Altered Lipid Metabolism in Preeclampsia and HELLP Syndrome: Links to Enhanced Platelet Reactivity and Fetal Growth

Abstract

Normal pregnancy is a physiological condition of balanced hypercoagulability. However, in preeclamptic pregnancies, the coagulation and fibrinolytic cascades are highly activated, accompanied by pathological blood rheology and endothelial dysfunction. This may result in disseminated intravascular coagulation (DIC). Atherosclerosis research showed that lipids may interfere with coagulation and cause endothelial dysfunction. Therefore, we analyzed the lipoprotein distribution and platelet counts in uncomplicated preeclamptic and HELLP syndrome pregnancies. In addition, a correlation between the fetal circulation determined by Doppler velocimetry and the maternal lipid metabolism was investigated. Fasting serum was collected from 24 women in the third trimester of uncomplicated pregnancies, 9 women with severe preeclampsia, and 6 women with HELLP syndrome. Cholesterol (CH), triglycerides (TGs), and apolipoproteins were analyzed in serum and in very-low-density (VLDL), intermediate-density (IDL), low-density (LDL), and high-density (HDL) lipoproteins separated by ultra-centrifugation. Compared with normal pregnancies, TGs in serum, VLDL, IDL, LDL, and HDL were significantly increased in preeclampsia; no difference in CH concentrations was observed. During HELLP syndrome, IDL-TGs were increased compared with normal pregnancies. There was no clear correlation between fetal hemodynamics and maternal lipid metabolism, but there was a significant negative correlation between maternal platelet counts and serum TG levels. Because TG-rich particles may play an important role in thrombin generation and may induce platelet aggregation, the observed changes in lipoprotein metabolism in preeclampsia and HELLP syndrome may contribute to the coagulopathy seen in these conditions.

A Study on Alter Ation of Serum Lipid Profile in Gestational Proteinuric Hypertension

“…This finding in the present study is similar to that reported by N sattar et al 12 and Wetzksa B et al 13 Due to the increased lipolytic activity by heightened insulin resistance occurring in preeclampsia, there is overproduction of VLDL by liver.…”

Pravastatin improves pregnancy outcomes in obstetric antiphospholipid syndrome refractory to antithrombotic therapy

“…Although placenta malperfusion is unique to pregnancy, there are many biological and pathological similarities as well as risk factors in common with cardiovascular disease (CVD). Normal development of maternal hyperlipidemia of pregnancy is exaggerated in PE (18). In addition, acute atherosis affects uteroplacental spiral arteries in 20% to 40% of cases of PE and resembles the early stages of atherosclerosis characterized by lipid deposition and inflammatory cells in the walls of maternal uterine arteries (19,20).…”

Identification of ACOX2 as a shared genetic risk factor for preeclampsia and cardiovascular disease

“…21 Similarly, triglyceride-rich lipoproteins have been suggested to trigger endothelial dysfunction 28 and artherothrombosis, 29 and they also play an important role in thrombin formation and may induce platelet aggregation, which can contribute to coagulopathy, another characteristic of PE. 30 An alternative explanation to downregulation of ACOX2 in PE might be through the bile acid intermediates. Although ACOX2 plays a direct role in the formation of bile acids, it is likely that there also is a connection between ACOX2 and the level of bile acid intermediates.…”