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Letters to JMG
Paternal contribution to the risk for pre-eclampsia
  1. P L M Zusterzeel1,
  2. R te Morsche2,
  3. M T M Raijmakers2,
  4. E M Roes1,
  5. W H M Peters2,
  6. E A P Steegers3
  1. 1Department of Obstetrics and Gynaecology, University Medical Centre, Nijmegen, The Netherlands
  2. 2Department of Gastroenterology, University Medical Centre, Nijmegen, The Netherlands
  3. 3Department of Obstetrics and Gynaecology, Erasmus University Medical Centre, Rotterdam, The Netherlands
  1. Correspondence to:
 Dr E A P Steegers, Department of Obstetrics and Gynaecology, Erasmus University Medical Centre, Rotterdam, The Netherlands;
 eapsteegers{at}gyna.azr.nl

https://doi.org/10.1136/jmg.39.1.44

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    Pre-eclampsia is a major cause of fetal and maternal morbidity and mortality with a still obscure aetiology. A major feature in pre-eclampsia is placental maladaptation, probably because of inadequate invasion of fetal trophoblast cells in the myometrium and spiral arteries that might be related to local oxidative stress. Reactive oxygen species (ROS), lipid peroxides, and other toxic compounds are metabolised by biotransformation enzymes in scavenging and detoxifying processes. Increasing evidence suggests an important function of antioxidants and detoxification enzymes in pre-eclampsia. We recently proposed that the 105Ile→Val polymorphisms in the glutathione S-transferase P1 gene (GSTP1), associated with lower enzyme detoxification capacity, enhanced maternal susceptibility to pre-eclampsia.1 Glutathione S-transferase P1-1 (GSTP1-1) is an important detoxification enzyme and is the main GST isoform in placenta and decidua.2 The GSTP1-1 level was found to be lower in placental and decidual tissue of pre-eclamptic women as compared with corresponding tissues of normal pregnant women.2 Since placenta is of fetal origin and therefore characterised by both maternal and paternal contribution, the risk for pre-eclampsia might be modified by maternal as well as paternal genetic variations in detoxification activities. We therefore studied GSTP1 polymorphisms in a cohort …

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