Fetus
Poster Session 1
Tess N. van Schoor, BS (she/her/hers)
Medical Student
Keck School of Medicine
Los Angeles, CA, United States
Matthew E. Thornton, BS, MS
Research Specialist
Maternal Fetal Medicine Division, Department of Obstetrics and Gynecology, Keck School of Medicine
Los Angeles, CA, United States
JC Rodman, BS, MPH
USC CTSI
Los Angeles, CA, United States
Arlyn Llanes, MHA, RN
University of Southern California
Los Angeles, CA, United States
Catherine Hamzeh, BS
University of Southern California
Los Angeles, CA, United States
RH Chmait, MD
Los Angeles Fetal Surgery
Los Angeles, CA, United States
Brendan Grubbs, MD
Los Angeles General Hospital + USC Medical Center
Los Angeles, CA, United States
AF was collected at the time of diagnosis (Early 21-22 weeks, n=6) or immediately prior to fetoscopic repair (Late 26-27 weeks, n=7). Control samples (21-22 weeks, n=3) were amniocentesis samples collected for advanced maternal age and did not have OSB. Activity levels of amylase and PLA2 were measured in control, early gestation, and late gestation groups utilizing commercial assay kits. The Wilcoxon-Signed Rank Test was used to compare amylase activity in the control vs. early groups and the early vs. late groups. A one-sided T-Test was used to compare PLA2 activity the control vs. early groups and the early vs. late groups.
Results:
The Amylase Activity of the early group (median=0.204 nmol/ml/min) was not significantly different from that of the control group (median= 0.183 nmol/ml/min); p=0.4, but was significantly less than that of the Late Group (median=0.253 nmol/ml/min); p< 0.0045. The PLA2 Activity of the early group (mean=3.84 nmol) was not significantly different from that of the control group (mean=4.1 nmol); p=0.3, and was not significantly less than that of the Late Group (mean=5.09 nmol); p=0.892.
Conclusion: Amylase activity levels in the AF of human fetuses with MMC appear to increase throughout the 2nd trimester. The increase in PLA2 activity did not reach statistical significance and may be due to a lack of power. These, as well as other neurotoxic enzymes may contribute to the “second hit” of OSB and suggest the RA rat as a valid model for the human defect.