Anne Eskild1, Lars Monkerud2, Anne Marie Jukic3, Bjørn Olav Åsvold4, Kari Kveim Lie5. 1. Department of Obstetrics and Gynecology, Akershus University Hospital, 1478, Lørenskog, Norway; Institute of Clinical Medicine, University of Oslo, 0313, Oslo, Norway. Electronic address: anne.eskild@medisin.uio.no. 2. Norwegian Institutes for Urban and Regional Research (NIBR), Oslo and Akershus University College of Applied Sciences, 0130, Oslo, Norway. 3. Chronic Disease Epidemiology, Yale School of Public Health, New Haven, 06510, CT, United States. 4. Department of Public Health and Nursing, Norwegian University of Science and Technology, 7491, Trondheim, Norway; Department of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, 7006, Trondheim, Norway. 5. Division of Epidemiology, Norwegian Institute of Public Health, 0403, Oslo, Norway.
Abstract
BACKGROUND: Intrauterine conditions may be important in the development of cerebral palsy in the child. The hormone, human chorionic gonadotropin (hCG), is synthesized in the placenta, and hCG plays an important role in placental angiogenesis and development. Thus, maternal hCG concentrations may be an indicator of placental function and thereby the intrauterine environment for the offspring. We studied the associations of maternal concentrations of hCG during pregnancy with cerebral palsy in the child. METHODS: We performed a case-control study nested within a cohort of 29,948 pregnancies in Norway during 1992-1994. Cases were all women within the cohort who gave birth to a singleton child with cerebral palsy diagnosed before five years of age (n = 63). Controls were a random sample of women with a singleton child without cerebral palsy (n = 182). RESULTS: The adjusted odds ratio (OR) for cerebral palsyin the child was 0.78 (95% CI: 0.55-1.10) per log-transformed unit of maternal hCG in the 1 st trimester, and the OR was 1.42 (95% CI: 0.94-2.16) in the 2nd trimester. Thus, women who did not have high hCG concentrations in the 1 st trimester and low hCG concentrations in the 2nd trimester, had increased risk for giving birth to a child with cerebral palsy. Adjustments were made for pregnancy week of serum sampling, maternal age and parity. CONCLUSIONS: The abnormal hCG concentrations in pregnancies with cerebral palsy in the offspring, could suggest placental factors as causes of cerebral palsy.
BACKGROUND: Intrauterine conditions may be important in the development of cerebral palsy in the child. The hormone, humanchorionic gonadotropin (hCG), is synthesized in the placenta, and hCG plays an important role in placental angiogenesis and development. Thus, maternal hCG concentrations may be an indicator of placental function and thereby the intrauterine environment for the offspring. We studied the associations of maternal concentrations of hCG during pregnancy with cerebral palsy in the child. METHODS: We performed a case-control study nested within a cohort of 29,948 pregnancies in Norway during 1992-1994. Cases were all women within the cohort who gave birth to a singleton child with cerebral palsy diagnosed before five years of age (n = 63). Controls were a random sample of women with a singleton child without cerebral palsy (n = 182). RESULTS: The adjusted odds ratio (OR) for cerebral palsyin the child was 0.78 (95% CI: 0.55-1.10) per log-transformed unit of maternal hCG in the 1 st trimester, and the OR was 1.42 (95% CI: 0.94-2.16) in the 2nd trimester. Thus, women who did not have high hCG concentrations in the 1 st trimester and low hCG concentrations in the 2nd trimester, had increased risk for giving birth to a child with cerebral palsy. Adjustments were made for pregnancy week of serum sampling, maternal age and parity. CONCLUSIONS: The abnormal hCG concentrations in pregnancies with cerebral palsy in the offspring, could suggest placental factors as causes of cerebral palsy.
Authors: Richard J Levine; Chun Lam; Cong Qian; Kai F Yu; Sharon E Maynard; Benjamin P Sachs; Baha M Sibai; Franklin H Epstein; Roberto Romero; Ravi Thadhani; S Ananth Karumanchi Journal: N Engl J Med Date: 2006-09-07 Impact factor: 91.245