Circulating vascular cell adhesion molecule–1 in pre-eclampsia, gestational hypertension, and normal pregnancy: Evidence of selective dysregulation of vascular cell adhesion molecule–1 homeostasis in pre-eclampsia

Abstract

OBJECTIVE: Our purpose was to investigate circulating levels of vascular cell adhesion molecule–1 in the peripheral and uteroplacental circulations during normotensive and hypertensive pregnancies. STUDY DESIGN: This prospective observational study involved 2 patient groups. Group 1 consisted of 22 women with pre-eclampsia and 30 normotensive women followed up longitudinally through pregnancy and post partum. There were an additional 13 women with established gestational hypertension. Group 2 consisted of 20 women with established pre-eclampsia and 19 normotensive control subjects undergoing cesarean delivery. Plasma levels of vascular cell adhesion molecule–1 were measured in blood drawn from the antecubital vein (group 1) and from both the antecubital and uterine veins (group 2). Data were analyzed by analysis of variance. RESULTS: In group 1 vascular cell adhesion molecule–1 levels did not change significantly throughout normal pregnancy and post partum. Women with established pre-eclampsia had increased vascular cell adhesion molecule–1 levels compared with the normotensive pregnancy group ( P = .01). Vascular cell adhesion molecule–1 levels were not elevated in women with established gestational hypertension. In group 2 significantly higher levels of vascular cell adhesion molecule–1 were detected in the uteroplacental ( P < .0001) and peripheral ( P < .0001) circulations of pre-eclamptic women by comparison with normotensive women. In the pre-eclamptic group there was a tendency toward higher vascular cell adhesion molecule–1 levels in the peripheral circulation than in the uteroplacental circulation ( P = .06). In contrast to vascular cell adhesion molecule–1, circulating levels of E-selectin and intercellular adhesion molecule–1, other major leukocyte adhesion molecules expressed by the endothelium, were not different in pre-eclamptic and normotensive pregnancies. CONCLUSION: Established pre-eclampsia is characterized by selective dysregulation of vascular cell adhesion molecule–1 homeostasis. This event is not an early preclinical feature of pre-eclampsia, does not persist post partum, is not a feature of nonproteinuric gestational hypertension, and is not observed with other major leukocyte adhesion molecules. Induction of vascular cell adhesion molecule–1 expression in pre-eclampsia may contribute to leukocyte-mediated tissue injury in this condition or may reflect perturbation of other, previously unrecognized, functions of this molecule in pregnancy. (Am J Obstet Gynecol 1998;179:464-9.)