Aim: To investigate the influence of maternal corticosteroid administration on neutrophil apoptosis in early onset preeclampsia.
Methods: We investigated five groups: early onset preeclampsia (EOPET, <34 weeks, n = 10); late-onset preeclampsia (LOPET, > or =34 weeks, n = 7); normotensive intrauterine growth restriction (nIUGR, n = 11); normal pregnancy (NPC, n = 22); and non-pregnancy (n = 10). We examined, by flow cytometry, spontaneous neutrophil apoptosis after 18 h culture (hypodiploid DNA, Annexin V binding, propidium iodide [PI] permeability).
Results: For the 10 women with EOPET exposed to betamethasone in the previous 48 h, we found that neutrophil apoptosis was not inappropriately inhibited, in contrast to our previous findings in women not thus exposed. Neither LOPET nor nIUGR differed from normal pregnancy.
Conclusion: Betamethasone alters the rate of spontaneous neutrophil apoptosis in EOPET. The anti-inflammatory influence of betamethasone may explain some of the differences between our previous and present findings with respect to neutrophil apoptosis in EOPET. Corticosteroids ameliorate the course of antenatal and postnatal preeclampsia. These results may reflect the mechanisms that underlie the transient improvements seen with antenatal dexamethasone use.