Abstract
Fetal growth restriction (FGR) is mainly caused by failure of the uteroplacental unit. The exact pathogenesis remains unclear. The cause is thought to be related to abnormal platelet activation, which may result in microthrombus formation in the small vessels of the placenta. Reactive oxygen species (ROS) may initiate the pathological process of platelet activation. This study aimed to evaluate selected platelet parameters in pregnancy complicated by FGR and relate them to the severity of hemodynamic abnormalities. A total of 135 women (pregnant with FGR, with an uncomplicated pregnancy, and non-pregnant) were enrolled to study different platelet parameters: count (PLT), mean volume (MPV), ROS levels, intracellular oxygen level, oxygen consumption, and aggregation indices. No abnormalities in PLT and MPV were found in the FGR group, although it revealed increased ROS levels in platelets, lower platelet oxygen consumption, and intraplatelet deprivation. Aggregation parameters were similar as in uncomplicated pregnancy. No significant relationships were observed between hemodynamic abnormalities and the studied parameters. Platelets in pregnancies complicated by FGR may reveal an impaired oxidative metabolism, which may, in turn, lead to oxidative stress and, consequently, to an impaired platelet function. This study adds to the understanding of the role of platelets in the etiology of FGR.
Highlights
Fetal growth restriction (FGR) is a common pregnancy complication, affecting approximately 4–6% of all pregnancies, and has been associated with various adverse perinatal outcomes [1]
This study examined several platelet-related parameters in pregnancy complicated by FGR
Platelet Reactive oxygen species (ROS) levels were significantly increased in FGR, indicating oxidative stress, which promotes the activation and aggregation of thrombocytes initiating the inflammation
Summary
Fetal growth restriction (FGR) is a common pregnancy complication, affecting approximately 4–6% of all pregnancies, and has been associated with various adverse perinatal outcomes [1]. FGR has been defined as the inability of the fetus to reach its intrinsic (i.e., genetically determined) growth potential [2]. It has been classically identified at an estimated fetus weight (EFW) below the 10th percentile for gestational age [3]. The leading cause of FGR is a failure of the uteroplacental unit, which results in decreased blood flow across the placenta [4,5]. This condition likely results from impaired normal trophoblast invasion of the uterine vasculature early in pregnancy [6,7]. The normal conversion of the spiral arteries into low-resistance vessels is impaired, resulting in reduced delivery of oxygen and nutrients to the fetus [8]
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