Marie Therese Vinnars1,2, Sara Falkare1, Nikos Papadogiannakis3,4, Josefine Nasiell1,4. 1. a Department of Clinical Science , Intervention and Technology, Division of Obstetrics and Gynecology, CLINTEC, Karolinska Institutet , Stockholm , Sweden . 2. b Örnsköldsviks Hospital , Örnsköldsvik , Sweden . 3. c Department of Laboratory Medicine , Division of Pathology, Karolinska Institutet , Stockholm , Sweden , and. 4. d Karolinska University Hospital , Stockholm , Sweden.
Abstract
OBJECTIVE: To ascertain whether the protective effect of smoking during preeclampsia (PE) can be visualized in the placenta. METHODS: The study cohort consisted of placentas (n = 523) from pregnancies complicated by PE, delivered at Karolinska University Hospital in Stockholm during the period 2000-2009. Of the women included in the study, 488 were non-smokers and 35 were smokers at first visit to maternity care. Outcome variables were placental infarctions and decidual arteriopathy. RESULTS: Infarctions (affecting ≥5% of the placental tissue) were found in 15.6% of the placentas from non-smokers and in 25.7% of the placentas from smokers (OR 1.88: CI 0.84-4.16, p = 0.12). Decidual arteriopathy was found in 27.5% of the placentas from non-smokers and in 40.0% of the placentas from smokers (1.76: CI 0.87-3.56, p = 0.12). When diagnosed histopathologically, placental abruption was found in 15.4% among non-smokers and in 17.1% among smokers (1.14: CI 0.46-2.84, p = 0.98). Those differences did not show any statistical significance. CONCLUSION: No significant differences concerning placental infarctions, decidual arteriopathy or abruption were found between preeclamptic placentas from non-smokers compared to smokers.
OBJECTIVE: To ascertain whether the protective effect of smoking during preeclampsia (PE) can be visualized in the placenta. METHODS: The study cohort consisted of placentas (n = 523) from pregnancies complicated by PE, delivered at Karolinska University Hospital in Stockholm during the period 2000-2009. Of the women included in the study, 488 were non-smokers and 35 were smokers at first visit to maternity care. Outcome variables were placental infarctions and decidual arteriopathy. RESULTS:Infarctions (affecting ≥5% of the placental tissue) were found in 15.6% of the placentas from non-smokers and in 25.7% of the placentas from smokers (OR 1.88: CI 0.84-4.16, p = 0.12). Decidual arteriopathy was found in 27.5% of the placentas from non-smokers and in 40.0% of the placentas from smokers (1.76: CI 0.87-3.56, p = 0.12). When diagnosed histopathologically, placental abruption was found in 15.4% among non-smokers and in 17.1% among smokers (1.14: CI 0.46-2.84, p = 0.98). Those differences did not show any statistical significance. CONCLUSION: No significant differences concerning placental infarctions, decidual arteriopathy or abruption were found between preeclamptic placentas from non-smokers compared to smokers.