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SUBSEQUENTLY SEVERE PREECLAMPSIA SHIN-YOUNG KIM, HYUN-MEE RYU, JAEHYUG YANG, MOON-YOUNG KIM, HYUN-KYONG AHN, JOONG-SIK SHIN, JUNSEEK CHOI, SO-YEON PARK, JIN-MI KIM, BOM-YI LEE, DO-JIN KIM, Samsung Cheil Hospital & Women’s Healthcare Center, Laboratory of Medical Genetics, Seoul, Korea, South Korea, Samsung Cheil Hospital & Women’s Healthcare Center, Sungkyunkwan University School of Medicine, Obstetrics and Gynecology, Seoul, Korea, South Korea OBJECTIVE: It has been shown that maternal serum inhibin-A levels are increased in women with preeclampsia. Little is known about inhibin-A levels in amniotic fluid. The aim of this study was to determine whether amniotic fluid and maternal serum inhibin-A levels are elevated in the early second trimester of women who subsequently develop severe preeclampsia. STUDY DESIGN: We studied the levels of inhibin-A in amniotic fluid and maternal serum at 15-20 weeks’ gestation from normal pregnant women (n = 80) and from pregnant women with subsequently severe preeclampsia (n = 50). All samples were assayed for inhibin-A by enzyme-linked immunosorbent assay (ELISA). RESULTS: Amniotic fluid and maternal serum inhibin-A levels were significantly increased in severe preeclampsia compared to normal pregnant women (P ! .001 for both). With a specific cutoff value, the estimated odds for severe SMFM Abstracts S35

(MTHFR C677T AND A1298C) AND METHIONINE SYNTHASE REDUCTASE (MTRR A66G) GENE AS MATERNAL RISK FACTORS FOR FETAL ANEUPLOIDY HYUNMEE RYU, DO-JIN KIM, MOON-YOUNG KIM, SO-YEON PARK, JIN-WOO KIM, SHIN-YOUNG KIM, JAE-HYUG YANG, JOUNG-YEOL HAN, JOO OH KIM, JINHOON CHUNG, Samsung Cheil Hospital and Women’s Healthcare Center, Sungkyunkwan University School of Medicien, Obstetrics and Gynecology, Seoul, Korea, South Korea, Samsung Cheil Hospital and Women’s Healthcare Center, Laboratory of Medical Genetics, Seoul, Korea, South Korea OBJECTIVE: The purpose of this study was to address the association of MTHFR (C677T/A1298C) and MTRR (A66G) polymorphisms as maternal risk factors for fetal aneuploidy. STUDY DESIGN: We studied the presence of MTHFR C677T/A1298C and MTRR A66G in an aneuploidy group (n = 30) who had fetal aneuploidy and in a control group (n = 78) who had given birth to at least two healthy children without a history of miscarriage or abnormal pregnancy. To determine the polymorphism of these enzymes, we performed PCR/RFLP (Restriction Fragment Length Polymorphism). RESULTS: There were no statistical differences in the prevalence of MTHFR 677 variant T allele (P = .519) and 1298 variant C allele (P = .051) in both groups. Frequency of MTRR G allele in aneuploidy group was higher than in control group. Mother with MTRR 66 AG mutation had a 2.9-fold higher risk of having a fetus with aneuploidy than mother without the G substitute (odds ratio: 2.9; 95% CI: 1.5-5.3; P = .001). CONCLUSION: This study suggests that there was an increased risk of fetal aneuploidy in mother carriers of MTRR G allele, not in MTHFR C677T and A1298C. The MTRR A66G variant may be a significant risk factor for producing a child with chromosome aneuploidy.