Investigation of serum and placental salusin-ghrelin levels in patients with HELLP syndrome

The syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP) is a life-threatening ailment, often seen as a severe variant of preeclampsia.In this study, we intended to investigate the maternal serum?placental levels of acylated ghrelin, desacyl ghrelin, salusin- ? and salusin- ? levels in normotensive pregnant women and pregnant women complicated with HELLP syndrome. Also we intended to investigate the possible associations between these biochemical markers and HELLP syndrome. All of these peptides have potential effect of hypotension on cardiovascular system.We involved 15 normotensive pregnant women who were delivered by abdominal way, 15 normotensive pregnant women who were delivered by vaginal way and 15 pregnant women complicated with HELLP syndrome in our study. We collected serum samples from all patients during prepartum and postpartum period. The serum and placental levels of these biochemical markers were analysed by enzyme-linked immunosorbent assay. The immunocytochemical analysis of placental tissues were performed by Avidin-Biotin-Peroxidase Complex method.The prepartum and postpartum levels of desacyl ghrelin (p<0.01) and salusin- ? ( p<0.05) in serum of pregnant women complicated with HELLP syndrome were significantly lower than levels of normotensive pregnant women. But salusin- ? (p<0.01) levels were significantly higher than normotensive pregnant women and only prepartum acylated ghrelin (p<0.05) levels of women complicated with HELLP syndrome were significantly higher than normotensive women. The placental desacyl ghrelin and salusin- ? levels of women complicated with HELLP syndrome were significantly lower than normotensive women but, placental acylated ghrelin levels of women complicated with HELLP syndrome were significantly higher than normotensive women.In conclusion, we thougt that acylated ghrelin, desacyl ghrelin, salusin- ? and salusin- ? could play an important role in the pathogenesis of HELLP syndrome by the mechanism of vasoconstruction.