Hyperhomocyst(e)inemia and Elevated Soluble Vascular Cell Adhesion Molecule-1 Concentrations Are Associated with an Increased Risk of Preeclampsia

Abstract

Hyperhomocyst(e)inemia (HHcy) is a risk factor of endothelial dysfunction and preeclampsia. Soluble vascular cell adhesion molecule-1 (sVCAM-1), a specific marker of endothelial dysfunction, is elevated in preeclampsia. Few have assessed the joint contribution of these biomarkers in predicting preeclampsia. We assessed the extent to which HHcy and elevated sVCAM-1 are independently and jointly associated with preeclampsia. We conducted a case-control analysis of 100 preeclampsia cases and 100 controls to test our study hypothesis. Maternal plasma was collected before labor onset. Total plasma homocysteine (tHcy) was measured using high-performance liquid chromatography with electrochemical detection procedures. Plasma sVCAM-1 was determined using ELISA. Using the distribution of each analyte among controls, elevated tHcy was defined as plasma tHcy >6.6 µmol/l and elevated sVCAM-1 was defined as plasma concentrations >845 ng/ml (i.e., values above the median). Odds ratios (OR) and 95% confidence intervals (CIs) were calculated. Compared with women without elevated tHcy and without elevated sVCAM-1 (the referent group), those with elevated sVCAM-1 alone had a 4.1-fold increased risk of preeclampsia (95% CI 1.2–13.8). The OR for women with elevated tHcy alone was 2.2 (95% CI 0.6–7.9). The OR for women with elevated tHcy and sVCAM-1 was 13.2 (95% CI 4.1–42.2). Elevated tHcy and sVCAM-1 together were strongly associated with an increased risk of preeclampsia. Larger, prospective studies are needed to confirm these findings and to determine the extent to which elevated tHcy and sVCAM-1 together in early pregnancy are predictive of preeclampsia risk.

Contribution of Dietary Intakes of Antioxidants to Homocysteine-Induced Low Density Lipoprotein (LDL) Oxidation in Atherosclerotic Patients

“…Since elevated Hcy strongly correlates with smoking and low blood folate levels were found in the PRIME case-control study, Hcy levels might be a secondary risk factor to low blood folate and smoking 22. Elevated Hcy may also be involved in hypertension because it is associated with impaired endothelial function due to the generation of oxidative stress, VCAM-1 and reduction of NO bioavailability 23,24. High dietary intake of sodium is also a cause of hypertension.…”

“…Both Hcy and Ox-LDL could participate in thrombosis by increasing VCAM-1 and ICAM-1, caused by endothelial cell activation due to fibrinogen-platelet GPIIb-lIIa formation. Ox-LDL affects both initial and progressive stages of arteriosclerosis 11,12,23,32. On the other hand, circulating Hcy reduced NO-induced detoxification, vasodilation, and endothelial function 10.…”

Endocan, a putative endothelial cell marker, is elevated in preeclampsia, decreased in acute pyelonephritis, and unchanged in other obstetrical syndromes

“…It is unclear if endothelial cell activation and dysfunction have different molecular fingerprints; indeed, they appear to coexist. Preeclampsia is considered to be characterized by endothelial cell activation/dysfunction [17-24], and this condition is associated with a significant increase in the maternal circulating concentrations of s E-selectin [57,58,60,158,159] and sVCAM-1 [57,60,158,160,161], which are markers of endothelial cell activation/dysfunction [136,162]. However, there is no increase in the concentration of sICAM-1 and sPECAM-1 [57,60,163,164], indicating that there are some unique features of endothelial cell activation/dysfunction in preeclampsia.…”

Interactions Between Total Plasma Homocysteine, Oxidized LDL Levels, Thiolactonase Activities and Dietary Habits in Tunisian Diabetic Patients

“…Both Hcy and Ox-LDL could participate in thrombosis by increasing VCAM-1 and ICAM-1, caused by endothelial cell activation due to fibrinogen-platelet GPIIb-lIIa formation. Ox-LDL affects both initial and progressive stages of arteriosclerosis (Jakubowski, 2000;Dardik et al, 2000;Vadachkoria et al, 2004;Erl et al, 2000). On the other hand, circulating Hcy reduces NO-induced detoxification, vasodilation, and endothelial function (Rocchi et al, 2007).…”