Investigating the Origins of Biochemical Dysregulation in Trisomy 21 Pregnancy
Authors' conclusion
The AF/P ratio supports a fetal origin for SOD, TAC, TOC, and adiponectin, while lower SIRT1 implies disrupted fetal oxidative regulation.
Study context
- Population
- Women referred for prenatal testing, without maternal chronic or acute diseases
- Participants
- 20 vs 20
- Comparison
- T21 vs euploid pregnancies
- T21n = 20
- Euploidn = 20reference
- Outcome
- Oxidative and metabolic markers in maternal plasma and amniotic fluid (AF), and AF/plasma (AF/P) ratio
Main finding
As reported in the abstract
- Maternal plasma in T21: decreased total antioxidant capacity (TAC), superoxide dismutase (SOD), FOXO and leptin
- P < .05
- AF in T21: reduced FOXO and leptin; elevated SOD, TAC, total oxidative capacity (TOC), adiponectin and 8-OHdG
- P < .05
- AF/P ratio increased for SOD
- P = .027
- AF/P ratio increased for TAC
- P < .001
- AF/P ratio increased for TOC
- P < .0001
- AF/P ratio increased for adiponectin
- P = .002
- Decreased SIRT1
- P = .036
Observational data: associations, not effects.
Further findings
Plasma biomarker panel (SOD, TAC, leptin; regression modeling) distinguishing T21 from euploid pregnancies
- AUC
- .92
- P
- P < 0.001
Original publication
Investigating the Origins of Biochemical Dysregulation in Trisomy 21 Pregnancy. J Clin Endocrinol Metab. Published 9 June 2025. doi:10.
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