Search

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2006.03.087 Byline: Ronald J. Wapner (a), Yoram Sorokin (b), Elizabeth A. Thom (c), Francee Johnson (d), Donald J. Dudley (e), Catherine Y. Spong (f), Alan M. Peaceman (g), Kenneth J. Leveno (h), Margaret Harper (i), Steve N. Caritis (j), Menachem Miodovnik (k), Brian Mercer (l), John M. Thorp (m), Atef Moawad (n), Mary Jo O'Sullivan (o), Susan Ramin (p), Marshall W. Carpenter (q), Dwight J. Rouse (r), Baha Sibai (s), Steven G. Gabbe (t) Abstract: The purpose of this study was to determine if weekly corticosteroids improve neonatal outcome without undue harm. Author Affiliation: (a) Department of Obstetrics and Gynecology, Drexel University College of Medicine, Philadelphia, PA (b) Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI (c) The Biostatistics Center, George Washington University Biostatistics Center, Rockville, MD (d) Department of Obstetrics and Gynecology, Ohio State University, Columbus, OH (e) Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, Utah (f) The National Institute of Child Health and Human Development, Bethesda, MD (g) Department of Obstetrics and Gynecology, Northwestern University, Chicago, IL (h) Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas, TX (i) Department of Obstetrics and Gynecology, Wake Forest University School of Medicine, Winston-Salem, NC (j) Department of Obstetrics and Gynecology, Magee Womens Hospital, Pittsburgh, PA (k) Departments of Obstetrics and Gynecology, Columbia University, New York, NY, and University of Cincinnati, Cincinnati, OH (l) Department of Obstetrics and Gynecology, Case Western Reserve University, Cleveland, OH (m) Department of Obstetrics and Gynecology, University of North Carolina Chapel Hill, Chapel Hill, NC (n) Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL (o) Department of Obstetrics and Gynecology, University of Miami, Miami, FL (p) Department of Obstetrics and Gynecology, University of Texas Houston, Houston, TX (q) Department of Obstetrics and Gynecology, Brown University, Providence, RI (r) Department of Obstetrics and Gynecology, University of Alabama, Birmingham, AL (s) Department of Obstetrics and Gynecology, University of Tennessee, Memphis, TN (t) Department of Obstetrics and Gynecology, Vanderbilt University, Nashville, TN Article History: Received 10 October 2005; Revised 16 February 2006; Accepted 21 March 2006 Article Note: (footnote) Supported by grants from the National Institute of Child Health and Human Development (HD21410, HD21414, HD27869, HD27917, HD27905, HD27860, HD27861, HD27915, HD34122, HD34116, HD34208, HD34136, HD40500, HD40485, HD40544, M01-RR-000080, HD40545, HD40560, HD40512, HD36801). Presented at the annual meeting of the Society for Maternal-Fetal Medicine, 24th Annual Meeting, New Orleans, La, February, 2004.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2004.06.055 Byline: Harish M. Sehdev, Soraya Abbasi, Patricia Robertson, Lytia Fisher, Dominic A. Marchiano, Jeffrey S. Gerdes, Jack Ludmir Abstract: The purpose of this study was to determine whether the interval between antenatal steroid exposure and delivery influences neonatal outcome in very low birth weight infants. Author Affiliation: Section of Maternal-Fetal Medicine and Newborn Pediatrics, Pennsylvania Hospital, Philadelphia, Pa, Departments of Pediatrics and Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia, Pa Article Note: (footnote) Presented at the Twenty-Fourth Annual Meeting of the Society for Maternal-Fetal Medicine, February 2-7, 2004, New Orleans, La.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1067/mob.2000.104789 Byline: Soraya Abbasi, Daniel Hirsch, Jonathan Davis, Jorge Tolosa, Nicole Stouffer, Robert Debbs, Jeffrey S. Gerdes Keywords: Betamethasone; prematurity; respiratory distress syndrome; intrauterine growth Abstract: Objective: Treatment of pregnant mothers with a single course of antenatal corticosteroids significantly reduces neonatal mortality and morbidity. Multiple weekly courses are often given. However, the safety and efficacy of repeated courses of antenatal corticosteroids have not been adequately studied. Study Design: A retrospective study was performed for 609 mothers and their 713 infants who were treated with 1 to 12 courses of antenatal corticosteroids. Data for 369 singleton preterm infants born at [less than or equal to]34 weeks' gestation, 210 multiple gestations, and 134 infants delivered at [greater than or equal to]35 weeks' gestation were analyzed separately. Results: The incidence of respiratory distress syndrome was 45% for single-course and 35% for multiple-course groups (P = .005; odds ratio, 0.44; 95% confidence interval, 0.25-0.79). The multiple-course group also had significantly