birth defects + the number of live births without defects. Results Among 414 first-trimester exposures to LTG monotherapy, 12 outcomes with major birth defects were reported (2.9%, 95% CI 1.6 to 5.1%). Among the 88 first-trimester exposures to LTG polytherapy including valproate, 11 outcomes with major birth defects were reported (12.5%; 95% CI 6.7 to 21.7%). Among 182 first-trimester exposures to LTG polytherapy excluding valproate, 5 outcomes with major birth defects were reported (2.7%, 95% CI 1.0 to 6.6%). No distinctive pattern of major birth defects was apparent among the offspring exposed to LTG monotherapy or polytherapy. Conclusions The risk of all major birth defects after first-trimester exposure to LTG monotherapy (2.9%) was similar to that in the general population and in other registries enrolling women exposed to antiepileptic monotherapy (3.3 to 4.5%). However, the sample size was too small to detect any but very large increases in specific birth defects. Critical Relationship between Sodium Valproate Dose and Human Teratogenicity: Results of the Australian Register of Anti-Epileptic Drugs in Pregnancy Vajda FJ, O'Brien TJ, Hitchcock A, Graham J, Cook M, Lander C, Eadie MJ J Clin Neurosci 2004;11:854–858 Purpose To compare the incidence of foetal malformations (FMs) in pregnant women with epilepsy treated with different antiepileptic drugs (AEDs) and doses, and the influence of seizures, family and personal history, and environmental factors. A prospective, observational, community-based cohort study. Methods A voluntary, Australia-wide, telephone-interview–based register prospectively enrolling three groups of pregnant women: taking AEDs for epilepsy; with epilepsy not taking AEDs; and taking AEDs for a nonepilepsy indication. Four hundred fifty eligible women were enrolled over a 40-month period. Three hundred ninety-six pregnancies had been completed, with 7 sets of twins, for a total of 403 pregnancy outcomes. Results The 354 (87.8%) pregnancy outcomes resulted in a healthy live birth; 26 (6.5%) had an FM; 4 (1%), a death in utero; 1 (0.2%), a premature labour with stillbirth; 14 (3.5%), a spontaneous abortion; and 4, lost to follow-up. The FM rate was greater in pregnancies exposed to sodium valproate (VPA) in the first trimester (16.0%) compared with those exposed to all other AEDs (16.0 vs. 2.4%; P < 0.01) or no AEDs (16.0% vs.3.1%; P < 0.01). The mean daily dose of VPA taken in pregnancy with FMs was significantly greater than in those without (1975 vs. 1128 mg, P < 0.01). The incidence of FM with VPA doses ≥1100 mg was 30.2% versus 3.2% with doses <1100 mg ( P < 0.01). Conclusions A dose–effect relation occurs for FM and exposure to VPA during the first trimester of pregnancy, with higher doses of VPA associated with a significantly greater risk than with lower doses or with other AEDs. These results highlight the need to limit, where possible, the dose of VPA in pregnancy. Neuropsychological Effects of Exposure to Anticonvulsant Medication In Utero Vinten J, Adab N, Kini U, Gorry J, Gregg J, Baker GA; Liverpool and Manchester Neurodevelopment Study Group Neurology 2005;64:949–954 Purpose To investigate the long-term differential drug effects on cognitive functioning in school-aged children exposed to antiepileptic drugs (AEDs) in utero. Methods Mothers with epilepsy were recruited from specialist epilepsy clinics and obstetric clinics from the Liverpool and Manchester region. The mothers and their children were recruited without prior knowledge of their AED treatment during pregnancy or the health of the offspring. A battery of neuropsychological tests was applied to each mother–child pair to obtain a neuropsychological profile for each child. Results Neuropsychological investigation was performed on 249 children between the ages of 6 and 16 years. Children exposed to sodium valproate had a significantly lower verbal IQ when compared with children exposed to other AEDs or not exposed at all. The same children were more likely to have an IQ below 69 and more likely to have memory impairment when compared with the other groups. The mothers’ IQs, exposure to sodium valproate, and the number of tonic–clonic seizures during pregnancy were significant predictors of verbal IQ in this population. Conclusions This retrospective study highlights the potential harmful effects of sodium valproate exposure in utero on neuropsychological development.

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Cosden, Merith, Stacey Peerson, and Katherine Elliott. "Effects of Prenatal Drug Exposure on Birth Outcomes and Early Child Development." Journal of Drug Issues 27, no. 3 (July 1997): 525–39. http://dx.doi.org/10.1177/002204269702700306.

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Public attention has been drawn to the needs of children who have been exposed to drugs, alcohol, and tobacco in utero. Despite initial concerns that prenatal substance exposure could have global and permanent effects, current research suggests that many of these children do not have significant birth outcomes. Developmental outcomes are also mixed. This paper presents a review of the literature on the impact of prenatal drug exposure on infants and young children. In addition, birth outcome and development data are presented on 80 children who were exposed to multiple substances in utero and who were with their mothers in a treatment facility. Both intra-uterine and extra-uterine factors related to children's outcomes are discussed.

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12

Jackson, Adam, Heather Ward, Rebecca Louise Bromley, Charulata Deshpande, Pradeep Vasudevan, Ingrid Scurr, John Dean, et al. "Exome sequencing in patients with antiepileptic drug exposure and complex phenotypes." Archives of Disease in Childhood 105, no. 4 (September 3, 2019): 384–89. http://dx.doi.org/10.1136/archdischild-2018-316547.

