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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Ultrasound diagnosis of fetal anomalies associated with in utero cocaine exposure: further support for cocaine-induced vascular disruption teratogenesis.

The dramatic increase in cocaine use over the past decade has led to a concern about its possible teratogenicity. We have identified 6 structural fetal anomalies which we postulate may have cocaine-induced vascular accidents as the teratogenic mechanism: 2 complex choroid plexus cysts, gastroschisis, meconium peritonitis, urethral stenosis, and radial hypoplasia. Two additional anomalous neonates were born to perinatal cocaine users. Eight of 51 (15.7%) cocaine-exposed perinates exhibited anomalies versus 120 of 2,194 (5.4%) perinates without known cocaine exposure during this time period. This represents a 3-fold relative risk (RR = 2.87, OR = 3.22, chi square = 9.68, p < 0.005) for the cocaine-exposed fetus. Subjects were all identified as cocaine users prior to ultrasound-detected anomaly and ultrasonologists were blinded to maternal drug history. The vascular disruption model as the plausible mechanism for cocaine-associated teratogenesis is supported by the type of anomalies reported. In addition, cocaine use was prospectively determined to have occurred at the critical developmental period in each case.[1]

References

  1. Ultrasound diagnosis of fetal anomalies associated with in utero cocaine exposure: further support for cocaine-induced vascular disruption teratogenesis. Hume, R.F., Gingras, J.L., Martin, L.S., Hertzberg, B.S., O'Donnell, K., Killam, A.P. Fetal. Diagn. Ther. (1994) [Pubmed]
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