Volume 192, Issue 2 , Pages 604-609, February 2005
Persistent elevation of cell-free fetal DNA levels in maternal plasma after selective laser coagulation of chorionic plate anastomoses in severe midgestational twin-twin transfusion syndrome
Objective
This study was undertaken to determine whether laser thermocoagulation for twin-twin transfusion syndrome (TTTS) causes increased cell-free fetal DNA levels in maternal plasma, potentially as a result of placental injury.
Study design
We enrolled 34 patients with twin pregnancies complicated by severe TTTS who underwent fetoscopic selective laser ablation of placental vascular anastomoses. Blood samples were drawn before and sequentially after the procedure. Fetal DNA in maternal plasma was quantified by polymerase chain reaction amplification of a Y-chromosome sequence.
Results
Compared with baseline, median elevations of fetal DNA levels were 0.8% at 30 minutes (P
=
.32), 15.8% at 60 minutes (P
=
.1), 179.5% at 24 hours (P
=
.003), and 172.9% at 48 hours (P
=
.003). Factors associated with increased fetal DNA levels at 24 hours after procedure included longer operation time, higher number of vessels ablated, and subsequent in utero fetal death (P
=
.01, .04, and .04, respectively).
Conclusions
Persistent elevation of fetal DNA levels in maternal plasma after laser ablation suggests that circulating fetal DNA could derive from placental injury. Plasma fetal DNA analysis may be an additional prognostic marker for fetal outcome after laser therapy.
Key words: Cell-free fetal DNA, Twin-twin transfusion syndrome, Fetoscopic laser ablation, Placental pathology, In utero fetal death
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The Maternal-Fetal Medicine Fellowship (TW) was supported in part by the Anandamahidol Foundation, Thailand. The fellowship (JJ) and the clinical trials were supported by the European Commission (EURO TWIN 2 TWIN, GLC1-CT-2002-01632). L. Lewi is a recipient of a doctoral fellowship of the Flemish Government (VIS/00/009). Funding was also received from The Spanish Fondo de Investigaciones Cientificas (FIS 02/0738 to EG) and the United States National Institutes of Health (N01-HD43204 and R01-HD42053 to DWB).
PII: S0002-9378(04)00777-X
doi:10.1016/j.ajog.2004.07.019
© 2005 Elsevier Inc. All rights reserved.
Volume 192, Issue 2 , Pages 604-609, February 2005