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IntroductionFetal anticonvulsant syndrome (FACS) describes the pattern of physical and developmental problems seen in those children exposed to certain antiepileptic drugs (AEDs) in utero. The diagnosis of FACS is a clinical one and so excluding alternative diagnoses such as genetic disorders is essential.MethodsWe reviewed the pathogenicity of reported variants identified on exome sequencing in the Deciphering Developmental Disorders (DDD) Study in 42 children exposed to AEDs in utero, but where a diagnosis other than FACS was suspected. In addition, we analysed chromosome microarray data from 10 patients with FACS seen in a Regional Genetics Service.ResultsSeven children (17%) from the DDD Study had a copy number variant or pathogenic variant in a developmental disorder gene which was considered to explain or partially explain their phenotype. Across the AED exposure types, variants were found in 2/15 (13%) valproate exposed cases and 3/14 (21%) carbamazepine exposed cases. No pathogenic copy number variants were identified in our local sample (n=10).ConclusionsThis study is the first of its kind to analyse the exomes of children with developmental disorders who were exposed to AEDs in utero. Though we acknowledge that the results are subject to bias, a significant number of children were identified with alternate diagnoses which had an impact on counselling and management. We suggest that consideration is given to performing whole exome sequencing as part of the diagnostic work-up for children exposed to AEDs in utero.

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13

Takcı, Sahin, Cihangül Bayhan, Tolga Celik, and Sule Yiğit. "Hypotonia and poor feeding in an infant exposed to lamotrigine and valproic acid in utero." Turkish Journal of Pediatrics 55, no. 5 (October 25, 2013): 546–48. http://dx.doi.org/10.24953/turkjped.2013.1551.

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Lamotrigine has been considered a safe new-generation antiepileptic drug during the perinatal period for both mothers and infants. Despite the concerns regarding its possible teratogenic effect, very limited data have been reported on the adverse effects of perinatal lamotrigine exposure. Herein, we report a case of an infant with hypotonicity and poor feeding who was exposed to lamotrigine in utero. The drug interaction probability scale indicated a probable relationship between sepsis-like symptoms and exposure to lamotrigine and valproic acid in utero in this infant.

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14

&NA;. "New guidelines concerning in utero drug exposure during pregnancy." Reactions Weekly &NA;, no. 298 (April 1990): 1. http://dx.doi.org/10.2165/00128415-199002980-00001.

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15

Ehrenkranz, R. A. "In utero antiepileptic drug exposure: Fetal death and malformations." Yearbook of Neonatal and Perinatal Medicine 2007 (January 2007): 47–49. http://dx.doi.org/10.1016/s8756-5005(08)70032-5.

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16

Meador, K. J., G. A. Baker, R. H. Finnell, L. A. Kalayjian, J. D. Liporace, D. W. Loring, G. Mawer, P. B. Pennell, J. C. Smith, and M. C. Wolff. "In utero antiepileptic drug exposure: Fetal death and malformations." Neurology 67, no. 3 (August 7, 2006): 407–12. http://dx.doi.org/10.1212/01.wnl.0000227919.81208.b2.

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Brooks-Gunn, Jeanne. "Effects of In Utero Drug Exposure on Children's Development." Archives of Pediatrics & Adolescent Medicine 148, no. 1 (January 1, 1994): 33. http://dx.doi.org/10.1001/archpedi.1994.02170010035007.

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18

Hattan, David G. "In Utero Phase Carcinogenicity Testing." International Journal of Toxicology 17, no. 3 (April 1998): 337–53. http://dx.doi.org/10.1080/109158198226611.

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Early experimentation with transplacental exposure (1940s) demonstrated that expression of lung tumors in mice was enhanced when urethane was given during development in utero. In 1970, a U. S. Food and Drug Administration (FDA) expert panel on the safety evaluation of food additives and pesticides met and recommended that an in utero exposure phase be added to carcinogenicity testing (U.S. FDA, 1 971). An analysis was conducted of studies in the open scientific literature, in food additive studies available in FDA files and in studies performed by the National Institute of Environmental Health Sciences (NIEHS). While exposure to rodents during only the adult phase provided qualitatively similar results, early neonatal exposure typically provided slightly higher incidences of turnors, and decreased latency to turn or onset in certain scientific studies. In a series of studies recently performed by the NIEHS with three known animal carcinogens, neonatal or adult exposure produced similar tumors in similar tissues. The food additive saccharin, which shows bladder tumors, and eugenol reliably produced tumors only with neonatal exposure. Implieations for carcinogenicity testing of food additives are discussed in light of these experi-mental findings.

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19

Bada, H. S. "Central and autonomic system signs with in utero drug exposure." Archives of Disease in Childhood - Fetal and Neonatal Edition 87, no. 2 (September 1, 2002): 106F—112. http://dx.doi.org/10.1136/fn.87.2.f106.

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20

Sibiude, Jeanne, Josiane Warszawski, and Stéphane Blanche. "Tolerance of the newborn to antiretroviral drug exposure in utero." Expert Opinion on Drug Safety 14, no. 5 (March 1, 2015): 643–54. http://dx.doi.org/10.1517/14740338.2015.1019462.

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21

de Castro, Ana, Hendreé E. Jones, Rolley E. Johnson, Teresa R. Gray, Diaa M. Shakleya, and Marilyn A. Huestis. "Maternal Methadone Dose, Placental Methadone Concentrations, and Neonatal Outcomes." Clinical Chemistry 57, no. 3 (March 1, 2011): 449–58. http://dx.doi.org/10.1373/clinchem.2010.154864.

