Abstract

Introduction During pregnancy close interactions between the maternal and fetal system exist with the placenta as the organ situated between the two individuals. In cases where this crosstalk is disturbed, preeclampsia may develop. During the last decades a number of hypotheses have been developed to describe the etiology of this syndrome. However, so far all of them have failed. Objectives One of the current hypotheses – although wrong as well – is still strongly supported by the scientific community although it has become clear in recent years that a variety of arguments that are needed to support this hypothesis are not valid at all. Methods This list comprises the following arguments, known to be wrong today: (1) Failure in trophoblast invasion is a prerequisite for preeclampsia. (2) Placental hypoxia is present in cases suffering from preeclampsia. (3) During preeclampsia, the placenta is the main source for angiogenic factors in maternal blood. Additionally, another important issue needs attention: (4) The quality of a biomarker only depends on its concentration in maternal blood. Results These four arguments and issues will be discussed. It will become clear that (1) changes in trophoblast invasion are not related to preeclampsia; (2) placental hypoxia does not exist at all in cases with preeclampsia; (3) the maternal vascular system is the main source for angiogenic factors; and (4) pre-analytics are increasingly important to maintain the quality of samples to test for biomarkers. Conclusion Due to the availability of new data it is more than needed to update the hypotheses on the etiology of preeclampsia. It is quite detrimental to keep with old but no longer valid hypotheses and hindering the rise of newer and better hypotheses. Therefore, the above mentioned arguments including trophoblast invasion, placental hypoxia and the source of angiogenic factors need to be taken into account when further discussing the etiology of preeclampsia.

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