Cocaine Use during Pregnancy: Perinatal Outcomes

Handler, Arden; Kistin, Naomi; Davis, Faith G.; Ferré, Cynthia

doi:10.1093/oxfordjournals.aje.a115961

Cited by 165 publications

(44 citation statements)

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“…27 Other studies continue to show a relationship between drug use and increased risk of perinatal mortality. 4,28 The relationship between drug use and fetal and neonatal mortality may be related to improvements in the medical management of high-risk mothers and infants in hospitals, a factor which was not analyzed in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Women who use illicit drugs during pregnancy have higher risks of placental abruption, premature rupture of membranes, 1 and polyhydramnios, 2 and their infants have higher rates of prematurity and low birth weight. [3][4][5][6][7] These health outcomes, by themselves, have been associated with increased morbidity and mortality. [8][9][10][11][12] Although mortality is only one measure of the health of pregnant women and their infants, it represents an important indicator.…”

Section: Introductionmentioning

confidence: 99%

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Mortality Risk Associated with Perinatal Drug and Alcohol Use in California

et al. 2004

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mortality Risk Associated with Perinatal Drug and Alcohol Use in California

et al. 2004

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“…One such pathway for cocaine-exposed infants may be via compromised fetal growth. Reduced blood flow and fetal vasoconstriction have been implicated as causal mechanisms for the effects of prenatal cocaine exposure on poor fetal growth (Handler, Kistin, Davis, & Ferre, 1991;Oro & Dixon, 1987). Maternal cocaine use is also associated with poor maternal nutrition, lack of prenatal care, and lower pre-pregnancy weight, thus exacerbating the likelihood of poor fetal growth in this group of children (Amaro, Zuckerman, & Cabral, 1989).…”

Section: Indirect Effects and Moderationmentioning

confidence: 99%

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Schuetze

Eiden

Coles

2007

Developmental Psychobiology

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This study examined the association between prenatal exposure to cocaine and autonomic regulation at 7 months of age. Heart rate (HR) and respiratory sinus arrhythmia (RSA) were obtained from 154 (79 exposed, and 75 nonexposed) infants during baseline and tasks designed to elicit positive and negative affect. Cocaine-exposed infants had higher HR during the positive affect task. There was a significant suppression of RSA during the negative affect task for nonexposed infants but not for exposed infants. Fetal growth and maternal caregiving behavior did not mediate or moderate this association. These results provide additional support for an association between prenatal cocaine exposure and dysregulation during infancy.

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“…A number of developmental disorders in human infants have been attributed to cocaine exposure in utero. These include decreased birth weight and head circumference, sudden infant death syndrome, systemic hypertension, and tachycardia (Handler et al, 1991;Silvestri et al, 1991). Cocaine can cross the placenta and accumulate in the fetus (Schenker et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Cocaine Induces Apoptosis in Fetal Rat Myocardial Cells through the p38 Mitogen-Activated Protein Kinase and Mitochondrial/CytochromecPathways

Guo-hu¹,

Xiao²,

Zhang³

2004

J Pharmacol Exp Ther

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Cocaine induces apoptosis in fetal rat myocardial cells (FRMCs). However, the mechanisms are not clear. The present study examined the role of p38 mitogen-activated protein kinase (MAPK) and cytochrome c release in the cocaine-induced apoptosis in primary culture of FRMCs prepared from the fetal heart of gestational age of 21 days. Cocaine induced timedependent, concurrent increases in cytochrome c release and activities of caspase-9 and caspase-3, which preceded apoptosis. Caspase-8 was not activated. In accordance, cyclosporin A and the inhibitors of caspase-9 and caspase-3 inhibited cocaineinduced caspase activation and apoptosis. Cocaine stimulated a transient increase in the p38 MAPK activity at a time point of 15 min but reduced the extracellular signal-regulated kinase (ERK) activity at 5 and 15 min in FRMCs. The p38␣ MAPK inhibitor SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole] inhibited cocaine-induced activation of caspases and apoptosis. In contrast, the p38␤ MAPK and mitogen-activated protein kinase kinase/ERK inhibitors SB 202190 [4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole] and PD98059 (2Ј-amino-3Ј-methoxyflavone), respectively, increased apoptosis in the absence of cocaine and potentiated cocaine-induced apoptosis. Consistent with its inhibition of apoptosis, SB203580 inhibited cocaine-induced cytochrome c release and activation of caspase-9 and caspase-3. In addition, cocaine induced a decrease in Bcl-2 protein levels, with no effect on Bax levels. The cocaine-mediated reduction of Bcl-2 levels was not affected with SB203580 and the caspase inhibitors. The results suggest that in FRMCs, p38␣ MAPK plays an important role in the cocaine-induced apoptosis by promoting cytochrome c release, downstream or independent of Bcl-2 protein-mediated regulation. In contrast, p38␤ MAPK and ERK protect fetal myocardial cells against apoptosis.Cocaine abuse among women of childbearing age is prevalent in the United States. A number of developmental disorders in human infants have been attributed to cocaine exposure in utero. These include decreased birth weight and head circumference, sudden infant death syndrome, systemic hypertension, and tachycardia (Handler et al., 1991;Silvestri et al., 1991). Cocaine can cross the placenta and accumulate in the fetus (Schenker et al., 1993). Our recent studies have demonstrated that maternal cocaine administration during pregnancy induces apoptosis in the fetal heart . Cocaine also directly induces an increase in apoptotic cell death in fetal rat myocardial cells (FRMCs) . However, the cellular and molecular mechanisms responsible for cocaine-induced cardiac myocyte apoptosis are presently not clear.Apoptotic cell death is characterized by the activation of a unique class of aspartate-specific proteases, i.e., caspases. Sequential activation of caspases results in cleavage of substrate proteins and breakdown of DNA molecules. It has been well documented that the caspase cascade involved in apoptosis includes...

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Cocaine Use during Pregnancy: Perinatal Outcomes

Cited by 165 publications

References 0 publications

Mortality Risk Associated with Perinatal Drug and Alcohol Use in California

Mortality Risk Associated with Perinatal Drug and Alcohol Use in California

Prenatal cocaine and other substance exposure: Effects on infant autonomic regulation at 7 months of age

Cocaine Induces Apoptosis in Fetal Rat Myocardial Cells through the p38 Mitogen-Activated Protein Kinase and Mitochondrial/CytochromecPathways

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