The Great Obstetrical Syndromes

The Journal of Maternal–Fetal and Neonatal Medicine was born when two biomedical journals merged: The Journal of Maternal–Fetal Medicine and Prenatal and Neonatal Medicine. The new name for what is now known as the ‘Black Journal’ represents the need for dialogue and communication between maternal– fetal medicine specialists and neonatologists. The last editorial board meeting took place in San Diego at the Annual Meeting of the Society for Maternal-Fetal Medicine. The editors and publisher were pleased to inform the members of the editorial board about the scientific and financial success of the journal. In this issue of the journal, we reprint the opening editorial of Prenatal and Neonatal Medicine, entitled ‘Prenatal Medicine: The Child is the Father of the Man’, which articulated the agenda of the journal in 1996 and remains topical and visionary in 2009 [1]. The two themes of the editorial were the emphasis on the developmental origins of adult disease (also known as the ‘‘Barker hypothesis’’) and the concept of the ‘great obstetrical syndromes’. The first theme has gained worldwide acceptance thanks to imaginative epidemiologic studies conducted around the world. The concept has served to establish the International Society for Developmental Origins of Health and Disease, which holds congress and workshops on a regular basis where scientists and clinicians aim at understanding the mechanisms responsible for programming, and also, to translate what has been learned into clinical practice. The next congress of the society will be in Santiago, Chile from 19 November to 22 November 2009 (for details, see www.dohad2009.com). The second theme aimed at re-examining the nature of disease in obstetrics, and proposed that the clinical conditions responsible for maternal and perinatal morbidity and mortality is syndromic in nature. The term ‘the great obstetrical syndromes’ was coined to refer to conditions with the following characteristics: (1) multiple etiologies; (2) a long preclinical period; (3) adaptive in nature; (4) fetal involvement and (5) the result of complex interactions between the maternal and fetal genome and the environment [1–4]. The complexity and importance of the interaction between the fetal and maternal genomes is now being explored [1– 4]. The definition of environmental exposure in utero is also a challenge. Accumulating observations now indicate that preterm labor, preterm premature rupture of membranes [5–10], preeclampsia [11–30], small for gestational age (SGA) [31–33], large for gestational age (LGA) [34–44], stillbirth [45–54] and many other conditions that we deal with in clinical practice are not discrete entities, but are syndromes with more than one cause. The purpose of the term ‘the great obstetrical syndromes’ was to try to explain the disappointing results when we tried to predict and prevent obstetrical diseases [1]. It called attention to the idea that etiologic heterogeneity was followed by a common pathway [1]. Therefore, the concept predicted that no single test would identify the patient destined to develop preterm labor, preeclampsia, SGA, etc. and that there would not be a single treatment [1]. Medicine is now committed to identifying biomarkers to predict disease. This is also the case for maternal–fetal medicine and obstetrics. It is hoped that prediction will lead to prevention, however, this has not been the case in obstetrics thus far. A positive fetal fibronectin or a short cervix can identify patients at risk for spontaneous preterm delivery. We are yet to prove that prediction can be used for prevention – perhaps such proof is around the corner. The Journal of Maternal-Fetal and Neonatal Medicine, August 2009; 22(8): 633–635