Health Dictionary
Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Pre-eclampsia pathophysiology
Introduction
Overview
Overview
Preeclampsia may be the result of placental factors in maternal circulation leading to endothelial dysfunction, hypertension, and proteinuria. Increased levels of an angiogenic factor named fms-like tyrosine kinase 1 in the placenta is correlated with endothelial dysfunction. In villous trophoblast of preeclamptic women, apoptosis was considered. Following uteroplacental ischemia, and invasion spiral arteries by trophoblasts, releasing some angiogenic factors causes other organ involvement. Incomplete penetration in recessive or dominant genes was noticed in pathogenesis of preeclampsia.
Pathophysiology
Pathophysiology
- The pathogenesis of preeclampsia is characterized by the following :[1][2]
- Chronic uteroplacental ischemia[3]
- Genetic susceptibility
- Very-low-density lipoprotein toxicity
- Increased trophoblast apoptosis or necrosis[4]
- Increased Maternal inflammatory response to fetal trophoblast
- Imbalance of angiogenic factors [5]
- Imbalance of prostacycline and thromboxan-A2
References
References
- ↑ Johansen, M; Redman, C.W.G; Wilkins, T; Sargent, I.L (1999). “Trophoblast Deportation in Human Pregnancy—its Relevance for Pre-eclampsia”. Placenta. 20 (7): 531–539. doi:10.1053/plac.1999.0422. ISSN 0143-4004.
- ↑ Dekker, Gustaaf A.; Sibai, Baha M. (1998). “Etiology and pathogenesis of preeclampsia: Current concepts”. American Journal of Obstetrics and Gynecology. 179 (5): 1359–1375. doi:10.1016/S0002-9378(98)70160-7. ISSN 0002-9378.
- ↑ Espinoza, J. (2012). “Uteroplacental ischemia in early- and late-onset pre-eclampsia: a role for the fetus?”. Ultrasound in Obstetrics & Gynecology. 40 (4): 373–382. doi:10.1002/uog.12280. ISSN 0960-7692.
- ↑ Crocker, Ian P.; Cooper, Suzanne; Ong, Stephen C.; Baker, Philip N. (2003). “Differences in Apoptotic Susceptibility of Cytotrophoblasts and Syncytiotrophoblasts in Normal Pregnancy to Those Complicated with Preeclampsia and Intrauterine Growth Restriction”. The American Journal of Pathology. 162 (2): 637–643. doi:10.1016/S0002-9440(10)63857-6. ISSN 0002-9440.
- ↑ Levine, Richard J.; Maynard, Sharon E.; Qian, Cong; Lim, Kee-Hak; England, Lucinda J.; Yu, Kai F.; Schisterman, Enrique F.; Thadhani, Ravi; Sachs, Benjamin P.; Epstein, Franklin H.; Sibai, Baha M.; Sukhatme, Vikas P.; Karumanchi, S. Ananth (2004). “Circulating Angiogenic Factors and the Risk of Preeclampsia”. New England Journal of Medicine. 350 (7): 672–683. doi:10.1056/NEJMoa031884. ISSN 0028-4793.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Ogheneochuko Ajari, MB.BS, MS [3]