Pentraxina 3 come potenziale marcatore di danno endoteliale in gravidanze complicate da preeclampsia e ritardato accrescimento intrauterino.

Objectives: Endothelial dysfunction typical of preeeclampsia (PE) is the result of an excessive maternal inflammatory response to pregnancy. PE can occur alone or together with intrauterine growth restriction (IUGR). We investigated PTX3 in maternal, fetal and placental compartments in complicated pregnancies. Study design: Maternal blood samples were collected during the III trimester in 53 PE, 43 IUGR and 50 normal pregnancies. Fetal samples were collected from the umbilical vein in 26 PE, 23 IUGR and 26 normal pregnancies at elective cesarean section. PTX3 plasma levels were determined by ELISA. Pattern and site of expression of PTX3 was studied by immunohistochemistry (IHC) on placenta, decidual bed and maternal peritoneum. Results: PE and IUGR pregnancies showed significantly higher median maternal PTX3 levels vs normal pregnancies (24.8 and 9.9 vs 3.8 ng/ml; p<0.001). IUGR showed significantly lower levels than PE (p<0.001). Severe PE revealed higher levels (33.1 vs 17.1 ng/ml, p<0.001) than mild PE. Severe PE with HELLP presented significantly higher levels. IHC on placenta and decidual bed biopsies showed similar expression in pathologic compared to normal cases. Maternal peritoneum expressed a significantly higher signal in the endothelium of pathological vs normal pregnancies. PTX3 was detected in the fetal circulation with values significantly higher in IUGR thsn in normal fetuses with a trend towards higher values in correlation with IUGR severity. Conclusions: We report elevated maternal levels of PTX3 in PE and IUGR pregnancies. PTX3 levels correlated to clinical severity of disease with higher PTX3 levels in severe than in mild PE, IUGR without clinical PE were significantly different from both normal and PE pregnancies. PTX3 increase may represent the expression of endothelial systemic damage on the maternal side. Moreover, PTX3 is detected in fetal blood and is significantly incresased in IUGR fetuses likely reflecting endothelial damage.