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J Matern Fetal Med. 1999 Nov-Dec;8(6):270-4.

Distribution of apolipoprotein(a) isoforms in normotensive and severe preeclamptic women.

Author information

1
First Department of Obstetrics and Gynecology, Semmelweis University Medical School, Budapest, Hungary. naba@noi1.sote.hu

Abstract

OBJECTIVE:

Preeclampsia is a pregnancy-related disorder constituting one of the primary causes of worldwide maternal and fetal mortality, but despite intensive research its pathogenesis remains unclear. Lipids have been implicated in the development of preeclampsia, although this possible association remains controversial and not yet fully investigated. This study set out to examine the potential association between lipoprotein(a) and the development of severe preeclampsia. The focus of this study was to investigate the potential utility of apolipoprotein(a) isoforms as possible diagnostic markers for identifying women at risk for developing preeclampsia.

METHODS:

Study participants included a control group of nonpregnant female volunteers (n = 59), a group of healthy pregnant (normotensive) female volunteers (n = 51), and a group of severe preeclamptic female volunteers (n = 59). Serum lipoprotein(a) concentrations were measured using double-antibody ELISA methods and were found to be 17.0+/-23.6 mg/dl among nonpregnant controls (n = 51), 15.9+/-15.8 mg/dl among healthy pregnant normotensives (n = 51), and 16.2+/-16.7 mg/dl in the preeclamptic group (n = 59). In addition, apolipoprotein (a) isoforms were identified using high-resolution SDS-agarose electrophoresis followed by immunoblotting.

RESULTS:

We detected no significant differences between the groups studied in the distribution of isoforms (Chi-square = 1.21, df = 4, P = 0.89); however, in a 1-week interval we detected a 42.2% rise in Lp(a) levels as well as a 67.1% rise in C-reactive protein concentrations among 10 volunteers in the preeclamptic group (median = 9.6; P < 0.05).

CONCLUSIONS:

Although the exact mechanism of pathogenesis continues to elude investigators, our results suggest that lipoprotein(a) may act as an acute-phase reactant during preeclampsia. Although our results are preliminary, they are consistent with growing evidence implicating lipids as among those factors involved in the etiology of preeclampsia. Changes in apolipoprotein(a) may be among those important biochemical markers that are found to be useful in the early identification of high-risk women and warrant further study.

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