Hi Jaroslaw,
These three (3) conditions have one thing in common as complication, that is, disseminated intravascular coagulation (DIC). STBM triggered thrombin generation in normal plasma in a tissue factor dependent manner, indicating that TF activity is expressed by STBM. STBM shed during these pregnancy complications contain increased levels of active tissue factor and that this activate the coagulation system. . Please refer to the following articles for further information.
1. Chris Gardiner et al. (2011). Syncytiotrophoblast Microvesicles Released from Pre-Eclampsia Placentae Exhibit Increased Tissue Factor Activity. PLoS One. 2011; 6(10): e26313. Published online Oct 14, 2011. doi: 10.1371/journal.pone.0026313
2. Aharon A, Brenner B, Katz T, Miyagi Y, Lanir N. Tissue factor and tissue factor pathway inhibitor levels in trophoblast cells: implications for placental hemostasis. Thromb Haemost. 2004; 92:776–786. [PubMed]
3. Aharon A, Katzenell S, Tamari T, Brenner B. Microparticles bearing tissue factor and tissue factor pathway inhibitor in gestational vascular complications. J Thromb Haemost. 2009; 7:1047–1050. [PubMed]
Regards
Only in preeclampsia TF transported by the microparticles from the placenta may play a role. In early pregnancy STBM with syncytiotropfoblast enters through placental circulation in the blood of pregnant and causes the activation of thrombin generation. Thrombin activates in loco clotting and inflammation causing further damage of endothelial cells during pregnancy. The placental abruption in pregnancy and amniotic fluid embolism - STBM not get into the amniotic fluid. We found the presence of microparticles in the amniotic fluid but different origin. There are microparticles resulting from apoptosis of epithelial cells of the fetus (the respiratory tract, gastrointestinal tract, especially the epidermal cells and amnion cells). TF in the amniotic fluid is a lot of what we wrote in the work of 2001.2002 years. However, the DIC supply pathomechanism is probably a little different. Microparticles have little relevance here. There are too few. TF contained in the amniotic fluid causes the promotion of thrombin and activation of the coagulation cascade. This leads to consumption coagulopathy and clotting factors of DIC.
What is interesting is that there are fewer STBM microparticles in the circulation of normotensive women with pregnancies complicated by IUGR than in normal pregnancy (Duna Goswami) - as there is also less syncytial volume in these placentae (Ian Crocker). This contrasts with early-onset pre-eclampsia, where both syncytial volume and circulating STBM concentrations are higher than in GA-matched normal pregnancy. Late-onset pre-eclampsia does not appear to differ greatly from normal pregnancy in this regard. Whereas changes in angiogenic balance appear to be shared between placental IUGR and pre-eclampsia (Samantha Benton), the STBM response to imperfect placentation is discordant between IUGR and pre-eclampsia - this makes STBM very important as a specific inciter of the pre-eclampsia response in my view.
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