OBJECTIVE: In the pathogenesis of pre-eclampsia, endothelial cell activation or dysfunction is the central theme and marked dyslipidemia may contribute to endothelial cell dysfunction. The objective of this study was to evaluate the association between pre-eclampsia and the Asp9Asn mutation and the -93G promotor mutation. STUDY DESIGN: DNA was extracted from whole blood or cheek swabs of 224 pre-eclamptic patients, 265 controls, and 106 babies from pre-eclamptic patients. Controls consisted of women who had undergone at least two term pregnancies unaffected by pre-eclampsia. All samples were genotyped for all the polymorphisms using Polymerase Chain Reaction (PCR) of known allelic variants. Sequences were confirmed on an Applied Biosystems 373 DNA Sequencer. Results were analyzed with a x2 contingency table. RESULTS: The prevalences of the LPL Asp9Asn mutation and the LPL -93G promotor mutation were not significantly different between the patients with pre-eclamptic patients, severe pre-eclamptic patients, and HELLP syndrome patients and controls and also not significantly different between the babies born from pre-eclamptic mothers and controls. CONCLUSION: In this caucasian population, the LPL Asp9Asn mutation and the LPL -93G promotor mutation are not associated with an increased risk for pre-eclampsia and HELLP syndrome.
Cheek ; DNA ; Dyslipidemias ; Endothelial Cells ; Female ; HELLP Syndrome ; Humans ; Hypertension, Pregnancy-Induced* ; Lipoprotein Lipase* ; Lipoproteins* ; Mothers ; Polymerase Chain Reaction ; Pre-Eclampsia ; Pregnancy ; Prevalence