Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor, Senior Consultant Anna-Karin Wikström, Uppsala University, Sweden
- Second opponent: Associate Professor, Consultant Obstetrician Jacob Alexander Lykke, Rigshospitalet University Hospital, Denmark
- Third member and chair of the evaluation committee: Associate Professor Anne Cecilie Kjeldsen Larstorp, University of Oslo
Chair of the Defence
Professor II Trond M. Michelsen, University of Oslo
Principal Supervisor
Associate Professor Katariina Laine, University of Oslo
Summary
Hypertensive disorders of pregnancy include preeclampsia and gestational hypertension. Preeclampsia is a leading cause of maternal mortality, stillbirth and preterm delivery, and has potential long-term health consequences for both mother and child. Low-dose aspirin can help prevent preeclampsia in high-risk women, but for those women who develop the disease, there is no known effective treatment other than delivery.
The thesis was a population-based retrospective cohort study using data from the Maternal Birth Register of Norway, Statistics Norway and the Norwegian Prescription Database. The main aims of the thesis were to assess the prevalence of and risk factors for hypertensive disorders of pregnancy in Norway over two decades, and to interpret the findings using established models of preeclampsia pathogenesis.
Foreign-born women and women with low education had the same or lower risks of hypertensive diseases in pregnancy compared to women born in Norway, regardless of parity. Nulliparous women with diabetes, chronic hypertension or obesity had increased risk of early, intermediate and late-onset preeclampsia. BMI did not modify the risk of preeclampsia in women with pre-gestational diabetes or chronic hypertension. However, BMI partially modified the risk of late-onset preeclampsia in women with gestational diabetes.
Preeclampsia prevalence decreased 37% over two decades while the proportion of women with risk factors for preeclampsia increased. Observed population changes could not fully explain the 44% decreased risk of preeclampsia over the study period. However, concurrent with decreasing preeclampsia prevalence, labor inductions and low-dose aspirin use among young women in the general population increased.
The above findings support the concept of the 2-stage model of multifactorial pathways to hypertensive disorders of pregnancy as well as the threshold liability model and competing risk model.
Additional information
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