Are long‐term health risks of pre‐eclampsia and intrauterine growth restriction really the same?

Pre-eclampsia and intrauterine growth restriction (IUGR) represent divergent clinical manifestations of placental disease. Although the underlying aetiology of these complications is of placental origin, the mechanisms leading to the differential maternal and fetal responses are not understood. Likewise, although pre-eclampsia and IUGR are risk factors for future maternal health conditions, it is not clear whether the degree of risk is indeed equal for these women (Smith et al. Lancet 2001;357:2002–2006). In this issue of BJOG, Al-Nasiry et al. compared the metabolic syndrome (defined according to criteria outlined by the WHO) in women with a history of pre-eclampsia, compared with women who were normotensive and who delivered a small-for-gestational age (SGA) infant (defined as birthweight <10th percentile for gestational age at delivery and sex). The calculated odds ratios for the metabolic syndrome and its components several months postpartum were increased for women with a history of pre-eclampsia compared with SGA. These findings suggest that the divergent response to placental disease corresponds to differing health risks for women who develop pre-eclampsia versus those who deliver an SGA infant. The development of pre-eclampsia rather than IUGR may relate to the intrinsic maternal threshold for (mal)adapting to the compensatory mechanisms, primarily inflammation, activated in the presence of abnormal placentation (Ness and Sibai Am J Obstet Gynecol 2006;195:40–49). If there are intrinsic differences for coping with systemic inflammation in women who develop pre-eclampsia versus IUGR, it would seem plausible that long-term health risks would indeed differ between these groups. Better understanding of the interaction between placental disease and maternal threshold will help to refine the association between pre-eclampsia and IUGR and the future health of these mothers. It should be noted that this study used SGA as a (poor) proxy for IUGR. As commented by the authors, their SGA group thus contains both constitutionally small fetuses and those with true growth restriction. We would argue that the majority of the women in this group probably delivered constitutionally small fetuses (RCOG Guideline No. 31, 2013), and thus the true association (if any) between the fetal response to placental disease (IUGR) and subsequent maternal risk of the metabolic syndrome may be masked. Future studies should aim to use more concrete criteria to define IUGR, although we recognise that this is problematic in retrospective studies. Overall, this study highlights a finding of differing risk for the metabolic syndrome for mothers with a history of pre-eclampsia or normotensive SGA. Such studies are needed to clarify the association between these complications and long-term health in order to provide women attending postpartum clinics an accurate estimate of their future health risk mechanisms as well as potentially elucidating the mechanisms leading to the divergent maternal and fetal responses to placental disease. The authors have received unrestricted in-kind funding from Alere International.

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