|
|
||||||||
Letters to the Editor |
1 Institut National de la Santé et de la Recherche Médicale (INSERM) U4892 Department of Gynecology and Obstetrics3 Department of Biochemistry and4 Department of Nephrology, Hôpital Tenon, Paris, France
aAddress correspondence to this author at: Hôpital Tenon, 4 rue de la Chine, NA 75020 Paris, France. Fax 33-1-43645448; e-mail alexandre.hertig@tnn.ap-hop-paris.fr.
| The first 20% of the full text of this article appears below. |
To the Editor:
Preeclampsia is a leading cause of maternal and fetal morbidity and mortality worldwide. It occurs in two phases: abnormal implantation of the placenta leads to impaired placental blood flow, which in turn induces the release of a critical placental substance into the maternal circulation (1). Clinical onset usually occurs in the third trimester of pregnancy, long after initiation of the underlying process.
Recently, Maynard et al. (2) compared the gene expression profile in placental tissue from women with and without preeclampsia and identified soluble Flt1 (sFlt1), a vascular endothelial growth factor receptor, as a molecule of particular pathophysiologic interest. It is now suspected that trophoblastic injury markedly enhances placental sFlt1 production, antagonizing the endothelial protective role of vascular endothelial growth factor and/or placental growth factor and eventually leading to clinical preeclampsia (2)(3). A recent study pointed out that, compared with women with a retrospective diagnosis of normal pregnancy (i.e., without hypertension), preeclamptic women had increased serum sFlt1 several weeks before
The following articles in journals at HighWire Press have cited this article:
![]() |
S. E. Maynard and R. Thadhani Pregnancy and the Kidney J. Am. Soc. Nephrol., January 1, 2009; 20(1): 14 - 22. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Huppertz Placental Origins of Preeclampsia: Challenging the Current Hypothesis Hypertension, April 1, 2008; 51(4): 970 - 975. [Full Text] [PDF] |
||||
![]() |
N. Berkane, G. Lefevre, and A. Hertig Angiogenic factors in preeclampsia: so complex, so simple? Nephrol. Dial. Transplant., October 1, 2007; 22(10): 2753 - 2756. [Full Text] [PDF] |
||||
![]() |
S. Rana, S. A. Karumanchi, R. J. Levine, S. Venkatesha, J. A. Rauh-Hain, H. Tamez, and R. Thadhani Sequential Changes in Antiangiogenic Factors in Early Pregnancy and Risk of Developing Preeclampsia Hypertension, July 1, 2007; 50(1): 137 - 142. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Cudmore, S. Ahmad, B. Al-Ani, T. Fujisawa, H. Coxall, K. Chudasama, L. R. Devey, S. J. Wigmore, A. Abbas, P. W. Hewett, et al. Negative Regulation of Soluble Flt-1 and Soluble Endoglin Release by Heme Oxygenase-1 Circulation, April 3, 2007; 115(13): 1789 - 1797. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Stepan, A. Unversucht, N. Wessel, and R. Faber Predictive Value of Maternal Angiogenic Factors in Second Trimester Pregnancies With Abnormal Uterine Perfusion Hypertension, April 1, 2007; 49(4): 818 - 824. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Levine, C. Lam, C. Qian, K. F. Yu, S. E. Maynard, B. P. Sachs, B. M. Sibai, F. H. Epstein, R. Romero, R. Thadhani, et al. Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. N. Engl. J. Med., September 7, 2006; 355(10): 992 - 1005. [Abstract] [Full Text] [PDF] |
||||
![]() |
K.-A. Wathen, E. Tuutti, U.-H. Stenman, H. Alfthan, E. Halmesmaki, P. Finne, O. Ylikorkala, and P. Vuorela Maternal Serum-Soluble Vascular Endothelial Growth Factor Receptor-1 in Early Pregnancy Ending in Preeclampsia or Intrauterine Growth Retardation J. Clin. Endocrinol. Metab., January 1, 2006; 91(1): 180 - 184. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Lam, K.-H. Lim, and S. A. Karumanchi Circulating Angiogenic Factors in the Pathogenesis and Prediction of Preeclampsia Hypertension, November 1, 2005; 46(5): 1077 - 1085. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |