Etiology of preeclampsia: maternal vascular predisposition and couple disease - mutual exclusion or complementarity?
Date
2007
Authors
Robillard, P.
Dekker, G.
Chaouat, G.
Hulsey, T.
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Journal article
Citation
Journal of Reproductive Immunology, 2007; 76(1-2):1-7
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Pierre-Yves Robillard, Gustaaf Dekker, Gérard Chaouat, Thomas C. Hulsey
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Abstract
Developed countries represent 20% of the population in the world, but only 12% of human births annually, while 98% of medical publications are issued from these areas. What we can read on preeclampsia is correct, but only for 12% of human pregnancies! In addition, reproductive patterns in the developed world, but only for the last three decades, are different from elsewhere and during the first 70 years of the 20th century. A major difference is in the number of children in families but also, and mainly, in the ages at first pregnancies in primiparae (approaching now 30 years in many developed countries). This is probably why current epidemiological data seem different than that of the 20th century. The purpose of this article is to analyse to what extent the 'primipaternity model' may give clues for the comprehension of epidemiological descriptions past and present--and, indeed, it works in many respects. However, it is evident also that a proportion of preeclampsia cases cannot be explained by paternity patterns, and vascular disease predisposition in women (diabetes, obesity, thrombophilias, etc.) evidently comes into play. For these latter, maternal age is also strongly associated with these complications. Here, we reflect on what can be respective parts of the disease in preeclamptic couples, and on preeclampsia as a marker of subjects susceptible to vascular disease.
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© 2007 Elsevier Ireland Ltd. All rights reserved.