less patent ductus arteriosus (20% vs 13%; P = .016). Incidence of death before discharge and other neonatal morbidities were similar. The multiple-course group had a reduction of 0.46 [+ or -] 0.19 cm in head circumference at birth (P = .013) when adjusted for gestational age and preeclampsia. The 2 groups had similar birth weights. Infants born at [greater than or equal to]35 weeks' gestation, multiple-gestation infants, and infants who were born >7 days after the last corticosteroid dose had similar outcomes, regardless of the number of courses they received. Mothers treated with multiple courses compared with a single course had a significantly higher incidence of postpartum endometritis (P = .013), even though they had a lower incidence of prolonged rupture of membranes (24% vs 33%, P = .06) and similar cesarean delivery rates. Conclusion: Exposure to multiple courses of antenatal corticosteroids compared with a single course resulted in a significant reduction in the incidence of respiratory distress syndrome in singleton preterm infants delivered within a week of the last corticosteroid dose. This was associated with a reduction in birth head circumference and an increased incidence of maternal endometritis. Whether the potential benefits of repeated therapy clearly outweigh the risks will ultimately be determined in randomized prospective controlled trials. (Am J Obstet Gynecol 2000;182:1243-9.) Author Affiliation: Philadelphia, Pennsylvania, and Mineola, New York From the Section on Newborn Pediatrics, Pennsylvania Hospital, the Departments of Pediatrics and Obstetrics and Gynecology and the Division of Biostatistics, University of Pennsylvania School of Medicine and Winthrop University Hospital, and the State University of New York at Stonybrook School of Medicine Article History: Received 28 September 1999; Accepted 2 December 1999 Article Note: (footnote) [star] Reprint requests: Soraya Abbasi, MD, Section on Newborn Pediatrics, Pennsylvania Hospital, Eighth and Spruce St, Philadelphia, PA 19107.

Byline: Alan H. Jobe, John P. Newnham, Karen E. Willet, Peter Sly, M.Gore Ervin, Cindy Bachurski, Fred Possmayer, Mikko Hallman, Machiko Ikegami Keywords: Compliance; inflammation; lung maturation; respiratory distress syndrome; surfactant Abstract: Objective: We hypothesized that the proinflammatory response to intra-amniotic endotoxin would induce lung maturation in preterm lambs. Study Design: Ewes were randomly assigned to receive 20 mg Escherichia coli endotoxin by intra-amniotic injection, maternal betamethasone (0.5 mg/kg), or sodium chloride solution. Preterm lambs were delivered at 125 days' gestation and underwent ventilation to assess lung function. Lung gas volume, surfactant concentrations, and inflammation were subsequently evaluated, with data analyzed by analysis of variance. Results: Fetal endotoxin exposure 6 days before delivery increased compliance by 59%, increased lung gas volume 2.3-fold, increased concentrations of surfactant lipids, increased surfactant A and B protein levels, and increased messenger ribonucleic acid expressions for surfactant proteins (all P < .01, vs control group). Betamethasone exposure resulted in less consistent effects. White blood cell counts were increased in fetal membranes and lungs after endotoxin exposure, but there was no severe inflammation. Conclusion: A single fetal exposure to endotoxin resulted in large improvements in postnatal lung function and increases in surfactant concentrations after preterm delivery. These effects were qualitatively larger than those achieved with betamethasone. (Am J Obstet Gynecol 2000;182:401-8.) Author Affiliation: Cincinnati, Ohio, Murfreesboro, Tennessee, Perth, Western Australia, Australia, London, Ontario, Canada, and Oulu, Finland From the Division of Pulmonary Biology, Children's Hospital Medical Center,.sup.a the Department of Obstetrics, Women and Infants Research Foundation, University of Western Australia,.sup.b the Division of Clinical Science, TVW Telethon Institute for Child Health Research, University of Western Australia,.sup.c the Department of Biology, Middle Tennessee State University,.sup.d the Department of Obstetrics and Gynecology, University of Western Ontario,.sup.e and the Department of Pediatrics, Oulu University..sup.f Article History: Received 3 March 1999; Revised 25 June 1999; Accepted 31 August 1999 Article Note: (footnote) [star] Supported by grant HD-12714 from the National Institute of Child Health and Human Development and the Women and Infants Research Foundation, Perth, Western Australia, Australia., [star][star] Reprint requests: Alan H. Jobe, MD, PhD, Children's Hospital Medical Center, Division of Pulmonary Biology, 3333 Burnet Ave, Cincinnati, OH 45229-3039.

