Fasting serum triglycerides, free fatty acids, and malondialdehyde are increased in preeclampsia, are positively correlated, and decrease within 48 hours post partum,☆☆,,★★

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Abstract

OBJECTIVE: We tested the hypothesis that serum free (nonesterified) fatty acid and triglyceride concentrations are increased in nulliparous women with preeclampsia relative to women with uncomplicated pregnancies and that these lipids decrease post partum, consistent with the known resolution of clinical symptoms. The relationships between serum concentrations of these lipids and the lipid peroxidation metabolite malondialdehyde were also examined. STUDY DESIGN: Predelivery and 24 to 48 hour postpartum venous blood samples were collected from eight women with preeclampsia and nine women with uncomplicated pregnancies after an 8- to 10-hour fast. Sera were analyzed for concentrations of triglycerides, free fatty acids, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and malondialdehyde. RESULTS: Antepartum serum triglyceride and free fatty acid concentrations were increased approximately twofold in women with preeclampsia relative to uncomplicated pregnancies (p < 0.02 and 0.004, respectively). Total, high-density lipoprotein, and low-density lipoprotein cholesterol concentrations did not differ between groups. Concentrations of all lipids decreased significantly in both groups within 48 hours post partum. However, triglyceride and free fatty acid concentrations remained higher in women with preeclampsia (p < 0.006, both variables). Triglyceride and free fatty acid concentrations correlated positively, both ante partum (R2 0.42, p < 0.01) and post partum (R2 0.39, p < 0.02). Antepartum concentrations of malondialdehyde were 50% higher in women with preeclampsia (p < 0.01) and decreased post partum (p < 0.02) but did not decrease in controls (p = 0.07). Antepartum serum triglycerides and free fatty acids correlated positively with malondialdehyde concentrations (R2 0.38, p < 0.02, in both cases). CONCLUSION: Triglycerides and free fatty acids, but not cholesterol, are increased in preeclampsia and correlate with the lipid peroxidation metabolite malondialdehyde. We speculate that these interactions may contribute to endothelial cell dysfunction in preeclampsia. (AM J OBSTET GYNECOL 1996;174:975-82.)

Section snippets

Subjects

Seventeen nulliparous subjects were recruited at the time of admittance to the labor and delivery ward at Magee-Womens Hospital as part of an investigation of preeclampsia. This study was approved by the hospital institutional review board. Demographic and clinical data were collected at routine obstetric visits. Eight subjects had preeclampsia, defined by the criteria of hypertension, proteinuria, hyperuricemia, and reversal of hypertension and proteinuria after delivery.2 Gestational

RESULTS

By definition, preeclamptic parturients had elevated blood pressures (p < 0.001) and serum uric acid levels (p < 0.01) relative to normal pregnancy (Table I). Gestational age at time of delivery and infant birth weights were less for preeclamptic than normal pregnancies (p < 0.001, Table I). None of the infant birth weights in the normal pregnant group were <10th percentile for gestational age (small for gestational age) and two were >10th percentile for gestational age (large for gestational

COMMENT

During the first half of normal pregnancy increased maternal fat accumulation (relative anabolic state) is presumed to be important for the subsequent hypertriglyceridemia normally occurring in late gestation (relative catabolic state).17 Circulating concentrations of very-low-density lipoprotein (VLDL) and LDL normally increase with gestational age, as reflected by marked increases in serum triglycerides and cholesterol (250% and 25% by term, respectively).3, 18 The hypertriglyceridemia is due

Acknowledgements

We thank Jacqueline I. Ojimba, BS, for excellent technical assistance and Cindy Schatzman, RN, and the nursing staff of Magee-Womens Hospital for invaluable help in sample collection. We gratefully acknowledge Ariel Many, MD, for advice and suggestions concerning this study.

References (25)

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From the Magee-Womens Research Institute, and the Departments of Obstetrics and Gynecology and Epidemiology, University of Pittsburgh.

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Supported in part by National Institutes of Health grant No. HD30367. C.A.H. was the recipient of Individual National Research Service Award No. HL 08786 from the National Heart, Lung, and Blood Institute and the Irene McLenahan Young Investigator Research Fund Award, Magee-Womens Hospital.

Reprint requests: Carl A. Hubel, PhD, Magee-Womens Research Institute, 204 Craft Ave., Pittsburgh, PA 15213.

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