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BACKGROUND Few investigations have used placenta as an alternative matrix to detect in utero drug exposure, despite its availability at the time of birth and the large amount of sample. Methadone-maintained opioid-dependent pregnant women provide a unique opportunity to examine the placental disposition of methadone and metabolite [2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP)], to explore their correlations with maternal methadone dose and neonatal outcomes, and to test the ability to detect in utero exposure to illicit drugs. METHODS We calculated the correlations of placental methadone and EDDP concentrations and their correlations with maternal methadone doses and neonatal outcomes. Cocaine- and opiate-positive placenta results were compared with the results for meconium samples and for urine samples collected throughout gestation. RESULTS Positive correlations were found between placental methadone and EDDP concentrations (r = 0.685), and between methadone concentration and methadone dose at delivery (r = 0.542), mean daily dose (r = 0.554), mean third-trimester dose (r = 0.591), and cumulative daily dose (r = 0.639). The EDDP/methadone concentration ratio was negatively correlated with cumulative daily dose (r = −0.541) and positively correlated with peak neonatal abstinence syndrome (NAS) score (r = 0.513). Placental EDDP concentration was negatively correlated with newborn head circumference (r = −0.579). Cocaine and opiate use was detected in far fewer placenta samples than in thrice-weekly urine and meconium samples, a result suggesting a short detection window for placenta. CONCLUSIONS Quantitative methadone and EDDP measurement may predict NAS severity. The placenta reflects in utero drug exposure for a shorter time than meconium but may be useful when meconium is unavailable or if documentation of recent exposure is needed.

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22

Vajda, F. J. E., T. J. O'Brien, J. Graham, A. A. Hitchcock, C. M. Lander, and M. J. Eadie. "Anti-epileptic drug exposure and risk of foetal death in utero." Acta Neurologica Scandinavica 137, no. 1 (August 31, 2017): 20–23. http://dx.doi.org/10.1111/ane.12816.

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23

Hite, Cecelia, and Michael Shannon. "Clinical Profile of Apparently Healthy Neonates With In Utero Drug Exposure." Journal of Obstetric, Gynecologic & Neonatal Nursing 21, no. 4 (July 1992): 305–9. http://dx.doi.org/10.1111/j.1552-6909.1992.tb01741.x.

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24

Kutlay, Baran, Sim Bayramoglu, A. Irfan Kutlar, and Narter Yesildaglar. "An acardiac acephalic monster following in-utero anti-epileptic drug exposure." European Journal of Obstetrics & Gynecology and Reproductive Biology 65, no. 2 (April 1996): 245–48. http://dx.doi.org/10.1016/0301-2115(95)02337-2.

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25

Littlejohns, Carl S., David J. Clarke, and John A. Corbett. "Tourette-Like Disorder in Asperger's Syndrome." British Journal of Psychiatry 156, no. 3 (March 1990): 430–33. http://dx.doi.org/10.1192/bjp.156.3.430.

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An eight-year-old boy with Asperger's syndrome was given haloperidol to control agitation and aggressive outbursts. Withdrawal of the drug after two years was followed by Tourette-like symptoms. Subsequently neither haloperidol nor a second antipsychotic drug altered the core features of Asperger's syndrome, despite suppressing the movement disorder. His first exposure to neuroleptics was in utero.

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Napiorkowski, Beata, Barry M. Lester, M. Catherin Freier, Susan Brunner, Laura Dietz, Andrea Nadra, and William Oh. "Effects of In Utero Substance Exposure on Infant Neurobehavior." Pediatrics 98, no. 1 (July 1, 1996): 71–75. http://dx.doi.org/10.1542/peds.98.1.71.

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Objective. This study had two objectives: (1) to assess infant behavior by using the NICU Network Neurobehavioral Scale (NNNS), an assessment designed specifically for prenatally drug-exposed infants; and (2) to control for the effects of polydrug use involving alcohol, marijuana, and cigarettes on the neurobehavioral status of the newborn infant. Methods. The subjects and controls in this study were full-term infants of appropriate gestational age with no medical problems. At 1 to 2 days of age, 20 infants exposed to cocaine, alcohol, marijuana, and cigarettes; 17 infants exposed to alcohol and/or marijuana and cigarettes; and 20 drug-free infants were evaluated by using the Neonatal Intensive Care Unit Network Neurobehavioral Scale. The data were reduced to reflect clinically defined categories of neurobehavioral function and were analyzed by using analysis of variance and X2 statistics. Results. Cocaine-exposed infants showed increased tone and motor activity, more jerky movements, startles, tremors, back arching, and signs of central nervous system and visual stress than unexposed infants. They also showed poorer visual and auditory following. There were no differences in how the examination was administered to cocaine-exposed and nonexposed infants. Reduced birth weight and length were also observed in cocaine-exposed infants. Conclusions. Differences attributable to cocaine-exposed infants were related to muscle tone and motor performance, following during orientation, and signs of stress. However, cocaine-exposed infants were not more difficult to test, nor did they require an alteration in the examination. Both neurobehavioral patterns of excitability and lethargy were observed. Findings may have been due to the synergistic effects of cocaine with alcohol and marijuana.

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Ginsberg, Gary, Dale Hattis, Richard Miller, and Babasaheb Sonawane. "Pediatric Pharmacokinetic Data: Implications for Environmental Risk Assessment for Children." Pediatrics 113, Supplement_3 (April 1, 2004): 973–83. http://dx.doi.org/10.1542/peds.113.s3.973.

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Pharmacology and toxicology share a common interest in pharmacokinetic data, especially as it is available in pediatric populations. These data have been critical to the clinical pharmacologist for many years in designing age-specific dosing regimens. Now they are being used increasingly by toxicologists to understand the ontogeny of physiologic parameters that may affect the metabolism and clearance of environmental toxicants. This article reviews a wide range of physiologic and metabolic factors that are present in utero and in early postnatal life and that can affect the internal dose of an absorbed chemical and its metabolites. It also presents a child/adult pharmacokinetic database that includes data for 45 therapeutic drugs organized into specific children’s age groupings and clearance pathways. Analysis of these data suggests that substantial child/adult differences in metabolism and clearance are likely for a variety of drugs and environmental chemicals in the early postnatal period. These results are also relevant to in utero exposures, where metabolic systems are even more immature, but exposures are greatly modified by the maternal system and placental metabolism. The implications of these child/adult differences for assessing children’s risks from environmental toxicants is discussed with special focus on physiologically based pharmacokinetic modeling strategies that could simulate children’s abilities to metabolize and eliminate chemicals at various developmental stages.

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Concheiro, Marta, Eva González-Colmenero, Elena Lendoiro, Ana Concheiro-Guisán, Ana de Castro, Angelines Cruz-Landeira, and Manuel López-Rivadulla. "Alternative Matrices for Cocaine, Heroin, and Methadone In Utero Drug Exposure Detection." Therapeutic Drug Monitoring 35, no. 4 (August 2013): 502–9. http://dx.doi.org/10.1097/ftd.0b013e31828a6148.

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29

Hodel, E. M., C. Marzolini, C. Waitt, and N. Rakhmanina. "Pharmacokinetics, Placental and Breast Milk Transfer of Antiretroviral Drugs in Pregnant and Lactating Women Living with HIV." Current Pharmaceutical Design 25, no. 5 (June 3, 2019): 556–76. http://dx.doi.org/10.2174/1381612825666190320162507.

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Background:Remarkable progress has been achieved in the identification of HIV infection in pregnant women and in the prevention of vertical HIV transmission through maternal antiretroviral treatment (ART) and neonatal antiretroviral drug (ARV) prophylaxis in the last two decades. Millions of women globally are receiving combination ART throughout pregnancy and breastfeeding, periods associated with significant biological and physiological changes affecting the pharmacokinetics (PK) and pharmacodynamics (PD) of ARVs. The objective of this review was to summarize currently available knowledge on the PK of ARVs during pregnancy and transport of maternal ARVs through the placenta and into the breast milk. We also summarized main safety considerations for in utero and breast milk ARVs exposures in infants.Methods:We conducted a review of the pharmacological profiles of ARVs in pregnancy and during breastfeeding obtained from published clinical studies. Selected maternal PK studies used a relatively rich sampling approach at each ante- and postnatal sampling time point. For placental and breast milk transport of ARVs, we selected the studies that provided ratios of maternal to the cord (M:C) plasma and breast milk to maternal plasma (M:P) concentrations, respectively.Results:We provide an overview of the physiological changes during pregnancy and their effect on the PK parameters of ARVs by drug class in pregnancy, which were gathered from 45 published studies. The PK changes during pregnancy affect the dosing of several protease inhibitors during pregnancy and limit the use of several ARVs, including three single tablet regimens with integrase inhibitors or protease inhibitors co-formulated with cobicistat due to suboptimal exposures. We further analysed the currently available data on the mechanism of the transport of ARVs from maternal plasma across the placenta and into the breast milk and summarized the effect of pregnancy on placental and of breastfeeding on mammal gland drug transporters, as well as physicochemical properties, C:M and M:P ratios of individual ARVs by drug class. Finally, we discussed the major safety issues of fetal and infant exposure to maternal ARVs.Conclusions:Available pharmacological data provide evidence that physiological changes during pregnancy affect maternal, and consequently, fetal ARV exposure. Limited available data suggest that the expression of drug transporters may vary throughout pregnancy and breastfeeding thereby possibly impacting the amount of ARV crossing the placenta and secreted into the breast milk. The drug transporter’s role in the fetal/child exposure to maternal ARVs needs to be better understood. Our analysis underscores the need for more pharmacological studies with innovative study design, sparse PK sampling, improved study data reporting and PK modelling in pregnant and breastfeeding women living with HIV to optimize their treatment choices and maternal and child health outcomes.

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Vajda, F. J. E., T. J. O'Brien, J. Graham, C. M. Lander, and M. J. Eadie. "Associations between particular types of fetal malformation and antiepileptic drug exposurein utero." Acta Neurologica Scandinavica 128, no. 4 (March 6, 2013): 228–34. http://dx.doi.org/10.1111/ane.12115.

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Bowman, Pamela, and Bijay Vaidya. "Suspected Spontaneous Reports of Birth Defects in the UK Associated with the Use of Carbimazole and Propylthiouracil in Pregnancy." Journal of Thyroid Research 2011 (2011): 1–5. http://dx.doi.org/10.4061/2011/235130.

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The concept of a carbimazole embryopathy underlies current Endocrine Society advice to avoid this drug in early pregnancy, favouring propylthiouracil as an alternative for the treatment of maternal hyperthyroidism. We aimed to establish whether suspected spontaneous reporting of adverse drug reactions in the UK via the Yellow Card Scheme supports a carbimazole embryopathy and the lack of association between propylthiouracil and congenital anomalies. All birth defects related to maternal treatment with carbimazole or propylthiouracil reported over a 47-year period via the Yellow Card Scheme were analysed. 57 cases with 97 anomalies were reported following in utero exposure to carbimazole. These anomalies included aplasia cutis, choanal atresia, tracheo-oesophageal fistula, and patent vitellointestinal duct, which have previously been reported in association with carbimazole/methimazole exposure in utero. Only 6 cases with 11 anomalies were reported for propylthiouracil, all within the last 15 years. Therefore, these findings may support a carbimazole embryopathy. There are few birth defects associated with propylthiouracil, but this should be interpreted in the context of higher historical prescription rates for carbimazole.

