Lai Xu1, Minjae Lee2, Arun Jeyabalan3, James M Roberts4. 1. Department of Internal Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA. 2. Biostatistics/Epidemiology/Research Design Core, Center for Clinical and Translational Sciences, University of Texas Health Science Center, Houston, TX. 3. Magee-Womens Research Institute and Foundation, University of Pittsburgh School of Medicine, Pittsburgh, PA; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA. 4. Magee-Womens Research Institute and Foundation, University of Pittsburgh School of Medicine, Pittsburgh, PA; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, PA; Department of Epidemiology, University of Pittsburgh School of Medicine, Pittsburgh, PA; Clinical and Translational Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA. Electronic address: jroberts@mwri.magee.edu.
Abstract
OBJECTIVE: Vitamin D deficiency has been linked to the pathogenesis of preeclampsia. Given the demonstrated antiinflammatory function of vitamin D in multiple organ systems including trophoblast cells and placenta, we hypothesized that vitamin D deficiency contributes to the development of preeclampsia through increased inflammation, as indicated by elevated interleukin (IL)-6 concentrations. STUDY DESIGN: Plasma samples from a large preeclampsia cohort study were examined in 100 preeclamptic and 100 normotensive pregnant women. Comparisons of vitamin D and IL-6 concentrations used Student t test and χ(2) test or their nonparametric counterparts. A logistic regression model assessed the association among vitamin D, IL-6 concentrations, and preeclampsia risk. RESULTS: The mean concentration of 25-hydroxyvitamin D was 49.4 ± 22.6 nmol/L in normotensives and 42.3 ± 17.3 nmol/L in preeclamptic women (P = .01). The median (interquartile range: Q1, Q3) concentrations of IL-6 were 2.0 (1.3, 3.4) pg/mL and 4.4 (2.2, 10.0) pg/mL in the control and preeclampsia groups, respectively (P < .01). We observed a significant association between IL-6 elevation and preeclampsia (odds ratio, 4.4; 95% confidence interval, 1.8-10.8; P < .01) and between vitamin D deficiency and preeclampsia (odds ratio, 4.2; 95% confidence interval, 1.4-12.8; P = .04). However, there was no association between vitamin D deficiency and IL-6 elevation. CONCLUSION: Third-trimester IL-6 elevation and vitamin D deficiency were independently associated with the risk of preeclampsia. We found no evidence to support the hypothesis that vitamin D deficiency alters the pathogenesis of preeclampsia by activation of inflammation as assessed by IL-6 concentration.
OBJECTIVE:Vitamin Ddeficiency has been linked to the pathogenesis of preeclampsia. Given the demonstrated antiinflammatory function of vitamin D in multiple organ systems including trophoblast cells and placenta, we hypothesized that vitamin Ddeficiency contributes to the development of preeclampsia through increased inflammation, as indicated by elevatedinterleukin (IL)-6 concentrations. STUDY DESIGN: Plasma samples from a large preeclampsia cohort study were examined in 100 preeclamptic and 100 normotensive pregnant women. Comparisons of vitamin D andIL-6 concentrations used Student t test and χ(2) test or their nonparametric counterparts. A logistic regression model assessed the association among vitamin D, IL-6 concentrations, and preeclampsia risk. RESULTS: The mean concentration of 25-hydroxyvitamin D was 49.4 ± 22.6 nmol/L in normotensives and 42.3 ± 17.3 nmol/L in preeclamptic women (P = .01). The median (interquartile range: Q1, Q3) concentrations of IL-6 were 2.0 (1.3, 3.4) pg/mL and 4.4 (2.2, 10.0) pg/mL in the control and preeclampsia groups, respectively (P < .01). We observed a significant association between IL-6 elevation and preeclampsia (odds ratio, 4.4; 95% confidence interval, 1.8-10.8; P < .01) and between vitamin Ddeficiency and preeclampsia (odds ratio, 4.2; 95% confidence interval, 1.4-12.8; P = .04). However, there was no association between vitamin Ddeficiency andIL-6 elevation. CONCLUSION: Third-trimester IL-6 elevation andvitamin Ddeficiency were independently associated with the risk of preeclampsia. We found no evidence to support the hypothesis that vitamin Ddeficiency alters the pathogenesis of preeclampsia by activation of inflammation as assessed by IL-6 concentration.
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