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1.
Croat Med J ; 56(2): 119-27, 2015 Apr.
Article in English | MEDLINE | ID: mdl-25891871

ABSTRACT

AIM: To identify characteristic risk factors of preterm birth in Central and Eastern Europe and explore the differences from other developed countries. METHOD: Data on 33,794 term and 3867 preterm births (<37 wks.) were extracted in a retrospective study between January 1, 2007 and December 31, 2009. The study took place in 6 centers in 5 countries: Czech Republic, Hungary (two centers), Romania, Slovakia, and Ukraine. Data on historical risk factors, pregnancy complications, and special testing were gathered. Preterm birth frequencies and relevant risk factors were analyzed using Statistical Analysis System (SAS) software. RESULTS: All the factors selected for study (history of smoking, diabetes, chronic hypertension, current diabetes, preeclampsia, progesterone use, current smoking, body mass index, iron use and anemia during pregnancy), except the history of diabetes were predictive of preterm birth across all participating European centers. Preterm birth was at least 2.4 times more likely with smoking (history or current), three times more likely with preeclampsia, 2.9 times more likely with hypertension after adjusting for other covariates. It had inverse relationship with the significant predictor body mass index, with adjusted risk ratio of 0.8 to 1.0 in three sites. Iron use and anemia, though significant predictors of preterm birth, indicated mixed patterns for relative risk ratio. CONCLUSION: Smoking, preeclampsia, hypertension and body mass index seem to be the foremost risk factors of preterm birth. Implications of these factors could be beneficial for design and implementation of interventions and improve the birth outcome.


Subject(s)
Healthcare Disparities/statistics & numerical data , Obstetric Labor, Premature/epidemiology , Premature Birth/epidemiology , Adult , Birth Rate , Body Mass Index , Europe, Eastern/epidemiology , Female , Humans , Hypertension/epidemiology , Infant, Newborn , Pre-Eclampsia/epidemiology , Pregnancy , Retrospective Studies , Risk Factors , Smoking/epidemiology
2.
Environ Res ; 130: 7-13, 2014 Apr.
Article in English | MEDLINE | ID: mdl-24517884

ABSTRACT

BACKGROUND: Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy. METHODS: In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10µm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound. RESULTS: Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3mm. For women residing within 5km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined. CONCLUSIONS: Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy.


Subject(s)
Air Pollution/adverse effects , Fetal Development/physiology , Maternal Exposure/adverse effects , Vehicle Emissions/toxicity , Adult , Carbon Monoxide/toxicity , Cohort Studies , Female , Humans , Infant, Newborn , Los Angeles , Male , Models, Theoretical , Nitrogen Oxides/toxicity , Ozone/toxicity , Particulate Matter/toxicity , Pregnancy , Prospective Studies , Ultrasonography, Prenatal , Young Adult
3.
J Womens Health (Larchmt) ; 30(1): 113-120, 2021 01.
Article in English | MEDLINE | ID: mdl-33021442

ABSTRACT

Background: Depression is a common complication of pregnancy and vitamin D deficiency is one biological risk factor for postpartum depression (PPD). Materials and Methods: We evaluated the ratio of 24,25(OH)2D and 25(OH)D serum concentrations referred to as the Vitamin D Metabolite Ratio (VMR), a new candidate biomarker during pregnancyand its relationship with PPD. Women were enrolled in the first trimester of pregnancy and followed through four timepoints. Results: A total of 89 women had complete depression, biomarker and demographic data and 34% were at risk for PPD (CES-D≥16). Stepwise multiple logistic regression models for PPD risk were carried out with eight predictors. Results showed that only lower VMR, OR = 1.43, 95% CI 1.10-1.86, p = 0.007, and Hispanic/Latina identification, OR = 3.83, 95% CI 1.44-10.92, p = 0.007 were significantly associated with higher PPD risk. Conclusion: Routine prenatal screening for vitamin D metabolites, particularly in Hispanic/Latina women, may identify women at risk for PPD.


Subject(s)
Depression, Postpartum , Vitamin D Deficiency , Depression, Postpartum/diagnosis , Depression, Postpartum/epidemiology , Female , Humans , Pregnancy , Risk Factors , Vitamin D , Vitamin D Deficiency/complications , Vitamin D Deficiency/diagnosis , Vitamin D Deficiency/epidemiology , Vitamins
4.
Clin Psychol Sci ; 1(3): 253-264, 2013 Jul 01.
Article in English | MEDLINE | ID: mdl-23997996

ABSTRACT

Three decades of research point to both biological and psychological risk factors for postpartum depression, but very little research integrates the two. This study bridged this gap by testing whether prenatal social support predicted depressive symptoms at 8 weeks postpartum in a multiethnic sample of 210 women and whether the stress hormone placental corticotropin-releasing hormone (pCRH), measured at 19, 29, and 37 weeks' gestation, mediated this relationship. We found that prenatal family support predicted significantly fewer depressive symptoms postpartum and more gradual increases in pCRH from 29 to 37 weeks' gestation. Furthermore, steeper increases in pCRH during this same period predicted more depressive symptoms postpartum. Finally, these changes in pCRH in late pregnancy mediated the relationship between prenatal family support and postpartum depressive symptoms. These results suggest that social and biological risk factors for postpartum depressive symptoms are intertwined and move us closer to an integrated biopsychosocial understanding of postpartum depression.