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Morrison, Janna L., K. Wayne Riggs, and Dan W. Rurak. "Fluoxetine during pregnancy: impact on fetal development." Reproduction, Fertility and Development 17, no. 6 (2005): 641. http://dx.doi.org/10.1071/rd05030.

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Women are at greatest risk of suffering from depression during the childbearing years and thus may either become pregnant while taking an antidepressant or may require a prescription for one during pregnancy. The antidepressant fluoxetine (FX) is a selective serotonin reuptake inhibitor (SSRI), which increases serotonin neurotransmission. Serotonin is involved in the regulation of a variety of physiological systems, including the sleep–wake cycle, circadian rhythms and the hypothalamic–pituitary–adrenal axis. Each of these systems also plays an important role in fetal development. Compared with other antidepressant drugs, the SSRIs, such as FX, have fewer side effects. Because of this, they are now frequently prescribed, especially during pregnancy. Clinical studies suggest poor neonatal outcome after exposure to FX in utero. Recent studies in the sheep fetus describe the physiological effects of in utero exposure to FX with an 8 day infusion during late gestation in the sheep. This is a useful model for determining the effects of FX on fetal physiology. The fetus can be studied for weeks in its normal intrauterine environment with serial sampling of blood, thus permitting detailed studies of drug disposition in both mother and fetus combined with monitoring of fetal behavioural state and cardiovascular function. Fluoxetine causes an acute increase in plasma serotonin levels, leading to a transient reduction in uterine blood flow. This, in turn, reduces the delivery of oxygen and nutrients to the fetus, thereby presenting a mechanism for reducing growth and/or eliciting preterm delivery. Moreover, because FX crosses the placenta, the fetus is exposed directly to FX, as well as to the effects of the drug on the mother. Fluoxetine increases high-voltage/non-rapid eye movement behavioural state in the fetus after both acute and chronic exposure and, thus, may interfere with normal fetal neurodevelopment. Fluoxetine also alters hypothalamic function in the adult and increases the magnitude of the prepartum rise in fetal cortisol concentrations in sheep. Fetal FX exposure does not alter fetal circadian rhythms in melatonin or prolactin. Studies of the effects of FX exposure on fetal development in the sheep are important in defining possible physiological mechanisms that explain human clinical studies of birth outcomes after FX exposure. To date, there have been insufficient longer-term follow-up studies in any precocial species of offspring exposed to SSRIs in utero. Thus, further investigation of the long-term consequences of in utero exposure to FX and other SSRIs, as well as the mechanisms involved, are required for a complete understanding of the impact of these agents on development. This should involve studies in both humans and appropriate animal models.

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Degiacomo, Jessica, and Sherry Luedtke. "Neonatal Toxicity From Escitalopram Use In Utero: A Case Report." Journal of Pediatric Pharmacology and Therapeutics 21, no. 6 (December 1, 2016): 522–26. http://dx.doi.org/10.5863/1551-6776-21.6.522.

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Selective serotonin reuptake inhibitor (SSRI) exposure during pregnancy can result in symptoms of serotonin syndrome or serotonin withdrawal. In contrast to other SSRIs, reports of serotonin behavioral syndrome following in utero exposure to escitalopram and citalopram are limited. We describe a case of suspected toxicity following in utero exposure to 20 mg escitalopram throughout pregnancy. The infant was transferred to our neonatal intensive unit at 9 hours of life for further evaluation of lethargy, weak cry, bradycardia, and non-reactive pupils. Hypoxic ischemic encephalopathy was suspected upon presentation, despite APGAR scores of 8 and 9. Upon admission, symptoms progressed to signs of hypertonia, irritability, high-pitched cry, and posturing. The patient was loaded with phenobarbital for empiric management of suspected seizures versus drug withdrawal. Both electroencephalogram and computed tomography scan results were normal; however, an electrocardiogram revealed a prolonged QTc interval of 531 milliseconds. Signs of irritability and QTc prolongation continued through day of life (DOL) 5. The infant was discharged on DOL 10 with no further symptoms. We hypothesize that this represented a case of serotonin toxicity due to in utero exposure to escitalopram and recommend close monitoring for neonatal behavioral syndrome symptoms and QTc prolongation in infants exposed to escitalopram during pregnancy.

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O'Donnell, Karen J., Geoffrey M. Georgi, Jeannine L. Gingras, Luanne McAdams, Richard Granowsky, and Allen P. Killam. "PRENATAL INTERVENTION FOR CHILDREN WITH IN UTERO EXPOSURE TO MATERNAL DRUG USE. 643." Pediatric Research 39 (April 1996): 110. http://dx.doi.org/10.1203/00006450-199604001-00665.

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Smith, Andrew L., Jeffrey A. Cohen, Daniel Ontaneda, and Mary Rensel. "Pregnancy and multiple sclerosis: Risk of unplanned pregnancy and drug exposure in utero." Multiple Sclerosis Journal - Experimental, Translational and Clinical 5, no. 4 (October 2019): 205521731989174. http://dx.doi.org/10.1177/2055217319891744.

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Kintz, P. "Contribution of in utero drug exposure when interpreting hair results in young children." Forensic Science International 249 (April 2015): 314–17. http://dx.doi.org/10.1016/j.forsciint.2014.09.014.

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Salmen, Teodor, Vlad Dima, Claudia Gabriela Potcovaru, Bianca Margareta Mihai, Delia Cinteza, and Roxana-Elena Bohiltea. "The neuroprotective effects of magnesium sulfate in utero exposure." Romanian Journal of Pediatrics 71, S2 (November 30, 2022): 36–39. http://dx.doi.org/10.37897/rjp.2022.s2.8.

