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Standardization of Amniotic Fluid Leptin Levels and Utility in Maternal Journal of Perinatology (2015) 35, 547–552 © 2015 Nature America, Inc. All rights reserved 0743-8346/15 www.nature.com/jp ORIGINAL ARTICLE Standardization of amniotic fluid leptin levels and utility in maternal overweight and fetal undergrowth M Scott-Finley1,6,JGWoo2,3,6, M Habli1,2, O Ramos-Gonzales2, JF Cnota2, Y Wang3, BD Kamath-Rayne4, AC Hinton1, WJ Polzin1,5, TM Crombleholme5 and RB Hinton2 OBJECTIVE: Leptin is an adipokine that regulates energy homeostasis. The objective of this study was to establish a gestational age-specific standard for amniotic fluid leptin (AFL) levels and examine the relationship between AFL, maternal overweight and fetal growth restriction. STUDY DESIGN: Amniotic fluid was obtained at mid-gestation from singleton gravidas, and leptin was quantified using enzyme- linked immunosorbent assay. Amniotic fluid samples from 321 term pregnancies were analyzed. Clinical data, including fetal ultrasound measurements and maternal and infant characteristics, were available for a subset of patients (n = 45). RESULTS: The median interquartile range AFL level was significantly higher at 14 weeks’ gestation (2133 pg ml − 1 (1703 to 4347)) than after 33 weeks’ gestation (519 pg ml − 1 (380 to 761), P trendo0.0001), an average difference of 102 pg ml − 1 per week. AFL levels were positively correlated with maternal pre-pregnancy body mass index (BMI) (r = 0.36, P = 0.03) adjusting for gestational age at measurement, but were not associated with fetal growth. CONCLUSIONS: AFL levels are higher at mid-gestation than at late gestation, and are associated with maternal pre-pregnancy BMI. Journal of Perinatology (2015) 35, 547–552; doi:10.1038/jp.2015.39; published online 30 April 2015 INTRODUCTION development.13–15 However, amniotic fluid leptin (AFL) has not Fetal growth restriction (FGR) is among the most significant been standardized or examined systematically during pregnancy. problems in perinatal medicine. It is the second leading cause of Little is known about how AFL levels change during pregnancy perinatal morbidity and mortality, exceeded only by prematurity.1 and relate to fetal growth. Understanding leptin dysregulation FGR is defined as an estimated fetal weight less than the tenth may elucidate mechanisms of FGR at the intersection of maternal percentile for gestational age and corresponds with small for health and fetal growth. In this study, we examined AFL in a cross- sectional manner across gestational ages with the goal of gestational age (SGA), which is defined as a birth weight less than establishing a gestational age-specific standard. Because maternal the tenth percentile for gestational age.2 Perinatal morbidity and weight has been associated with leptin regulation, we hypothe- mortality is significantly increased in the presence of low birth 3,4 sized that increased pre-pregnancy maternal body mass index weight for gestational age. In addition, FGR infants are at (BMI) is associated with increased AFL levels at mid-gestation. increased risk for a variety of long-term sequelae, including These observations have important clinical implications and may adult-onset metabolic diseases such as type 2 diabetes and 5,6 lead to applications that improve the diagnostic and prognostic hypertension. Despite the immediate and long-term importance assessment of fetal growth. of FGR, there are presently no predictive biomarkers or preventive treatment strategies. Growth abnormalities in the fetus may be caused by numerous METHODS insults that are generally classified as maternal, fetal or placental in Study population origin and include maternal preeclampsia, fetal genetic anomalies This study was approved by the Institutional Review Boards of Cincinnati and primary placental vasculopathies. However, the shared ’ fi Children s Hospital Medical Center and Good Samaritan Hospital pathogenesis of FGR is poorly understood. Placental insuf ciency (Cincinnati, OH. USA). Amniotic fluid was obtained from pregnancies at may be a common final pathway for FGR, but predicting placental both community and referral hospitals that underwent a genetic function is challenging.7 Several growth factors and signaling amniocentesis at any time during gestation; however, the specific molecules have been implicated in FGR, including vascular indications for testing are unknown because the study used discarded endothelial growth factor, placental growth factor and leptin.8–10 tissue that was anonymized. Inclusion criteria were a normal karyotype Leptin is an adipokine that regulates energy homeostasis and is analysis and the absence of fetal anomalies by ultrasound anatomic survey. Exclusion criteria included prematurity (o37 weeks’ gestation), multiple increased in obesity (anabolism) and decreased in cachexia gestation pregnancy, and fetal or neonatal demise. Patients were enrolled 11,12 (catabolism), and leptin is present in fetal tissue, including from May 2009 to October 2010. Detailed medical record information was the placenta, suggesting a direct role for leptin in fetal growth and reviewed in a small subset of high-risk cases from a single center owing to 1Division of Maternal Fetal Medicine, Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, OH, USA; 2Division of Cardiology, The Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; 3Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA; 4Perinatal Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA and 5Fetal Care Center, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA. Correspondence: Dr RB Hinton, Division of Cardiology, The Heart Institute, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 2003, Cincinnati, OH 45229, USA. E-mail: [email protected] 6These authors contributed equally to this work. Received 3 December 2014; Received 23 March 2015; accepted 24 March 2015; published online 30 April 2015 Standardization of amniotic fluid leptin M Scott-Finley et al 548 the fact that the majority of cases were derived from referring hospitals again and streptavidin–HRP was added for 20 min, after which a 1:1 where information was not accessible. Informed consent was obtained mixture of colors A and B was added. Plates were stopped with 2 N H2SO4 from this subset of patients. Archived placental tissue was identified in a and read at 450 nm minus 595 nm background. Values are expressed in subset of these cases. pg ml − 1. The Bradford assay was employed by adding 200 μl 1X solution (R&D Systems) to a plate, followed by 5 μl per sample. Plates were read at − Maternal health 595 nm. Values were expressed as μgml 1. Clinical records were reviewed for a subset (n = 45) with available data, with the following data collected: maternal age, calculated pre-pregnancy Placenta assessment BMI from self-reported weight and measured height, BMI at delivery, and Histochemistry and immunohistochemistry were used for exploratory weight gain during pregnancy. In addition, medical history of preexisting studies to assess placental tissue, which was obtained from 5/45 (11%) diabetes mellitus or gestational diabetes (GD) and preeclampsia was pregnancies from the subset of patients with medical record information in noted. Gestational diabetes was identified by an abnormal diagnostic the course of routine pathological processes. Antibodies directed against 100-g 3-hour oral glucose test defined as two elevated values. Finally, leptin (1:500, Lifespan Biosciences, Seattle, WA, USA), and leptin receptor estimated fetal weight by ultrasound within 2 weeks of amniocentesis, (1:50, Abcam, Cambridge, MA, USA) were used to assess the location and gestational age at the time of amniocentesis, gestational age at the time of relative amount of protein. The leptin antibodies required additional citrate delivery, birth weight, birth head circumference and infant gender were pretreatment. A semiquantitative scale was used to assess the 18 recorded. For the purposes of analysis, GD was defined as either an expression. Briefly, staining was graded on a scale of 0 to 3 based on abnormal glucose-tolerance test or confirmed clinical diagnosis of GD. the percentage of positive cells as follows: 0 = immunoreactivity in o10% Maternal pre-pregnancy BMI (in kg m − 2) was classified as normal weight of cells; 1 = 10 to 35%; 2 = 35 to 70%; and 3 = 470%. Quantification was (BMI o25) or overweight/obese (BMI ⩾ 25).16 performed by a single blinded reader. Fetal growth Statistical analyses Neonatal anthropometrics included birth weight and head circumference. Statistical analyses were conducted using SAS v.9.3 (SAS Institute, Cary, NC, USA). Because wide variability in AFL levels has been reported widely, AFL Growth z-scores were derived from the Olsen standard, a contemporary set − 1 of growth curves derived from a large, racially diverse USA sample, levels were analyzed both as concentration (pg ml ) and standardized to fl μ − 1 resulting in gestational age- and gender-specific z-scores.17 SGA was amniotic uid protein levels (pg g ). There were fewer samples per week ’ defined as a birth weight less than or equal to the tenth percentile (z-score after 26 weeks gestation, and thus later gestational ages required grouping fi ⩽ − 1.28), and for the purposes of this study was considered a surrogate for analysis. AFL levels were rst grouped by attained full weeks of measure of FGR. gestation at the time of measurement, except for the later weeks, which were grouped into 25 to 27, 28
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