Maternal familial hypercholesterolaemia (FH) confers altered haemostatic profile in offspring with and without FH.

INTRODUCTION: Patients with familial hypercholesterolaemia (FH) are characterized by high total and LDL cholesterol. Pregnant women with FH have higher absolute levels of total and LDL cholesterol, and a more pro-coagulant pattern compared with healthy pregnant women. Maternal hypercholesterolaemia has been shown to affect early atherosclerosis formation in the offspring. The aim of the present study was to investigate whether maternal FH leads to differences in plasma or serum levels of haemostatic and fibrinolytic markers in children with and without FH born of mothers with FH compared to control children born of non-FH mothers. METHODS AND RESULTS: Children with (n=9) and without (n=7) FH born of mothers with FH, as well as control children (n=16) born of non-FH mothers were included in the study. The concentrations of tissue plasminogen activator, plasminogen activator inhibitor (PAI-1), tissue factor (TF), TF pathway inhibitor (TFPI), thrombomodulin, fibrinogen, prothrombin fragment 1+2 and von Willebrand Factor were measured. Our findings show i) higher levels of PAI-1 and TFPI in children with and without FH born of mothers with FH compared with control children, ii) lower levels of thrombomodulin in children with FH compared with control children, and iii) significant correlations between maternal PAI-1 levels during pregnancy and PAI-1 levels in the offspring. CONCLUSIONS: We found that maternal FH may confer an unfavourable phenotype by affecting haemostatic and fibrinolytic markers in offspring independent of the children's FH status. However, the association between maternal hypercholesterolaemia and haemostatic risk markers in the offspring needs to be further elucidated.

Activation and inhibition of nuclear factor kappa B activity by cereal extracts: role of dietary phenolic acids.

The transcription factor nuclear factor kappa B (NF-kappaB) plays a critical role in stress, immune, and inflammatory responses, and the modulation of its activity can be a potentially effective preventive strategy for controlling certain diseases. Cereal grains contain phenolic compounds in concentrations comparable to those in fruits and vegetables, well-known for their beneficial effect on human health. In this study we aimed to examine the effect of different phenolic extracts from barley, oat, wheat, and buckwheat on the modulation of basal and lipopolysaccharide (LPS)-induced NF-kappaB activity and elucidate the role of phenolic acids in this modulation. Three extracts were prepared: extracts of free phenolic compounds (M1), extracts of free phenolic acids (M2), and extracts of bound phenolic acids (HY). Generally, extracts M2 showed the highest effect on modulation of NF-kappaB activity with strong inhibition of LPS-induced NF-kappaB activity at all concentrations and of the basal NF-kappaB activity at concentrations equal to or lower than 3 mg/mL. Most of extracts M1 and HY slightly increased both the basal and the LPS-induced NF-kappaB activation. However, at the highest concentrations (3 or 15 mg/mL) extracts HY inhibited LPS-induced NF-kappaB activation. Similar experiments with standard solutions of phenolic acids indicated their ability to modulate the NF-kappaB activity.