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Related Experiment Videos

Circulating angiogenic proteins in trisomy 13.

Yuval Bdolah1, Glenn E Palomaki, Yuval Yaron

  • 1Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

American Journal of Obstetrics and Gynecology
|January 4, 2006
PubMed
Summary

Trisomy 13 pregnancies show significantly higher soluble fms-like tyrosine kinase-1/placental growth factor ratios, suggesting a link to preeclampsia development. This imbalance in angiogenic factors may explain the increased preeclampsia risk in trisomy 13 cases.

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Area of Science:

  • Reproductive Medicine
  • Genetics
  • Maternal-Fetal Medicine

Background:

  • Trisomy 13 is associated with an increased risk of preeclampsia in pregnant women.
  • Elevated levels of soluble fms-like tyrosine kinase-1 (sFLT1) are implicated in preeclampsia pathogenesis.
  • The FLT1 gene, encoding sFLT1, is located on chromosome 13, suggesting a potential link between trisomy 13 and sFLT1 levels.

Purpose of the Study:

  • To investigate maternal circulating angiogenic proteins in pregnancies affected by trisomy 13.
  • To determine if trisomy 13 leads to altered levels of sFLT1 and placental growth factor (PlGF).
  • To assess the sFLT1/PlGF ratio as a potential biomarker in trisomy 13 pregnancies.

Main Methods:

  • Maternal serum samples from pregnancies with trisomy 13, 18, 21, and normal karyotypes were analyzed.

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  • 17 trisomy 13 cases were matched with 85 normal karyotype controls.
  • Levels of sFLT1 and PlGF were measured using enzyme-linked immunosorbent assay (ELISA).
  • Main Results:

    • The median sFLT1/PlGF ratio was significantly higher in trisomy 13 pregnancies (17.0) compared to controls (6.7) (P = .003).
    • No significant difference in sFLT1/PlGF ratios was observed for trisomy 18 or 21 pregnancies compared to controls.
    • The disparity in sFLT1/PlGF ratios between trisomy 13 and control groups was more pronounced in the second trimester.

    Conclusions:

    • Altered circulating angiogenic factors, specifically the sFLT1/PlGF ratio, may play a role in the pathogenesis of preeclampsia in trisomy 13.
    • These findings suggest a potential mechanism linking trisomy 13 to increased preeclampsia risk.
    • Further longitudinal studies are warranted to confirm the association between trisomy 13, angiogenic factor imbalance, and preeclampsia outcomes.