ELEVATED SERUM LEVELS OF VASCULAR ENDOTHELIAL GROWTH-FACTOR IN PATIENTS WITH PREECLAMPSIA

Objective: To determine whether altered levels of vascular endothelial growth factor (VEGF) may be implicated in the pathogenesis of preecla mpsia, and whether VEGF mediates the endothelial cell activation that is involved in the pathogenesis of the clinical syndrome. Methods: In a cross-sectional study, maternal serum samples in late pregnancy (at the time of clinical disease) were collected from 78 nulliparous women . These subjects were subdivided into those with preeclampsia (n = 27) , nonproteinuric pregnancy-induced hypertension (n = 15), and normal p regnant women (n = 36). In a nested case-control study, in addition to samples taken before delivery, samples were obtained in early pregnan cy (before clinical disease) and 24-48 hours postpartum from 12 of the patients with preeclampsia, 12 of those with nonproteinuric pregnancy -induced hypertension, and 12 of the normal pregnant subjects. Umbilic al cord blood was sampled from 14 of the preeclamptic and 16 of the no rmal pregnant subjects. We measured VEGF levels in all samples using a n immunofluorometric assay. Results: In most samples collected before delivery, VEGF levels were below the lower limit of detection. However , the proportion of detectable levels was higher in the preeclampsia g roup (seven of 27) than in the normotensive group (one of 36, P < .05) . The proportion in the nonproteinuric pregnancy-induced hypertension group (two of 15) did not differ significantly from the other groups. Levels in the patients with preeclampsia were not elevated before clin ical disease. Levels of VEGF in umbilical blood samples were higher th an in maternal venous blood, although there were no significant differ ences between groups. Conclusion: Serum VEGF levels were elevated in p atients with preeclampsia, which suggests that the growth factor has a role in the endothelial cell activation that occurs in the disease.