Byline: Trish Nicholls, Ilias Nitsos, David W. Walker Keywords: Excitotoxicity; fetus; kynurenine; kynurenic acid; neuroprotection; quinolinic acid; tryptophan; tryptophan 2,3-dioxygenase Abstract: Objective: The effects of a tryptophan load on the plasma concentration of kynurenine, the precursor for the production in the brain of the neuroactive products kynurenic acid and quinolinic acid, were determined in pregnant sheep at midgestation and late gestation and in nonpregnant sheep. Study Design: Pregnant ewes were given an intravenous infusion of 100 mg/kg L -tryptophan during 2 hours at 95 to 98 days' gestation (n = 4) or 135 to 138 days' gestation (n = 10). Nonpregnant ewes (n = 6) were studied in late estrus. Arterial blood samples taken from 2 hours before to 48 hours after the start of the infusion were used for analysis of plasma tryptophan, kynurenine, and cortisol concentrations. Results: Tryptophan loading at both gestational ages resulted in significantly greater increases in kynurenine concentrations in fetal plasma (at 95-98 days' gestation, from 5.7 [+ or -] 1.2 [mu]mol/L [baseline] to 247.9 [+ or -] 86.7 [mu]mol/L (peak); at 135-138 days' gestation, from 9.0 [+ or -] 2.3 [mu]mol/L [baseline] to 289.0 [+ or -] 194.0 [mu]mol/L [peak]) than in maternal plasma [at 95-98 days' gestation, from 4.6 [+ or -] 0.8 [mu]mol/L [baseline] to 118.0 [+ or -] 79.7 [mu]mol/L [peak]; at 135-138 days' gestation, from 4.8 [+ or -] 2.9 [mu]mol/L [baseline] to 98.3 [+ or -] 67.8 [mu]mol/L [peak]). It took longer for kynurenine concentrations to return to basal values in the fetus (24-30 hours) than in the ewe (8-12 hours). The kynurenine responses in pregnant and nonpregnant ewes were not different from each other. Conclusion: The production of kynurenine from tryptophan is significantly greater in the fetal lamb than in the pregnant or nonpregnant adult ewe. (Am J Obstet Gynecol 1999;181:1452-60.) Author Affiliation: Clayton, Victoria, Australia From the Department of Physiology, Monash University Article History: Received 12 February 1999; Revised 10 June 1999; Accepted 18 June 1999 Article Note: (footnote) [star] Supported by a grant from the National Health and Medical Research Council of Australia to D.W.W., [star][star] Reprint requests: David W. Walker, PhD, Department of Physiology, Monash University, Clayton, Victoria, Australia 3168., a 0002-9378/99 $8.00 + 0 6/1/100982

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0002-9378(99)70391-1 Byline: Trish Nicholls, Ilias Nitsos, David W. Walker Keywords: Excitotoxicity; fetus; kynurenine; kynurenic acid; neuroprotection; quinolinic acid; tryptophan; tryptophan 2,3-dioxygenase Abstract: Objective: The effects of a tryptophan load on the plasma concentration of kynurenine, the precursor for the production in the brain of the neuroactive products kynurenic acid and quinolinic acid, were determined in pregnant sheep at midgestation and late gestation and in nonpregnant sheep. Study Design: Pregnant ewes were given an intravenous infusion of 100 mg/kg L -tryptophan during 2 hours at 95 to 98 days' gestation (n = 4) or 135 to 138 days' gestation (n = 10). Nonpregnant ewes (n = 6) were studied in late estrus. Arterial blood samples taken from 2 hours before to 48 hours after the start of the infusion were used for analysis of plasma tryptophan, kynurenine, and cortisol concentrations. Results: Tryptophan loading at both gestational ages resulted in significantly greater increases in kynurenine concentrations in fetal plasma (at 95-98 days' gestation, from 5.7 [+ or -] 1.2 [mu]mol/L [baseline] to 247.9 [+ or -] 86.7 [mu]mol/L (peak); at 135-138 days' gestation, from 9.0 [+ or -] 2.3 [mu]mol/L [baseline] to 289.0 [+ or -] 194.0 [mu]mol/L [peak]) than in maternal plasma [at 95-98 days' gestation, from 4.6 [+ or -] 0.8 [mu]mol/L [baseline] to 118.0 [+ or -] 79.7 [mu]mol/L [peak]; at 135-138 days' gestation, from 4.8 [+ or -] 2.9 [mu]mol/L [baseline] to 98.3 [+ or -] 67.8 [mu]mol/L [peak]). It took longer for kynurenine concentrations to return to basal values in the fetus (24-30 hours) than in the ewe (8-12 hours). The kynurenine responses in pregnant and nonpregnant ewes were not different from each