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Prematurity affects 1 in 10 births and is associated with different degrees of disability and leads to a higher risk of neurological impairment and cerebral palsy (CP). Because its prevalence increase, but with a decrease in mortality rate, there is a burden of survivors that develop sequelae, a problem for the healthcare systems worldwide and for the patient’s social integration. Magnesium sulfate is a useful tool to limit the development of such complications. The risk factors for preterm brain injury act antenatally, intrapartum and postpartum. Even though there are several trials that tried to assess it benefits, magnesium sulfate is on the D list of U.S. Food and Drug Administration for pregnancy and several Societies of Obstetrics and Gynecology tried to implement national guidelines for its safe use. In conclusion it should be used with caution, within 24 hours before birth and under medical surveillance and to administer it only in pregnancies that are at high risk of premature childbirth. If there is a medical emergency involving the mother or the fetus, delivery should not be postponed in order to administer de magnesium sulfate.

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Reinarz, Susan, and Jenny Ecord. "Drug-of-Abuse Testing in the Neonate." Neonatal Network 18, no. 8 (December 1999): 55–61. http://dx.doi.org/10.1891/0730-0832.18.8.55.

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DRUG ABUSE I S A MAJOR psychiatric problem in the U.S.1The American Academy of Pediatrics (AAP) Committee on Substance Abuse notes that increasing numbers of women are reported to use licit and illicit substances during pregnancy.2Statistical data are insufficient because of the difficulty in obtaining accurate information from a medical history, but as many as one in ten infants has been estimated to have been exposed to illicit drugsin utero. The reported incidence is higher in inner-city hospitals.3Some of these infants are known to be experiencing complications related to drug exposure during the neonatal period. Others may be sent home with undetected problems. Long-term health and well-being of the infant and family may be negatively influenced by the lack of identification of drug exposure. This concern has prompted increased efforts to identify the exposed infant and the substance to which the infant was exposed.

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Barrau, Mathilde, Xavier Roblin, Leslie Andromaque, Aurore Rozieres, Mathias Faure, Stéphane Paul, and Stéphane Nancey. "What Should We Know about Drug Levels and Therapeutic Drug Monitoring during Pregnancy and Breastfeeding in Inflammatory Bowel Disease under Biologic Therapy?" Journal of Clinical Medicine 12, no. 23 (December 4, 2023): 7495. http://dx.doi.org/10.3390/jcm12237495.

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Data on the real long-term influences of in utero drug exposure in pregnant women on childhood development are scarce and remain not well determined and depend on the duration of in utero drug exposure and maternal drug levels. Therapeutic drug monitoring (TDM) during pregnancy may help limit fetal drug exposure while maintaining an effective dose for the treatment of the underlying inflammatory bowel disease (IBD) in women. Most antibody therapies used in patients with IBD are IgG molecules which are actively transported across the placenta, especially during the third trimester of the pregnancy. Here, we propose an up-to-date clinical review to summarize the available findings of serum drug levels in maternal blood during pregnancy, in the cord blood, infants at delivery and in breast milk of patients with IBD treated with biologics. Conversely, in comparison to adalimumab (ADA) levels, which are relatively stable during pregnancy, infliximab (IFX) drug clearance decreased significantly during the last two trimesters of the pregnancy, leading to increasing drug concentrations in the blood of the pregnant women. As most guidelines recommend using live vaccines in infants at the age of one or earlier in case of negative serum drug levels in newborns, statistical models could help clinicians in making a decision to adjust the last dose of the biologic during pregnancy and to determine the optimal date to vaccinate. Altogether, data from the literature offers strong reassurance in terms of safety for anti-TNFα therapies during pregnancy not only for IBD patients who intend to conceive, but also for pregnant women and for the physicians taking care of these patients. ADA and IFX levels in breast milk are detectable, but at very low levels, and therefore, it is recommended to pursue breast feeding under anti-TNFα therapy. Our knowledge on ustekinumab or vedolizumab levels in pregnant women remains unclear and scarce. These drugs are currently not recommended for patients with IBD in clinical practice. Therefore, TDM and proactive dose adjustment are not necessary during pregnancy since its impact on making a clinical decision have not yet been clearly demonstrated in routine practice. Overall, drug concentrations in the cord blood, an infant at birth and postpartum serum concentrations in infants, due to active placental drug transfer, may have a greater impact than the limited drug transfer in breast milk during lactation on the risk of infection and developmental outcomes. Ustekinumab and vedolizumab exposure during pregnancy and lactation are both considered low risk by the recent ECCO guidelines despite the limited data that are currently available.

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Perl, Anna Sechser, Blaine W. Robinson, Jaclyn A. Biegel, Elaine H. Zackai, Christos P. Kolaris, and Carolyn A. Felix. "Congenital Amniotic Band Syndrome and MLL Rearranged Neonatal Leukemia in an Infant with Multiple Pre-Conception and In Utero Exposures." Blood 108, no. 11 (November 16, 2006): 4286. http://dx.doi.org/10.1182/blood.v108.11.4286.4286.

