title: 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.
authors.affiliation: Department of Obstetrics and Gynecology, University of Freiburg, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Wetzka
authors.forename: K
authors.initials: K
authors.lastname: Winkler
authors.forename: M
authors.initials: M
authors.lastname: Kinner
authors.forename: I
authors.initials: I
authors.lastname: Friedrich
authors.forename: W
authors.initials: W
authors.lastname: März
authors.forename: H P
authors.initials: HP
authors.lastname: Zahradnik
mesh_terms: D000328:Adult; D001055:Apolipoproteins B / Q000097:blood / Q000378:metabolism; D001777:Blood Coagulation / Q000187:drug effects; D001783:Blood Flow Velocity; D001792:Blood Platelets / Q000378:metabolism; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D005314:Embryonic and Fetal Development; D005260:Female; D017359:HELLP Syndrome / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood* / Q000494:pharmacology; D008074:Lipoproteins / Q000737:chemistry / Q000378:metabolism; D010976:Platelet Count; D011225:Pre-Eclampsia / Q000097:blood / Q000378:metabolism*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D018608:Ultrasonography, Doppler; D014469:Umbilical Arteries
chemical_list: D001055:Apolipoproteins B; D008055:Lipids; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol