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Abstract

Aim: To explore the role of pharmacogenetics in determining the risk of congenital heart anomalies (CHA) with prenatal use of serotonin reuptake inhibitors. 

Methods: We included 33 case-mother dyads and 2 mother-only (child deceased) cases of CHA in a case-only study. Ten genes important in determining fetal exposure to serotonin reuptake inhibitors were examined: CYP1A2, CYP2C9, CYP2C19, CYP2D6, ABCB1, SLC6A4, HTR1A, HTR1B, HTR2A and HTR3B. 

Results: Among the exposed cases, polymorphisms that tended to be associated with an increased risk of CHA were SLC6A4 5-HTTLPR and 5-HTTVNTR, HTR1A rs1364043, HTR1B rs6296 and rs6298 and HTR3B rs1176744, but none reached statistical significance due to our limited sample sizes. 

Conclusion: We identified several polymorphisms that might potentially affect the risk of CHA among exposed fetuses, which warrants further investigation.

Original languageEnglish
Pages (from-to)987-1001
Number of pages15
JournalPharmacogenomics
Volume18
Issue number10
DOIs
Publication statusPublished - 1-Jul-2017

Keywords

  • gene-environment interaction
  • heart defects
  • pharmacogenetics
  • serotonin reuptake inhibitors
  • teratogenicity
  • GENE-ENVIRONMENT INTERACTIONS
  • ANTIDEPRESSANT THERAPY
  • P-GLYCOPROTEIN
  • ABCB1 GENE
  • PROMOTER POLYMORPHISM
  • CLINICAL-RESPONSE
  • MAJOR DEPRESSION
  • PREGNANT-WOMEN
  • MEDICATION USE
  • RISK-FACTORS

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