Ο ρόλος της ενδοθηλίνης στο αμνιακό υγρό ως δείκτης παθολογικών καταστάσεων της εγκυμοσύνης

Abstract

Endothelin-1 (ET-1) is a peptide consisting of 21 amino acids. It is a strong vasoconstrictor and mitogenic factor with significant activity on to the smooth muscle cells. High concentrations of ET-1 have been detected in plasma of patients with severe hypertension or preeclampsia. The exact role of ET-1 in relation to human reproduction is still largely an enigma. Maternal and fetal plasma concentrations of ET-1 have been studied recently in relation to pregnancy. These include intrauterine growth retardation (IUGR) and preeclampsia. The exact mechanisms of these pathological processes and increased plasma concentrations of ET-1 are still largely unknown, although there is evidence to suggest that ET-1 is associated with impaired endothelial cells. There is now some evidence that amniotic ET-1 concentrations are elevated in pregnancies associated with pre-eclampsia. The purpose of this prospective observational study was to record the ET-1 concentration in second trimester amniotic fluid and compare with the levels in women who develop preeclampsia, IUGR and premature rupture of membranes. The amniotic fluid samples were obtained from 125 women by amniocentesis during the second trimester of pregnancy. The levels of ET-1 were measured with a sensitive and specific radioimmunoassay examination (ELISA). The amniotic fluid concentrations of ET-1 are statistically significantly higher from the second trimester in women who later develop PPROM, PROM, IUGR with preeclampsia. This study showed that ET-1 levels correlated with the birth weight of newborns in the pregnancies complicated by IUGR, the birth weight of newborns and the gestational age for the group PPROM, and with the birth weight of newborns in pregnancies with preeclampsia . Investigating the levels of ET-1 in the second trimester amniotic fluid can be an extremely important research area in the future, and could shed more light on the early discovery of the pathophysiological process of placental dysfunction.