The onset and severity of Neonatal Abstinence Syndrome (NAS) in newborns exposed to prenatal opioids have shown significant variation. Because maternal opioid dosage does not appear to be linked to neonatal outcome, maternal, placental, and fetal genetic variations might have a role in NAS. Previous small cohort studies have linked variations in maternal and baby genes encoding the -Opioid Receptor (OPRM1), Catechol-O-methyltransferase (COMT), and Prepronociceptin (PNOC) to a shorter hospital stay and a lower requirement for therapy in newborns exposed to opioids in utero. The unbiased discovery of genomic variants and gene pathways associated with differences in maternal and fetal opioid pharmacokinetics and pharmacodynamics, as well as placental opioid transport and metabolism, will be enabled by falling genomic sequencing costs and computational approaches to predict variant function. The identification of pathogenic variations should allow for a more accurate assessment of the risk of acquiring more severe types of NAS. This study summarizes the existing involvement of genetic variables in the development of NAS and offers future genomic research initiatives.