5.
Reprod Sci ; 18(11): 1046-70, 2011 Nov.
Article in English | MEDLINE | ID: mdl-22031189

ABSTRACT

BACKGROUND: Understanding spontaneous preterm birth ([PTB] < 37 weeks) is difficult due to heterogeneities associated with multitudes of risk factors and pathophysiological pathways. Several biomarkers are routinely used clinically for predicting preterm labor; however, these factors are either nonspecific or detected too late. OBJECTIVE: Systematic review of literature on PTB biomarkers in the last 40 years to map out the existing knowledge and gaps in understanding PTB biomarkers. SEARCH STRATEGIES: Five electronic databases were searched for human studies on PTB biomarkers published in any language between 1965 and 2008. SELECTION CRITERIA: The phenotype of interest for final data extraction was exclusively spontaneous PTB with no rupture of membranes. Data extraction included (a) general characteristics of the study (clinical setting, period, and study design), (b) study/participant characteristics (inclusion and exclusion criteria, race/ethnicity, number of participants, gestational age at sampling, (c) characteristics of the biomarker (type, rationale for its selection, type of biological sample, and assay used, and (d) concentration of biomarkers in cases and controls. DATA COLLECTION AND ANALYSIS: The search yielded 7255 citations and data were extracted from 217 articles which met our inclusion and exclusion criteria. MAIN RESULTS: A total of 116 different biomarkers were reported and these were assayed 578 times in the 217 included studies. Over two thirds of the 217 studies were performed on North American or European populations. No reliable biomarkers emerged as a risk predictor of PTB. CONCLUSIONS: Identifying similar studies on biomarkers for the prediction of PTB was a very challenging task due heterogeneities in study design, sampling issues (types, timing and processing), assay methods, and analyses. Major areas of concern identified in this review include poor phenotype definition, nonideal study designs and poor rationale for biomarker selection and assays and population stratification issues.


Subject(s)
Biomarkers , Premature Birth , Biomarkers/analysis , Female , Humans , Infant, Newborn , Obstetric Labor, Premature , Pregnancy , Quality Control , Research Design , Risk Factors , Specimen Handling/methods
6.
Reprod Sci ; 15(5): 477-83, 2008 May.
Article in English | MEDLINE | ID: mdl-18579856

ABSTRACT

The objective of this study is to document differences in corticotrophin-releasing hormone (CRH), CRH receptor 1 (CRHR1), and CRH binding protein (CRHBP) gene expression in fetal membranes derived from African Americans and Caucasians in vitro in response to lipopolysaccharide (LPS) stimulation and to assess racial disparity in CRH concentrations in the amniotic fluid (AF) of women with spontaneous preterm birth (PTB). Fetal membranes (African American, n = 8; Caucasian, n = 8) at term, placed in an organ explant system, were stimulated with LPS. Microarray analysis documented differences in the mRNA expression pattern of CRH, CRHBP, and CRHR1 between races. CRH was measured in AF (a case [PTB]-control [term] study) and culture media. Between races, LPS significantly increased CRH and CRHR1 expression in African Americans and CRHBP in Caucasians, with no differences in controls. CRH was detectable only in LPS-stimulated African American membranes. AF CRH concentrations were higher in PTB compared with controls (P < .001), and no difference was noticed between races (P = .1). AF analysis did not document racial disparity in CRH concentrations in PTB. In fetal membranes, African Americans showed a higher expression and production of CRH in response to an in vitro stimulus.


Subject(s)
Amniotic Fluid/metabolism , Corticotropin-Releasing Hormone/biosynthesis , Extraembryonic Membranes/metabolism , Obstetric Labor, Premature/metabolism , Adult , Black or African American , Amniotic Fluid/drug effects , Carrier Proteins/biosynthesis , Carrier Proteins/genetics , Corticotropin-Releasing Hormone/genetics , Extraembryonic Membranes/drug effects , Female , Humans , In Vitro Techniques , Lipopolysaccharides/pharmacology , Obstetric Labor, Premature/genetics , Pregnancy , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Receptors, Corticotropin-Releasing Hormone/biosynthesis , Receptors, Corticotropin-Releasing Hormone/genetics , White People
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