Early Onset Preeclampsia and Nectin-4

Preeclampsia is assumed as a two-stage disorder arising from defective trophoblast invasion and failure of spiral artery remodeling as the main step responsible for the pathogenesis. PE is classified according to the disease onset time as early-onset PE before 34 weeks and late-onset PE after 34 weeks. Late-onset PE is more commonly seen and accepted as a mild maternal reaction to pregnancy. In early-onset PE, unlike the late-onset, due to the improper placental invasion, the diffuse placental ischemia and the resulting oxidative stress begin at early gestation. Thus, the early-onset PE may result in severe disease leading to perinatal and maternal morbidity and mortality.

The nectins are calcium-independent immunoglobulin-like celladhesion molecules and have a pivotal role at cellular junctions, as well as physiological regulations(8). Placenta expressesfor types of nectins; nectin-1, nectin-2, nectin-3, and nectin-4. They are localized at tight junctions and gap junctions of syncitiotrophoblasts(9). Nectin-4 is a relatively novel member of nectin family which has been detected only in placenta and airway epithelium in healthy subjects.

Despite, there has been no study published yet to reveal the soluble nectin-4 levels in preeclampsia as well as in early onset disease. In this study, we aimed to investigate the serum nectin-4 levels in early-onset preeclampsia in comparison of the healthy pregnancies.

Inclusion criteria

• spontaneous,
• singleton pregnancies
• above the 24 weeks of gestations
• positive fetal cardiac activity

Exclusion criteria

• multiple gestations,
• chronic hypertension
• hypothyroidism
• known malignancy,- diabetes mellitus,
• presence of fetal or maternal infection,
• clinical signs of chorioamnionitis (maternal fever, vaginal discharge, fetal tachycardia),
• hepatic or renal failure
• Placenta previa or pregnancies accompanied congenital fetal abnormalities or aneuploidies