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The Accuracy of Recalled versus Measured Pre-Pregnancy Weight for the Calculation of Pre-Pregnancy Body Mass Index

Tue, 05/13/2014 - 9:33am

Background: In 2009, the Institute of Medicine (IOM) published gestational weight gain (GWG) guidelines with the goal of optimizing maternal and fetal outcomes. GWG recommendations are specific to pre-pregnancy body mass index (BMI): 28-40 lbs for underweight (UW; BMI2), 25-35 lbs for normal weight (NW; 18.5≤BMI/m2), 15-25 lbs for overweight (OW; 25 ≤BMI/m2), and 11-20 lbs for obese (OB; BMI≥30 kg/m2) women. With upwards of 50% of pregnancies in the U.S. unplanned, measured pre-pregnancy weight is often unavailable in clinical and research settings. Evaluating the accuracy of recalled pre-pregnancy weight early in prenatal care is important in order to establish accuracy of pre-pregnancy BMI calculations in order to counsel about GWG accurately.

Objective: To examine differences in recalled versus measured pre-pregnancy weight and to examine factors associated with accuracy of recalled weights.

Methods: Medical record review of 1,998 randomly selected pregnancies. Eligible women received prenatal care in faculty and resident clinics at UMass Memorial Health Care (UMMHC), delivered between January 2007 and December 2012, and had available both: (1) a measured weight within one year of conception and (2) a pre-pregnancy weight self-reported at first prenatal visit. Data were obtained from the UMMHC paper or electronic prenatal record and the Allscripts EMR. We calculated the difference in weights as recalled pre-pregnancy weight minus most recent measured weight within one year of conception. Subjects were excluded if they received care at a non-faculty or non-resident practice, charts not available after three separate retrieval attempts, both weights of interest not available, or if measured weight occurred at a prenatal visit for a prior pregnancy. For women with more than one pregnancy during the study time frame, one was randomly selected for inclusion in the analytic data set.

Results: Of the 1,998 pregnancy charts reviewed, 400 records met eligibility criteria and were included in this analysis. Women were mean age 29.7 (SD: 6.2) years, 69.3% multigravida, 64.4% non-Hispanic white, 65.2% married, and 62.4% had a college or greater education. Based on recalled weight, 3.3% of women were underweight, 46.6% were normal weight, 25.9% overweight, and 24.2% obese. 63% received care in the faculty obstetric clinic. Recorded recalled weights were mean 2.4 (SD: 11.1) pounds lower than measured pre-pregnancy weight. This difference did not differ by age, location of care, pre-pregnancy BMI, marital status, race/ethnicity, primary language, gravity, education, or time between measured weight and conception, in unadjusted and adjusted models. For 88.7% of women, calculating pre-pregnancy BMI based on weight measured up to a year prior to conception or based on recalled pre-pregnancy weight reported at the first prenatal visit resulted in the same classification of pre-pregnancy BMI.

Conclusion: Prenatal care providers may calculate pre-pregnancy BMIs using recalled pre-pregnancy weights early in prenatal care and use such calculated BMIs to accurately provide GWG recommendations regardless of demographic variables, gravity, or location of care.

Myogenic Enhancers Regulate Expression of the Facioscapulohumeral Muscular Dystrophy-Associated DUX4 Gene

Mon, 05/12/2014 - 2:05pm

Facioscapulohumeral muscular dystrophy (FSHD) is linked to epigenetic dysregulation of the chromosome 4q35 D4Z4 macrosatellite. However, this does not account for the tissue specificity of FSHD pathology, which requires stable expression of an alternative full-length mRNA splice form of DUX4 (DUX4-fl) from the D4Z4 array in skeletal muscle. Here, we describe the identification of two enhancers, DUX4 myogenic enhancer 1 (DME1) and DME2 which activate DUX4-fl expression in skeletal myocytes but not fibroblasts. Analysis of the chromatin revealed histone modifications and RNA polymerase II occupancy consistent with DME1 and DME2 being functional enhancers. Chromosome conformation capture analysis confirmed association of DME1 and DME2 with the DUX4 promoter in vivo. The strong interaction between DME2 and the DUX4 promoter in both FSHD and unaffected primary myocytes was greatly reduced in fibroblasts, suggesting a muscle-specific interaction. Nucleosome occupancy and methylome sequencing analysis indicated that in most FSHD myocytes, both enhancers are associated with nucleosomes but have hypomethylated DNA, consistent with a permissive transcriptional state, sporadic occupancy, and the observed DUX4 expression in rare myonuclei. Our data support a model in which these myogenic enhancers associate with the DUX4 promoter in skeletal myocytes and activate transcription when epigenetically derepressed in FSHD, resulting in the pathological misexpression of DUX4-fl.