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Related Experiment Videos

Two live-born infants with trisomy 22.

J Phillipson1, K Benirschke, M Bogart

  • 1Department of Pathology, University of California San Diego Medical Center 92103.

Pediatric Pathology
|January 1, 1990
PubMed
Summary

Full trisomy 22, a genetic condition, was studied in two fetuses. Confined placental mosaicism may explain why some trisomy 22 pregnancies survive in the womb.

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Area of Science:

  • Genetics
  • Developmental Biology
  • Pathology

Background:

  • Trisomy 22 is a chromosomal abnormality characterized by the presence of an extra copy of chromosome 22.
  • Live-born fetuses with full trisomy 22 are rare, making detailed study challenging.
  • Understanding factors influencing intrauterine survival in chromosomal abnormalities is crucial.

Observation:

  • Autopsy findings and karyotypes were analyzed in two live-born fetuses diagnosed with full trisomy 22.
  • Confined placental mosaicism (CPM), a condition where placental cells have a different genetic makeup than fetal cells, was identified in one of the two cases.
  • The study examined the potential role of CPM in fetal development and survival.

Findings:

  • Karyotype analysis confirmed full trisomy 22 in both fetuses.
  • The presence of confined placental mosaicism in one case suggests a potential mechanism for partial genetic correction or influence on fetal growth.
  • Autopsy findings provided insights into the specific phenotypic manifestations associated with full trisomy 22.

Implications:

  • Confined placental mosaicism may be a significant factor contributing to the intrauterine survival of fetuses with trisomy 22.
  • Further research into CPM could offer new perspectives on managing and understanding other chromosomal abnormalities.
  • These findings highlight the complex interplay between placental and fetal genetics in determining pregnancy outcomes.

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