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To evaluate the association between psychotropic medication and inflammatory biomarkers in women with antenatal depressive symptoms (ADS). In this cross-sectional secondary analysis of a prospective multicenter observational study, 723 pregnant women underwent a depression screen using the Center for Epidemiologic Studies Depression Scale (CES-D) between 12 and 21 weeks gestation. Self-reported use of medications for depression and/or anxiety was corroborated with the medical record to document exposure to pharmacotherapy. Serum was collected and inflammatory biomarkers (IFNγ, IL13, IL6, IL8, TNFα, CRP) were measured concomitantly. Women were included if they fell into one of three categories: ADS responsive to treatment (CES-D < 16 with medication), ADS not responsive to medication (CES-D ≥ 23 despite medication), and untreated ADS (CES-D ≥ 23 with no medication). Levels of inflammatory biomarkers were compared among groups and multivariable regressions performed. Of the 85 women studied, 16 (19%) had ADS responsive to treatment, 12 (14%) had ADS not responsive to medication, and 57 (67%) had untreated ADS. TNFα concentrations significantly differed (P = 0.016) across the cohorts. Post hoc bivariate analyses demonstrated that women with ADS responsive to treatment had lower serum TNFα than non-responders (p = 0.02) and women with untreated ADS (p = 0.01). There were no differences in IFNγ, IL13, IL6, IL8, or CRP among the groups. Regressions demonstrated that, compared to women with ADS responsive to treatment, non-responders or women with untreated ADS had higher TNFα levels (β = 0.27, 95% CI 0.02-0.52 and β = 0.23, 95% CI 0.02-0.44, respectively). Pregnant women on pharmacotherapy who respond to treatment for ADS have lower TNFα compared to women not responsive to medication or women with untreated ADS. These data suggest the possibility that either the therapeutic response in the context of pharmacotherapy is accompanied by modulation of the immune system or that pre-existing higher levels of TNFα may be associated with a poorer response to traditional pharmacotherapy.

Problem: Maternal inflammation undergoes adaptations during pregnancy, and excessive inflammation has been associated with adverse outcomes. One mechanism may be maternal inflammation transmission to the fetal compartment. Links between maternal pregnancy inflammation and fetal inflammation are poorly characterized., Method: Principal components analysis was used to extract underlying inflammation components across cytokines (IFN-γ, IL-10, IL-13, IL-6, IL-8, TNF-α) in two pregnancy cohorts (SPAH N=87, MOMS N=539) assessed during the second and third trimesters. Links between maternal inflammation over pregnancy and fetal (cord blood) inflammation were assessed., Results: Substantial cytokine rank-order stability was observed in both cohorts, β's range .47-.96, P's <.001. Two consistent inflammatory components were extracted: a pro-inflammatory (IL-10, IL-6, IL-8, TNF-α, IFN-γ) component and anti-inflammatory (IL-13) component. Higher maternal pro-inflammatory and lower anti-inflammatory indices during pregnancy were associated with higher cord blood inflammation, P's>.04., Conclusion: Maternal inflammation indices over pregnancy were associated with inflammation in cord blood at birth. Results have implications for understanding pregnancy inflammatory processes and how maternal inflammation may be transmitted to fetal circulation., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

ObjectivesTo assess deviations in longitudinally measured cytokines with preterm birth (PTB).MethodsProspective longitudinal study targeting 80 subjects. Phlebotomy specimens for broad panel of cytokine analysis were obtained at three time (T) intervals: first trimester (T1: 8-14 weeks' gestation), second trimester (T2: 18-22 weeks' gestation), and third trimester (T3: 28-32 weeks' gestation). Important demographics and outcomes were tracked. Data were stratified and the target groups were analyzed as follows: "Uncomplicated" (delivered ≥37 weeks) or "Preterm Birth" (

