Plasma concentrations of Lp(a) lipoprotein and TGF‐β₁ are altered in preeclampsia

Abstract

This study was performed to investigate the possible association between preeclampsia and the plasma concentrations of Lp(a) lipoprotein and TGF‐β1 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‐β1 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‐β1 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‐β1 was statistically highly significant. Plasma concentrations of Lp(a) lipoprotein and the active form of TGF‐β1 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.

TGFB1 Functional Gene Polymorphisms (C‐509T and T869C) in the Maternal Susceptibility to Pre‐eclampsia in South Indian Women

“…Presence of two copies of the high-producing 'T' allele might result in augmentation of TGF-b1 plasma levels that in turn might lead to endothelial dysfunction by causing upregulation of endothelin-1. In accordance with these observations, raised plasma TGF-b1 concentrations in pregnant women with PE in comparison with normal pregnant women were reported by others [28,[41][42][43]. Additionally, existence of elevated TGF-b1 levels has been demonstrated to lead to upregulation of angiotensin II and stimulate the release of rennin from jaxtaglomerular cells with a consequent rise in blood pressure [26,44,45].…”

Epithelial-mesenchymal transition during extravillous trophoblast differentiation

“…TGFb1 is present at higher concentrations in the plasma and placentae of women with PE compared with that of normotensive controls. 82,83 A similar finding was also reported for TGFb2, 84 but other studies have produced contradictory results. 85,86 Numerous studies have also linked EGF and EGFR to placental dysfunction and to the pathophysiology of PE and FGR.…”

Abnormal Lipid levels as a risk factor of eclampsia, study conducted in tertiary care Hospitals of Khyber Pakhtunkhwa Province - Pakistan

“…Our results are in accordance to other studies 13 which shows elevated Lpa level in women with pregnancy induced hypertension but dissimilar to a study 14 presenting lower Lpa levels in women with pregnancy induced hypertension in contrast to healthy pregnant controls. Lipoprotein (a) can work as acute phase reactant in the presence of endothelial dysfunction or inflammation.…”