Abstract
ObjectivesPreeclampsia is divided into early-onset (delivery before 34 weeks of gestation) and late-onset (delivery at or after 34 weeks) subtypes, which may rise from different etiopathogenic backgrounds. Early-onset disease is associated with placental dysfunction. Late-onset disease develops predominantly due to metabolic disturbances, obesity, diabetes, lipid dysfunction, and inflammation, which affect endothelial function. Our aim was to use cluster analysis to investigate clinical factors predicting the onset and severity of preeclampsia in a cohort of women with known clinical risk factors.MethodsWe recruited 903 pregnant women with risk factors for preeclampsia at gestational weeks 12+0–13+6. Each individual outcome diagnosis was independently verified from medical records. We applied a Bayesian clustering algorithm to classify the study participants to clusters based on their particular risk factor combination. For each cluster, we computed the risk ratio of each disease outcome, relative to the risk in the general population.ResultsThe risk of preeclampsia increased exponentially with respect to the number of risk factors. Our analysis revealed 25 number of clusters. Preeclampsia in a previous pregnancy (n = 138) increased the risk of preeclampsia 8.1 fold (95% confidence interval (CI) 5.7–11.2) compared to a general population of pregnant women. Having a small for gestational age infant (n = 57) in a previous pregnancy increased the risk of early-onset preeclampsia 17.5 fold (95%CI 2.1–60.5). Cluster of those two risk factors together (n = 21) increased the risk of severe preeclampsia to 23.8-fold (95%CI 5.1–60.6), intermediate onset (delivery between 34+0–36+6 weeks of gestation) to 25.1-fold (95%CI 3.1–79.9) and preterm preeclampsia (delivery before 37+0 weeks of gestation) to 16.4-fold (95%CI 2.0–52.4). Body mass index over 30 kg/m2 (n = 228) as a sole risk factor increased the risk of preeclampsia to 2.1-fold (95%CI 1.1–3.6). Together with preeclampsia in an earlier pregnancy the risk increased to 11.4 (95%CI 4.5–20.9). Chronic hypertension (n = 60) increased the risk of preeclampsia 5.3-fold (95%CI 2.4–9.8), of severe preeclampsia 22.2-fold (95%CI 9.9–41.0), and risk of early-onset preeclampsia 16.7-fold (95%CI 2.0–57.6). If a woman had chronic hypertension combined with obesity, gestational diabetes and earlier preeclampsia, the risk of term preeclampsia increased 4.8-fold (95%CI 0.1–21.7). Women with type 1 diabetes mellitus had a high risk of all subgroups of preeclampsia.ConclusionThe risk of preeclampsia increases exponentially with respect to the number of risk factors. Early-onset preeclampsia and severe preeclampsia have different risk profile from term preeclampsia.
Highlights
Preeclampsia affects 3%[1] of all pregnancies
Cluster analysis to estimate the risk of preeclampsia were invited to participate in the order of arrival unless any of the exclusion criteria were present
After accounting for the number of tests the results correspond to false discovery rate false discovery rates (FDR) = 0.14 considered appropriate in this exploratory analysis
Summary
Preeclampsia affects 3%[1] of all pregnancies It is a systemic disease with a multifactorial background. Recent recommendation by the American College of Obstetricians and Gynecologists [2] further proposes that in the absence of proteinuria, preeclampsia could be diagnosed when newly diagnosed hypertension occurs in association with thrombocytopenia, impaired liver function, new development of renal insufficiency, pulmonary edema, or new-onset cerebral or visual disturbances. Earlyonset disease is associated with placental dysfunction It is often accompanied by intrauterine growth restriction, the risk runs in families and women with history of early-onset preeclampsia have an increased risk of cardiovascular disease later in life [5]. Late-onset preeclampsia develops due to metabolic disturbances, obesity, diabetes, lipid dysfunction, and inflammation [6] all of which affect endothelial function. Placental hypoplasia and vascular lesions frequently present in early-onset disease are often absent in the late-onset disease [7]
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