Hormone metabolic pattern in the preclinical stage of preeclampsia

Abstract

BACKGROUND: The imbalance of vascular endothelial cell metabolism determines the clinical manifestations of preeclampsia; however, the molecular mechanisms underlying the vessel destabilization are not fully understood. In recent years, researchers have focused on clarifying the role of dysmetabolic disorders in patients with obstetric pathology, including preeclampsia. This is due to the fact that pregnancy is accompanied by metabolic restructuring aimed at switching the energy supply of the pregnant womans body from the carbohydrate to the fat component in order to maintain an effective energoplastic supply of the developing fetus. Impairment of this evolutionary adaptation mechanism realized during pregnancy requires additional in-depth study.
 AIM: This study was aimed to identify and compare pathogenetic patterns that characterize early and late preeclampsia at the preclinical stage, based on dynamic clinical and laboratory examination of high-risk pregnant women.
 MATERIALS AND METHODS: A prospective clinical and laboratory examination of 180 pregnant women with independent factors of high risk of developing preeclampsia was carried out. Comparison groups were identified retrospectively, depending on the period of preeclampsia manifestation: Group I consisted of 31 pregnant women with early preeclampsia; Group II comprised 58 pregnant women with late preeclampsia; and Group III (control) included 30 healthy pregnant women with uncomplicated gestation. Pregnant women were examined twice at the preclinical stage of preeclampsia (11-14 and 18-21 weeks of gestation) and once at clinical manifestation of the disease (28-36 weeks of gestation). The markers of metabolic, hormonal, hemocirculatory, hemostasiological and placental disorders were evaluated.
 RESULTS: We found similar pathophysiological changes in pregnant women with both early and late PE, from early gestation periods. Those were characterized by pathological insulin resistance and hyperinsulinemia, as well as associated atherogenic changes in the lipid profile, hyperleptinemia, hyperuricemia, hypersympathicotonia, visceral fat deposition, and contra-insular hormonal deviations. The observed alterations reflected a single hormonal and metabolic pattern of the preclinical stage of preeclampsia. During pregnancy, there was shown an increase in clustering diabetogenic and atherogenic abnormalities and hormonal changes, which were supplemented by associated endothelial and hemostasiological dysfunction and, in early preeclampsia, placental dysfunction, thus accelerating the time of clinical implementation of preeclampsia.
 CONCLUSIONS: From the pathogenetic point of view, preeclampsia of various periods of manifestation is an indivisible category with a common basic developmental mechanism characterized by a hormone metabolic pattern from the early stages of pregnancy. These stable changes are the result of the pathologically transformed phylogenetic mechanism of energoplastic supply of the fetus. This transformation is realized via physiological insulin resistance and compensatory hyperinsulinemia development due to the contra-insular activity of placental hormones. The added structural and functional disorders of the embryo (feto) placental system potentiate basic mechanisms (pathological insulin resistance and hyperinsulinemia) and determine the period of preeclampsia clinical manifestation in each particular woman.