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Maternoembryonic transfusion and congenital malformations
D C van der Zee1, K M Bax, C Vermeij-Keers
1Department of Paediatric Surgery, University Children's Hospital, Wilhelmina Kinderziekenhuis, Utrecht, The Netherlands.
Prenatal Diagnosis
|January 1, 1997
Summary
Chorionic villus sampling (CVS) may cause limb defects by triggering antibody-mediated vascular disruption and cell death in embryos. This experimental model explains how maternoembryonic transfusion after CVS leads to congenital malformations.
Area of Science:
- Developmental Biology
- Reproductive Medicine
- Immunology
Background:
- Reports link chorionic villus sampling (CVS) to limb reduction defects and oromandibular-limb hypogenesis.
- Defect severity correlates with gestational age at CVS.
- Vascular disruption is a proposed mechanism for CVS-related malformations.
Purpose of the Study:
- To describe an experimental model explaining the pathogenesis of congenital malformations after CVS.
- To investigate the role of maternoembryonic transfusion in inducing these defects.
Main Methods:
- Whole rat embryo culture technique.
- Intracardiac injection of antisera to mimic transplacental transfusion post-CVS.
- Immunological staining to detect antibody-mediated reactions and apoptotic cell death.
Main Results:
- Antibody injection induced increased apoptotic cell death in rat embryos.
- Vulnerable, fenestrated endothelium in smaller embryonic vessels (pharyngeal arch, limb arteries) is susceptible to vascular disruption.
- Dorsal aortae with continuous endothelium showed transient effects.
Conclusions:
- Intracardiac antisera injection simulates maternoembryonic transfusion, causing antibody-mediated vascular disruption and apoptotic cell death.
- This process can lead to congenital malformations like transverse limb defects.
- Vascular development influences malformation risk throughout pregnancy.