Normal expression of cell adhesion molecules in placentae from women with systemic lupus erythematosus and the antiphospholipid syndrome

Pregnant women With active systemic lupus erythematosus (SLE) and/or the an tiphospholipid syndrome (APS) are prone to recurrent miscarriage, pre-eclam psia, intrauterine growth restriction and premature delivery. Placental dys function may account for these complications vet the mechanisms remain unce rtain. Amongst these, an inflammatory response in the placental vasculature could play a role, involving recruitment of neutrophils and platelets and the increased endothelial expression of cell adhesion molecules (CAM), cent ral to the recruitment process. The aim of this study was primarily to inve stigate CAM expression in the fetoplacental vasculature in women with SLE/A PS. Circulating maternal concentrations of soluble CAM were also elucidated . There were no differences in CAM immunostaining in placentae from patients with SLE and/or APS compared with controls. In both patients and controls m oderate immunostaining for the intercellular adhesion molecule-1 (ICAM-1) w as observed in placental vascular endothelium and mild immunostaining was p resent in the placental villous stroma, Strong immunostaining for platelet endothelial CAM (PECAM) occured in the placental vascular endothelium where as P-selectin was mildly expressed in the stem vessel endothelium only. Vas cular CAM-1 (VCAM-1) and E-selectin were undetectable in either study or co ntrol placentae. In contrast, ICAM-1 and VCAM-1 but not E-selectin, Is asse ssed by immunoassay (ELISA), Were elevated in maternal serum from SLE/APS p atients compared With controls. This study suggests that upregulation of CA M expression and subsequent activation of neutrophil and/or platelet activi ty within the placental villous tree is unlikely to be a mechanism by which the adverse pregnancy outcome arises in SLE/APS pregnancies. However, mate rnal endothelial cell activation (ECA) may play a more important role. (C): 2000 Harcourt Publishers Ltd.