Catherine L Haggerty1, Inge Panum2, Soren A Uldum2, Debra C Bass3, Jorn Olsen4, Toni Darville5, Jamie M Eastman3, Hyagriv N Simhan6, James M Roberts7, Roberta B Ness8. 1. Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States; Magee-Womens Research Institute, Pittsburgh, PA, United States. Electronic address: haggerty@pitt.edu. 2. Statens Serum Institut, Copenhagen, Denmark. 3. Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States. 4. University of Aarhus, Denmark School of Public Health and the Danish Epidemiology Science Centre, Aarhus, Denmark. 5. Children's Hospital of Pittsburgh, Pittsburgh, PA, United States; Pediatric Infectious Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States. 6. Magee-Womens Research Institute, Pittsburgh, PA, United States; Magee-Womens Hospital of UPMC, Pittsburgh, PA, United States; Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, United States. 7. Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, United States; Magee-Womens Research Institute, Pittsburgh, PA, United States; Magee-Womens Hospital of UPMC, Pittsburgh, PA, United States; Department of Obstetrics, Gynecology & Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA, United States. 8. University of Texas School of Public Health, Houston, TX, United States.
Abstract
BACKGROUND: Although the etiology of preeclampsia is not well understood, it has been suggested that excessive systemic inflammation may lead to oxidative stress, promoting the endothelial dysfunction characteristic of preeclampsia. Few prospective studies have examined the role of infection, an immune system stimulator, as a risk factor for preeclampsia. METHODS: We conducted a longitudinal study of the relationships between Chlamydia trachomatis (CT), Chlamydophila pneumoniae (CP), cytomegalovirus (CMV), herpes simplex virus (HSV) and preeclampsia among 509 preeclamptic cases and 336 normotensive controls nested within the Danish National Birth Cohort study. Antibodies were analyzed at a first prenatal visit (mean 17.0weeks) and at a late second/third trimester study visit. Prenatal infections were identified as IgG/IgM seroconversion or a fourfold rise in IgG antibody titers. Multiple regression models were adjusted for maternal age, BMI, smoking status, and time between blood draws. RESULTS: CT infection was associated with preeclampsia (ORadj 1.6, 95% CI 0.7, 3.6), severe preeclampsia (ORadj 1.8, 95% CI 0.6, 5.3), and preeclampsia resulting in preterm birth (ORadj 1.7, 95% CI 0.6-4.9) or birth of a small for gestational age infant (ORadj 2.1, 95% CI 0.6, 7.5), although CT infection was uncommon (n=33, 4.0%) and associations were not statistically significant. CP, CMV, and HSV infection were not associated with preeclampsia. CONCLUSIONS: Women with serological evidence of prenatal CT infection were more likely to develop preeclampsia, although infection was infrequent and confidence intervals were wide. Studies in populations at higher risk for STIs are needed to corroborate this association.
BACKGROUND: Although the etiology of preeclampsia is not well understood, it has been suggested that excessive systemic inflammation may lead to oxidative stress, promoting the endothelial dysfunction characteristic of preeclampsia. Few prospective studies have examined the role of infection, an immune system stimulator, as a risk factor for preeclampsia. METHODS: We conducted a longitudinal study of the relationships between Chlamydia trachomatis (CT), Chlamydophila pneumoniae (CP), cytomegalovirus (CMV), herpes simplex virus (HSV) and preeclampsia among 509 preeclamptic cases and 336 normotensive controls nested within the Danish National Birth Cohort study. Antibodies were analyzed at a first prenatal visit (mean 17.0weeks) and at a late second/third trimester study visit. Prenatal infections were identified as IgG/IgM seroconversion or a fourfold rise in IgG antibody titers. Multiple regression models were adjusted for maternal age, BMI, smoking status, and time between blood draws. RESULTS:CTinfection was associated with preeclampsia (ORadj 1.6, 95% CI 0.7, 3.6), severe preeclampsia (ORadj 1.8, 95% CI 0.6, 5.3), and preeclampsia resulting in preterm birth (ORadj 1.7, 95% CI 0.6-4.9) or birth of a small for gestational age infant (ORadj 2.1, 95% CI 0.6, 7.5), although CTinfection was uncommon (n=33, 4.0%) and associations were not statistically significant. CP, CMV, and HSV infection were not associated with preeclampsia. CONCLUSIONS:Women with serological evidence of prenatal CTinfection were more likely to develop preeclampsia, although infection was infrequent and confidence intervals were wide. Studies in populations at higher risk for STIs are needed to corroborate this association.
Authors: Catherine L Haggerty; Mark A Klebanoff; Inge Panum; Soren A Uldum; Debra C Bass; Jorn Olsen; James M Roberts; Roberta B Ness Journal: Pregnancy Hypertens Date: 2013-07-01 Impact factor: 2.899
Authors: Brandie D Taylor; Roberta B Ness; Jørn Olsen; David M Hougaard; Kristin Skogstrand; James M Roberts; Catherine L Haggerty Journal: Hypertension Date: 2014-12-15 Impact factor: 10.190
Authors: Brandie D Taylor; Gong Tang; Roberta B Ness; Jørn Olsen; David M Hougaard; Kristin Skogstrand; James M Roberts; Catherine L Haggerty Journal: Pregnancy Hypertens Date: 2015-11-10 Impact factor: 2.899
Authors: Anja Weinreich Olsen; Emma Kathrine Lorenzen; Ida Rosenkrands; Frank Follmann; Peter Andersen Journal: Front Immunol Date: 2017-12-11 Impact factor: 7.561
Authors: Cheuk-Lun Lee; Jan H W Veerbeek; Tirtha K Rana; Bas B van Rijn; Graham J Burton; Hong Wa Yung Journal: Am J Pathol Date: 2018-11-15 Impact factor: 4.307