Research suggests the health consequences of economic hardship can be transmitted across generations. Some of these disparities are thought to be passed to offspring during gestation. But this hypothesis has not been tested in contemporary American samples, and the mechanisms of transmission have not been characterized. Accordingly, this study had two goals: first, to determine if women exposed to economic hardship during childhood showed higher rates of adverse birth outcomes; and second, to evaluate the contribution of inflammation, psychosocial, lifestyle, and obstetric characteristics to this phenomenon. This prospective study enrolled 744 women with singleton pregnancies (59.1% White; 16.3% Black; 18.7% Latina; 5.9% Other). Childhood economic hardship was measured by self-report. Birth outcomes included length of gestation and incidence of preterm birth; birth weight percentile and small for gestational age; length of hospital stay and admission to Special Care Nursery. Analyses revealed that mothers' childhood economic hardship was independently associated with multiple adverse birth outcomes, even following adjustment for demographics, maternal education, and obstetrical confounders. Women raised in economically disadvantaged conditions had shorter gestation length and higher preterm delivery rates. Their babies had lower birth weights, were more likely to be small for gestational age, stayed in the hospital longer, and had more Special Care Nursery admissions. Mediation analyses suggested these associations arose through multiple pathways, and highlighted roles for inflammation, education, adiposity, and obstetric complications. Collectively, these findings suggest that childhood economic hardship predisposes women to adverse birth outcomes, and highlights likely behavioral and biological mechanisms.

Objective: To assess post-partum inflammation for patients delivering prior to 34 6/7 weeks by birth etiology. Methods: This was an observational study of early preterm birth (PTB) occurring between 20 0/7 and 34 6/7 weeks of gestation. Serum C-reactive protein (CRP) levels were measured 1 month post-partum. CRP measurements were compared by birth etiology. Results: A total of 399 women were analyzed. Distribution of birth etiology was 35% (n = 138) preterm labor (PTL), 28% (n = 115) preterm premature rupture of membranes (pPROM), and 37% (n = 141) indicated preterm birth (IPTB). Serum CRP varied by birth etiology (P = 0.036). Women with pPROM had elevated median CRP levels compared to women with PTL (P = 0.037). IPTB demonstrated elevated CRP levels when compared to PTL (P = 0.019). Pre-eclamptic/eclamptic subjects exhibited increased median CRP levels compared to PTL (P = 0.04). Conclusion: Post-partum inflammation varies by birth etiology. Such variation may serve as identification of subjects whose future pregnancies and, ultimately, overall health status may benefit from inter-pregnancy interventions aimed at reducing inflammatory-associated risk factors. [ABSTRACT FROM AUTHOR]

Research suggests the health consequences of economic hardship can be transmitted across generations. Some of these disparities are thought to be passed to offspring during gestation. But this hypothesis has not been tested in contemporary American samples, and the mechanisms of transmission have not been characterized. Accordingly, this study had two goals: first, to determine if women exposed to economic hardship during childhood showed higher rates of adverse birth outcomes; and second, to evaluate the contribution of inflammation, psychosocial, lifestyle, and obstetric characteristics to this phenomenon. This prospective study enrolled 744 women with singleton pregnancies (59.1% White; 16.3% Black; 18.7% Latina; 5.9% Other). Childhood economic hardship was measured by self-report. Birth outcomes included length of gestation and incidence of preterm birth; birth weight percentile and small for gestational age; length of hospital stay and admission to Special Care Nursery. Analyses revealed that mothers’ childhood economic hardship was independently associated with multiple adverse birth outcomes, even following adjustment for demographics, maternal education, and obstetrical confounders. Women raised in economically disadvantaged conditions had shorter gestation length and higher preterm delivery rates. Their babies had lower birth weights, were more likely to be small for gestational age, stayed in the hospital longer, and had more Special Care Nursery admissions. Mediation analyses suggested these associations arose through multiple pathways, and highlighted roles for inflammation, education, adiposity, and obstetric complications. Collectively, these findings suggest that childhood economic hardship predisposes women to adverse birth outcomes, and highlights likely behavioral and biological mechanisms. [ABSTRACT FROM AUTHOR]

The article presents a study which compares women with different chronic vaginal symptoms with a wide variety of sociodemographic, health, behavioral, and psychosocial characteristics. A questionnaire has been distributed to patients who underwent a standardized history, physical examination, and laboratory examination. Results of the study indicated that women with chronic vaginal symptoms have a variety of diagnoses, wherein most of them are non-infectious.