Objective. Hypothesising that metabolic syndrome may be associated with or useful in the prediction of pre-eclampsia, we investigated the association between all components of metabolic syndrome and C-reactive protein (CRP) in women with and without pre-eclampsia.Methods. A case–control study was performed. Cases had gestational hypertension or pre-eclampsia and controls were term deliveries. Clinical data and maternal serum was collected. The presence of metabolic syndrome (3/5 variables present) and a metabolic score (continuous 0–5) were investigated. Significant associations were evaluated using t-tests, and Pearson chi-square tests of association. Multivariable logistic regression was used to control for confounders.Results. One-hundred and one cases and 267 controls were evaluated. We observed a higher odds of pre-eclampsia when metabolic syndrome was present (AOR = 2.71 [1.1–6.67], p = 0.03). For every one-unit increase in metabolic score, there was a 39% increased odds of pre-eclampsia (AOR = 1.39 [1.06–1.82], p = 0.017). The odds of pre-eclampsia were nearly four times higher when hs- CRP was >8 (AOR = 3.61 [2.14–6.12], p < 0.001).Conclusions. Metabolic syndrome and hs-CRP are associated with pre-eclampsia. Investigation is crucial to determine if these abnormal lipid and inflammatory pathways observed in women with pre-eclampsia are present pre-pregnancy or develop as a result of the disease process of pre-eclampsia. Further investigation is also warranted to determine whether these abnormalities persist post-pregnancy and if so, their contribution to long-term cardiovascular disease.
Premature cervical ripening is believed to contribute to preterm birth (PTB). Preterm cervical ripening may be due to an aberrant regulation in timing of the same processes that occur at term, or may result from unique molecular mechanisms. Using mouse models of PTB, this study sought to investigate if the molecular mechanisms that govern cervical ripening were similar between preterm and term. Lipopolysaccharide (LPS) is infused into the uterine horn to create a mouse model of inflammation-induced PTB. For a noninfectious model of PTB, RU486 was administered. Both models result in delivery of pups in 8-24 h. Cervical tissues were collected from these models, as well as throughout gestation. Cervical tissues from E15 (preterm), E15 LPS (preterm inflammation), and E18.5 (term) were used for microarray analysis (n = 18). Additional experiments using gestational time course specimens were performed to confirm microarray results. Specific gene pathways were differentially expressed between the groups. Genes involved in immunity and inflammation were increased in the cervix in inflammation-induced PTB; term labor was not associated with differential expression of immune pathways. Cytokine expression was not increased in cervices during term labor, but was increased in the pospartum period. Epithelial cell differentiation pathway was significantly altered in term, but not preterm, labor. Activation of immune pathways may be sufficient for cervical ripening, but does not appear necessary. Differential expression of the epithelial cell differentiation pathway appears necessary in the process of cervical repair. Our results indicate that the molecular mechanisms governing preterm and term cervical ripening are distinctly different.