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Abstract Introduction: Patients with birth defects have a higher incidence of cancer; however, an association of amniotic band syndrome (vascular disruption syndrome) with congenital leukemia has never been reported. We characterized a case of MLL-rearranged leukemia in a neonate affected with this birth defect. Methods: The MLL translocation was characterized in peripheral AML blasts by karyotype analysis, multicolor FISH, Southern blot analysis and genomic and cDNA panhandle PCR. NQO1 genotype was determined by real-time PCR. Clinical history and results: The infant was born at 38 weeks gestation by C-section for suboccipital encephalocele to a 21 year-old gravida 3 para 2 mother with a history of cigarette, marijuana, cocaine and opiate use, and antidepressant, antipsychotic, barbiturate, caffeine and proton pump inhibitor treatment during pregnancy. Drug screen at delivery was positive for opioids and barbiturates. In addition to the encephalocele, a circular constriction of the right arm, consistent with amniotic band syndrome, and blueberry muffin lesions were noted at delivery. The CBC showed mild thrombocytopenia that resolved the next day. Congenital infection was excluded. The encephalocele was repaired. At 19–20 days of age the infant became septic and hepatosplenomegaly and hyperleukocytosis were observed. The peripheral smear and flow cytomery revealed acute myeloid leukemia with monocytic differentiation (CD45+ population positive for CD4, CD14, CD33, CD38, HLA-DR). Karyotype analysis showed a complex structural abnormality disrupting chromosomes 4, 11 and 19 involving MLL. M-FISH showed insertion of chromosome 11 material into a chromosome 19 and translocation between chromosomes 11q and 4q. The infant received cytosine arabinoside and daunomycin but succumbed to AML, sepsis and multi-organ failure within 4 days. Autopsy showed marrow, viscera, brain and skin infiltration with AML and Chiari type III brain malformation. Southern blot analysis detected two MLL bcr rearrangements. Panhandle PCR demonstrated fusion of MLL intron 6 and intron 1 of ELL from band 19p13.1. Short sequence homologies at the breakpoint junction suggested DNA damage resolution by NHEJ repair. The corresponding transcript joined MLL exon 6 to ELL exon 2. The infant was wild-type at NQO1 C609T. Conclusions: This is the first association of amniotic band syndrome and congenital AML, both of which are rare conditions. Although the cause(s) are unknown, both conditions originate in utero and maternal exposures during pregnancy may be relevant. There was a history of maternal fetal loss, which is a risk factor for leukemia in infants. The NQO1 substrate p-benzoquinone in cigarette smoke is a topoisomerase II poison, but the infant did not harbor the NQO1 variant that predisposes to leukemia. Cocaine is an in utero exposure implicated in amniotic band syndrome. The occurrence of amniotic band syndrome and congenital AML in this infant raises questions about potential host predisposition or gene-environment interactions common to both conditions. Alternatively, both rare conditions may have occurred by chance alone in the setting of the many in utero exposures.

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King, Terri A., Jeffrey M. Perlman, Abbot R. Laptook, Nancy Rollins, Gregory Jackson, and Bertis Little. "Neurologic Manifestations of In Utero Cocaine Exposure in Near-Term and Term Infants." Pediatrics 96, no. 2 (August 1, 1995): 259–64. http://dx.doi.org/10.1542/peds.96.2.259.

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Objective. To determine whether the incidence of neurosonographic and neurologic abnormalities is higher in cocaine-exposed infants at birth. Methods. In utero exposure to cocaine was investigated in 39 term and near-term infants with positive urine screens for cocaine only and 39 matched control infants without drug exposure admitted to the regular term newborn nursery. Serial evaluations were performed on each infant on postnatal days 1 and 2 and included a cranial sonogram, a neurologic and behavioral assessment for drug withdrawal, and Doppler interrogation of the anterior and middle cerebral arteries. Results. There were no differences between groups in neurosonographic abnormalities. Grade I or II intraventricular hemorrhage occurred in 11% of cocaine-exposed and 11% of control infants. There were no cases of grade III intraventricular hemorrhage, cystic periventricular leukomalacia, or neonatal stroke. Head size was smaller in cocaine-exposed infants, ie, 32.7 ± 0.1 cm versus 33.8 ± 0.1 cm. The neurologic examination was similar between groups with regard to tone, reflexes, and cranial nerves. Behavioral scores were higher on both days, in cocaine-exposed versus control infants, ie, 4.4 ± 0.5 versus 2.7 ± 0.3 on day 1 and 5.0 ± 0.5 versus 1.71 ± 0.31 on day 2. Cerebral blood flow velocity measurements in the anterior cerebral artery were similar between groups on both days of examination. However, cocaine-exposed infants demonstrated a significant increase in flow velocity from day 1 to day 2, ie, 0.48 ± 0.03 to 0.57 ± 0.04. There was a concomitant decrease in the pulsatility index from day 1 to day 2 in the cocaine-exposed, ie, 0.74 ± 0.02 to 0.69 ± 0.02, but not in the control infants. No differences were noted in the flow velocities in the middle cerebral arteries between groups. Conclusions. Term and near-term infants admitted to a regular nursery who are exposed to cocaine in utero: (1) do not exhibit an increased incidence of neurosonographic abnormalities; (2) do exhibit altered behavior consistent with drug withdrawal; and (3) do demonstrate changes in flow velocity in the anterior cerebral artery consistent with the vasoconstrictive effects of the drug. However, these changes were not accompanied by changes in the neurologic examination or altered care. The long-term neurodevelopmental implications of these subtle abnormalities in the neonatal period remain to be determined.

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McGlone, Laura, Helen Mactier, Huda Hassan, and Gail Cooper. "In utero drug and alcohol exposure in infants born to mothers prescribed maintenance methadone." Archives of Disease in Childhood - Fetal and Neonatal Edition 98, no. 6 (July 8, 2013): F542—F544. http://dx.doi.org/10.1136/archdischild-2013-304158.

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Kintz, P. "O1: Contribution of in-utero drug exposure when interpreting hair results in young children." Toxicologie Analytique et Clinique 26, no. 2 (June 2014): S4—S5. http://dx.doi.org/10.1016/s2352-0078(14)70009-5.

