Plasma concentrations of Lp(a) lipoprotein and TGF‐β 1 are altered in preeclampsia

• Published in: Clinical genetics Vol. 52; no. 5; pp. 371 - 376
• Main Authors: Djurovic, Srdjan, Schjetlein, Rune, Wisløff, Finn, Haugen, Guttorm, Husby, Henrik, Berg, Kåre
• Format: Journal Article
• Language: English
• Published: 01-11-1997
• ISSN: 0009-9163; 1399-0004
• DOI: 10.1111/j.1399-0004.1997.tb04356.x

This study was performed to investigate the possible association between preeclampsia and the plasma concentrations of Lp(a) lipoprotein and TGF‐β
1
in a large series of patients. Additionally, correlation between the concentrations of these molecules and the severity of preeclampsia or fetal growth retardation was evaluated. Following clinical examination and biochemical analyses, both electroimmunoassay and RIA technique were used for quantitative determinations of plasma Lp(a) lipoprotein. ELISA technique was used to measure the active form of TGF‐β
1
in plasma of pregnant normotensive and preeclamptic women. We examined 154 women with preeclampsia (preeclampsia group) and 76 healthy, pregnant normotensive women (control group). The preeclampsia group was further divided into the following subgroups: mild preeclampsia, severe preeclampsia and preeclampsia with fetal growth retardation. Plasma levels of Lp(a) lipoprotein were lower in the total preeclampsia group as well as in all preeclampsia subgroups (5.45 ± 7.41, 5.58 ± 8.02, 5.08 ± 5.38, and 4.32 ± 5.28 mg/dl in the total preeclampsia group, and in subgroups with mild preeclampsia, severe preeclampsia, and preeclampsia with fetal growth retardation, respectively) than in the control group (7.84 ± 9.26 mg/dl) as determined by quantitative electroimmunoassay. Corresponding results were obtained with a radioimmunoassay (166.03 ± 200.2 U/l in the total preeclampsia group vs. 229.18 ± 257.7 U/l in controls). There was good correlation between the two methods used for Lp(a) lipoprotein measurement. The differences between controls and the total preeclampsia group as well as each preeclampsia subgroup were statistically significant by a non‐parametric test (one‐way Kruskal‐Wallis test). Plasma concentrations of the active form of TGF‐β
1
were increased in all preeclampsia subgroups as well as in the total group (5.63 ± 1.68 ng/ml) compared to controls (4.67 ± 1.33 ng/ml). This increase in TGF‐β
1
was statistically highly significant. Plasma concentrations of Lp(a) lipoprotein and the active form of TGF‐β
1
did not differ significantly between the preeclampsia subgroups. The outcome of this study may suggest involvement of both parameters in the pathophysiology of preeclampsia and may substantiate the notion of a multifactorial etiology of the disease.