Abstract

Background: While several studies have demonstrated that obesity increases the risk of pre-eclampsia (PE), the mechanisms have yet to be elucidated. We assessed the association between maternal/paternal obesity and PE and hypothesized that maternal body mass index (BMI) would be associated with an adverse inflammatory and angiogenic profile. High-sensitivity C-reactive protein (hs-CRP) and following serum angiogenic markers were determined: soluble endoglin (sEng), soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF).

Methods: Data on BMI were available from 1450 pregnant women with PE and 1065 without PE. Serum concentrations of hs-CRP and angiogenic markers were available from a subset at first and third trimesters.

Results: Prepregnancy BMI was higher in the PE group than in controls (mean ± SD) 25.3 ± 5.2 vs. 24.1 ± 4,4, p < 0.001, adjusted for parity, mother’s age, and smoking status before pregnancy. Increased hs-CRP concentrations were observed in both PE and non-PE women similarly according to BMI category. In women with PE, a higher BMI was associated with lower sFlt-1 and sEng concentrations throughout the pregnancy (p = 0.004, p = 0.008, respectively). There were no differences in PlGF in PE women according to BMI.

Conclusions: We confirmed increased pre-pregnancy BMI in women with PE. Enhanced inflammatory state was confirmed in all women with overweight/obesity. Partly paradoxically we observed that PE women with obesity had less disturbed levels of angiogenic markers than normal weight women with PE. This should be taken into account when angiogenic markers are used in PE prediction.

FINNPEC Members

Hannele Laivuori2,7,8,9 (2Obstetrics and Gynecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland, 7Institute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science, University of Helsinki, Helsinki, Finland, 8Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland, 9Department of Obstetrics and Gynecology, Tampere University Hospital, Tampere, Finland), Seppo Heinonen2 (2Obstetrics and Gynecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland), Eero Kajantie10,11,12 (10Chronic Disease Prevention Unit, National Institute for Health and Welfare, Helsinki, Finland, 11Children’s Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland, 12PEDEGO Research Unit, MRC Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland), Juha Kere13,14,15 (13Department of Biosciences and Nutrition, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden, 14Molecular Neurology Research Program, University of Helsinki, Helsinki, Finland, 15Folkhälsan Institute of Genetics, Helsinki, Finland), Katja Kivinen16 (16Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK), Anneli Pouta13,17 (13Department of Biosciences and Nutrition, and Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden, 17Department of Government Services, National Institute for Health and Welfare, Helsinki, Finland)