PP118. Is the placental mass associated with the severity of preeclampsia?

INTRODUCTION

Preeclampsia contributes to an increased perinatal morbidity and mortality of both the mother and the fetus. The exact pathogenesis of PE is unclear; it is generally believed, however, that the placenta plays a pivotal role in this process.

OBJECTIVES

The aim of this study was to analyse the effect of the placental mass on the severity of PE.

METHODS

Following PE placentae were analyzed and their weights were compared with those of normal pregnancies [1]. Moderate and severe PE as well as HELLP syndrome were defined according to international guidelines. To compare placental weights obtained at different gestational ages, a ratio between observed (O) and expected (E) weights were calculated. Chi(2)-test and Kruskal-Wallis-test were used for statistical analysis and significance was considered when p<0.05.

RESULTS

Two hundred and eight placentae following singleton pregnancies complicated by preeclampsia were enrolled. The mean gestational age at birth was 31.8±3.8 weeks, 130 (62.5%) cases delivered before the 34th week. The group with severe PE delivered earlier than that with moderate PE (mean±SD, 32±3.9 vs. 34±3 weeks; p<0.01). Severe PE was found in 176 (84.6%) cases; 85 of this group were associated with a HELLP-syndrome. Isolated HELLP were found in 4 (1.9%) cases. In 144 (69.2%) cases placental weight was below the 10th percentile. The mean of the weights was higher in the group with moderate PE than in those with severe PE, PE with HELLP and isolated HELLP (410±67g, respectively, 376±79g, 344±86g, 341±88g). When normalized using the O/E-ratio (in order to correct for gestational age) these differences were not significant (moderate PE 0.75±0.24; severe PE 0.74±0.22, PE with HELLP 0.73±0.22; isolated HELLP 0.88±0.05; p=NS).

CONCLUSION

Our data show that the placental mass is not associated with the severity of PE. We hypothesize that once the pathogenesis of PE is triggered (by placental factors), the severity of the disease is modulated mainly by the maternal response and not by the placental mass.