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 language | English |
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Pages (from-to) | 987-1001 |
Number of pages | 15 |
Journal | Pharmacogenomics |
Volume | 18 |
Issue number | 10 |
DOIs | |
Publication status | Published - 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