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Yuan, Xia, Hongjun Liu, Yufeng Li, Wen Li, Huiqian Yu, and Xia Shen. "Ribbon Synapses and Hearing Impairment in Mice After in utero Sevoflurane Exposure." Drug Design, Development and Therapy Volume 14 (July 2020): 2685–93. http://dx.doi.org/10.2147/dddt.s253031.

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Reddy, Doodipala Samba, Jonathan Brewer, and Maunica Manchi. "Is Prenatal Valproate Exposure a Risk Factor for Autism." International Journal of Pharmaceutical Sciences and Nanotechnology 11, no. 2 (March 31, 2018): 4007–11. http://dx.doi.org/10.37285/ijpsn.2018.11.2.1.

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Sodium valproate (Depakene) and divalproex sodium (Depakote) are two commonly used drugs for epilepsy therapy. Sodium valproate, a first-generation antiepileptic drug, has commonly been used as a treatment for different forms of both epilepsy and psychiatric disorders ever since it was first clinically utilized in 1967. It is a simple 2-chain fatty acid that is believed to affect GABA metabolism, however, the mechanism is still unclear. It has been proven to have adverse side effects, such as neural tube defects if taken in utero during the first trimester of pregnancy and has therefore caused a reservation in the medical community for prescription of this drug in females. However, it is still one of the most commonly prescribed agents in young women of childbearing age with 23.4% of women actively receiving it for non-epileptic disorders, such as psychiatric disorders and 12% of women receiving it as an antiepileptic drug (AED). This may be cause for alarm due to the teratogenic effects that may result from usage of valproate. In this article, the potential of prenatal valproate to cause autism spectrum disorder will be outlined from a nonclinical and clinical perspective, as evident from this basic science report. Overall, valproate is clearly associated with teratogenic risks and hence should not be used in women with epilepsy during reproductive years.

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Ruda, Albert. "The DES Daughters in Spain: Liability for Damage Caused by the Exposure to a Defective Drug in Utero." European Review of Private Law 21, Issue 2 (March 1, 2013): 625–42. http://dx.doi.org/10.54648/erpl2013032.

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Abstract: The present paper presents an analysis of the legal situation concerning claims for liability for damage caused by the exposure to a defective drug in utero from the point of view of Spanish law. In contrast with other jurisdictions, proof of the causal link between such exposure and damage has not been a major hurdle for liability to be established. However, doubts as to the applicability of the development risk defence have been raised before the Spanish courts. Moreover, claims have been filed against the producer as well as the public authorities. At any rate, the number of claims is very small.

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Jevtovic-Todorovic, Vesna. "Exposure of Developing Brain to General Anesthesia." Anesthesiology 128, no. 4 (April 1, 2018): 832–39. http://dx.doi.org/10.1097/aln.0000000000002047.

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Abstract Recently, the U.S. Food and Drug Administration issued an official warning to all practicing physicians regarding potentially detrimental behavioral and cognitive sequelae of an early exposure to general anesthesia during in utero and in early postnatal life. The U.S. Food and Drug Administration concern is focused on children younger than three years of age who are exposed to clinically used general anesthetics and sedatives for three hours or longer. Although human evidence is limited and controversial, a large body of scientific evidence gathered from several mammalian species demonstrates that there is a potential foundation for concern. Considering this new development in public awareness, this review focuses on nonhuman primates because their brain development is the closest to humans in terms of not only timing and duration, but in terms of complexity as well. The review compares those primate findings to previously published work done with rodents.

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Boskovic, Rada, Julia Klein, Cindy Woodland, Tanya Karaskov, and Gideon Koren. "The role of the placenta in variability of fetal exposure to cocaine and cannabinoids: A twin study." Canadian Journal of Physiology and Pharmacology 79, no. 11 (November 1, 2001): 942–45. http://dx.doi.org/10.1139/y01-080.

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There is wide variability in the reported adverse fetal effects of cocaine and cannabinoids. The causes of this variability are largely unknown. We hypothesized that variability in placental handling of drugs affect fetal exposure. We used twin pregnancies as a paradigm to address the role of the placenta in this variability. We analyzed hair or meconium samples taken from dizygotic and monozygotic twins exposed in utero to illicit drugs. Out of 12 pairs, 5 had negative levels in both twins, and seven pairs of twins had chemical evidence of fetal exposure to cocaine (n = 5) or cannabinoids (n = 2). The one known monozygotic pair of twins had almost identical levels of cocaine. In contrast, the six dizygotic pairs had large disparities in either cocaine or cannabinoid concentrations. In three of these six dizygotic pairs, levels of cocaine (n = 2) or canabinoids (n = 1) were undetectable in one twin while positive in the other. Given that twins are theoretically exposed to similar maternal drug levels, our findings suggest that the placenta may have a major role in modulating the amounts of drug reaching the fetus.Key words: cocaine, cannabinoids, placenta, twins.

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Gupta, Manish, Alan O. Mulvihill, Gerassimos Lascaratos, Brian W. Fleck, and Nick D. George. "Nystagmus and Reduced Visual Acuity Secondary to Drug Exposure In Utero: Long-Term Follow-up." Journal of Pediatric Ophthalmology & Strabismus 49, no. 1 (March 15, 2011): 58–63. http://dx.doi.org/10.3928/01913913-20110308-01.

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Almgren, Malin, Bengt Källén, and Catharina Lavebratt. "Population-based study of antiepileptic drug exposure in utero—Influence on head circumference in newborns." Seizure 18, no. 10 (December 2009): 672–75. http://dx.doi.org/10.1016/j.seizure.2009.09.002.

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