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      Hypertensive Disorders of Pregnancy and Offspring Cardiometabolic Health at Midchildhood: Project Viva Findings

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          Exposure to preeclampsia or gestational hypertension is associated with higher offspring systolic blood pressure ( SBP), but less is known about associations with other cardiometabolic risk markers.

          Methods and Results

          We studied 1097 children from the Project Viva cohort born 1999‐2002. Exposures were preeclampsia or gestational hypertension and mean maternal SBP in each trimester from prenatal records. Outcomes were research measures in midchildhood (mean 8.0 years) of SBP, overall adiposity, and a global cardiometabolic risk score comprising measures of SBP, waist circumference, glycemia, and lipids. We conducted linear regression analyses adjusted for maternal characteristics and offspring sex and age. In adjusted models, maternal preeclampsia or gestational hypertension (n=98, 9.1%) versus normal blood pressure was associated with slightly higher offspring SBP z‐score (0.15 units; 95% confidence interval [CI] −0.03, 0.32) but otherwise predicted better cardiometabolic health markers including metabolic risk z‐score (−0.23 units; −95% CI 0.44, −0.03) and several of its components as well as lower body mass index z‐score (−0.27 units; 95% CI −0.48, −0.06) and lower fat mass index (−0.91 kg/m 2; 95% CI −1.35, −0.47). Similarly, higher mean third‐trimester maternal SBP was associated with higher offspring SBP z‐score (0.09 units per 10 mm Hg; 95% CI 0.02, 0.16) and lower overall and central adiposity but not with biomarkers of metabolic risk. Results for second‐trimester SBP were generally similar. First‐trimester blood pressure was associated with higher offspring blood pressure but not with other outcomes.


          Higher maternal late‐pregnancy SBP and hypertensive disorders of pregnancy were associated with higher offspring SBP but otherwise better cardiometabolic health.

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          Most cited references 24

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          2000 CDC Growth Charts for the United States: methods and development.

          This report provides detailed information on how the 2000 Centers for Disease Control and Prevention (CDC) growth charts for the United States were developed, expanding upon the report that accompanied the initial release of the charts in 2000. The growth charts were developed with data from five national health examination surveys and limited supplemental data. Smoothed percentile curves were developed in two stages. In the first stage, selected empirical percentiles were smoothed with a variety of parametric and nonparametric procedures. In the second stage, parameters were created to obtain the final curves, additional percentiles and z-scores. The revised charts were evaluated using statistical and graphical measures. The 1977 National Center for Health Statistics (NCHS) growth charts were revised for infants (birth to 36 months) and older children (2 to 20 years). New body mass index-for-age (BMI-for-age) charts were created. Use of national data improved the transition from the infant charts to those for older children. The evaluation of the charts found no large or systematic differences between the smoothed percentiles and the empirical data. The 2000 CDC growth charts were developed with improved data and statistical procedures. Health care providers now have an instrument for growth screening that better represents the racial-ethnic diversity and combination of breast- and formula-feeding in the United States. It is recommended that these charts replace the 1977 NCHS charts when assessing the size and growth patterns of infants, children, and adolescents.
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            A nearly continuous measure of birth weight for gestational age using a United States national reference

            Background Fully understanding the determinants and sequelae of fetal growth requires a continuous measure of birth weight adjusted for gestational age. Published United States reference data, however, provide estimates only of the median and lowest and highest 5th and 10th percentiles for birth weight at each gestational age. The purpose of our analysis was to create more continuous reference measures of birth weight for gestational age for use in epidemiologic analyses. Methods We used data from the most recent nationwide United States Natality datasets to generate multiple reference percentiles of birth weight at each completed week of gestation from 22 through 44 weeks. Gestational age was determined from last menstrual period. We analyzed data from 6,690,717 singleton infants with recorded birth weight and sex born to United States resident mothers in 1999 and 2000. Results Birth weight rose with greater gestational age, with increasing slopes during the third trimester and a leveling off beyond 40 weeks. Boys had higher birth weights than girls, later born children higher weights than firstborns, and infants born to non-Hispanic white mothers higher birth weights than those born to non-Hispanic black mothers. These results correspond well with previously published estimates reporting limited percentiles. Conclusions Our method provides comprehensive reference values of birth weight at 22 through 44 completed weeks of gestation, derived from broadly based nationwide data. Other approaches require assumptions of normality or of a functional relationship between gestational age and birth weight, which may not be appropriate. These data should prove useful for researchers investigating the predictors and outcomes of altered fetal growth.
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              Epidemiology of pre-eclampsia and the other hypertensive disorders of pregnancy.

              Hypertensive disorders of pregnancy include chronic hypertension, gestational hypertension, pre-eclampsia and chronic hypertension with superimposed pre-eclampsia. Pre-eclampsia complicates about 3% of pregnancies, and all hypertensive disorders affect about five to 10% of pregnancies. Secular increases in chronic hypertension, gestational hypertension and pre-eclampsia have occurred as a result of changes in maternal characteristics (such as maternal age and pre-pregnancy weight), whereas declines in eclampsia have followed widespread antenatal care and use of prophylactic treatments (such as magnesium sulphate). Determinants of pre-eclampsia rates include a bewildering array of risk and protective factors, including familial factors, sperm exposure, maternal smoking, pre-existing medical conditions (such as hypertension, diabetes mellitus and anti-phospholipid syndrome), and miscellaneous ones such as plurality, older maternal age and obesity. Hypertensive disorders are associated with higher rates of maternal, fetal and infant mortality, and severe morbidity, especially in cases of severe pre-eclampsia, eclampsia and haemolysis, elevated liver enzymes and low platelets syndrome. Copyright © 2011 Elsevier Ltd. All rights reserved.

                Author and article information

                J Am Heart Assoc
                J Am Heart Assoc
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                30 January 2018
                February 2018
                : 7
                : 3 ( doiID: 10.1002/jah3.2018.7.issue-3 )
                [ 1 ] Division of Chronic Disease Research Across the Lifecourse Department of Population Medicine Harvard Medical School and Harvard Pilgrim Health Care Institute Boston MA
                [ 2 ] Department of Chronic Disease Epidemiology Yale University New Haven CT
                [ 3 ] Department of Nutrition Harvard T.H. Chan School of Public Health Boston MA
                [ 4 ] Diabetes Unit Massachusetts General Hospital Boston MA
                Author notes
                [* ] Correspondence to: Emily Oken, MD, MPH, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, 401 Park Drive, Suite 401E, Boston, MA 02215. E‐mail: emily_oken@ 123456hphc.org
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                Page count
                Figures: 1, Tables: 4, Pages: 12, Words: 8991
                Funded by: US National Institutes of Health
                Award ID: R01 HD034568
                Award ID: K24 HD069408
                Award ID: UG3OD023286
                Funded by: Yale School of Public Health Weinerman Fellowship
                Original Research
                Original Research
                Custom metadata
                February 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version= mode:remove_FC converted:06.02.2018


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