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Editorials |
1 Unit of Hematology and Thrombosis, Department of Medicine, Surgery and Dentistry, Ospedale San Paolo, University of Milano, Via di Rudinì 8, 20142 Milan, Italy, Fax 39-0250320723, E-mail marco.cattaneo@unimi.it
| The first 20% of the full text of this article appears below. |
The association of inherited and acquired thrombophilias (which predispose to thrombotic vascular occlusions) with the risk of eclampsia, abruptio placentae, intrauterine growth restriction (IUGR), and stillbirth has been the object of many studies in the last few years (1). The rationale for these studies was based on the hypothesis that the formation of thrombi in the placental circulation of thrombophilic women could lead to impaired nutrition of the fetus. As a matter of fact, some studies have documented the presence of thrombotic lesions in the placentas of women with adverse pregnancy outcomes, although this has not been a consistent finding (2)(3)(4).
Early case-control studies of the prevalence of thrombophilia in women with adverse pregnancy outcomes gave contrasting results because each of them involved a relatively low number of participants (5)(6)(7). More recently, Infante-Rivard et al.(8) published a large study, which involved 493 women who gave birth to babies with IUGR and 472 women who had babies of normal size. The study, which had sufficient statistical power to detect odds ratios that had been estimated by previous reports, showed that there was no difference in the prevalence of the two most common thrombophilic polymorphisms (factor V Leiden and prothrombin G20210A) among cases and controls. In addition, the prevalence of placentas that had
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