other. Conclusion: The production of kynurenine from tryptophan is significantly greater in the fetal lamb than in the pregnant or nonpregnant adult ewe. (Am J Obstet Gynecol 1999;181:1452-60.) Author Affiliation: Clayton, Victoria, Australia From the Department of Physiology, Monash University Article History: Received 12 February 1999; Revised 10 June 1999; Accepted 18 June 1999 Article Note: (footnote) [star] Supported by a grant from the National Health and Medical Research Council of Australia to D.W.W., [star][star] Reprint requests: David W. Walker, PhD, Department of Physiology, Monash University, Clayton, Victoria, Australia 3168., a 0002-9378/99 $8.00 + 0 6/1/100982

Byline: Stephen T. Vermillion, Roger B. Newman Keywords: Indomethacin; tocolysis; neonatal complications Abstract: Objective: We sought to determine whether indomethacin tocolysis immediately before delivery is associated with any increased complications in neonates delivered between 24 and 32 weeks' gestation. Study Design: We performed a case-control analysis of neonates delivered between 24 and 32 weeks' gestation after maternal indomethacin treatment for preterm labor. All infants were delivered within 48 hours of indomethacin exposure. Seventy-five patients were matched with 150 control subjects in a patient/control ratio of 1:2. Matching variables in order of priority included gestational age at delivery, fetal number, betamethasone exposure >24 hours before delivery, magnesium sulfate use, mode of delivery, infant sex, and race. Data were analyzed by using the Student t test, I.sup.2 analysis, and the Fisher exact test and Yates' correction. Results: The gestational age at delivery (mean [+ or -] SD) was 28.7 [+ or -] 2.3 weeks in the indomethacin group and 28.3 [+ or -] 2.1 weeks for the control subjects. Birth weights (mean [+ or -] SD) were 1121 [+ or -] 243 and 1141 [+ or -] 287 g, respectively. All mothers received both magnesium sulfate and betamethasone before delivery. The median cumulative dose of indomethacin was 225 mg. The median interval from last dose of indomethacin until delivery was 12 hours. There were no significant differences between the groups in the incidence of necrotizing enterocolitis (odds ratio, 1.12; 95% confidence interval, 0.31-3.84), grade III/IV intraventricular hemorrhage (odds ratio, 0.37; 95% confidence interval, 0.10-1.19), patent ductus arteriosus (odds ratio, 0.85; 95% confidence interval, 0.44-1.64), bronchopulmonary dysplasia (odds ratio, 0.97; 95% confidence interval, 0.49-1.91), pulmonary hypertension (odds ratio, 0.49; 95% confidence interval, 0.02-4.80), anuria (odds ration, 1.21; 95% confidence interval, 0.22-6.01), thrombocytopenia (odds ratio, 1.14; 95% confidence interval, 0.53-2.42), sepsis (odds ratio, 1.21; 95% confidence interval, 0.22-6.01), or neonatal death (odds ratio, 1.34; 95% confidence interval, 0.55-3.25). Conclusion: Maternal indomethacin exposure immediately before delivery was not associated with increased neonatal complications for infants delivered between 24 and 32 weeks' gestation. (Am J Obstet Gynecol 1999;181:1083-6.) Author Affiliation: Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Medical University of South Carolina. Charleston, South Carolina Article Note: (footnote) [star] Reprint requests: Stephen T. Vermillion, MD, Department of Obstetrics and Gynecology, Medical University of South Carolina, 96 Jonathan Lucas St, Suite 634, Charleston, SC 29425., [star][star] 0002-9378/99 $8.00 + 0 6/6/100993

Byline: Beverly A. Banks, Avital Cnaan, Mark A. Morgan, Julian T. Parer, Jeffrey D. Merrill, Philip L. Ballard, Roberta A. Ballard Keywords: Antenatal corticosteroids; preterm delivery; lung disease Abstract: Objectives: We sought to examine outcome for premature neonates after multiple courses of antenatal corticosteroids compared with a single course. Study Design: We performed a post hoc nonrandomized analysis on 710 neonates of 25-32 weeks' gestation who were born to mothers enrolled in the North American Thyrotropin-Releasing Hormone Trial and who received 1, 2, or [greater than or equal to]3 courses of antenatal corticosteroids. Results: There was no detectable clinical difference in incidence of respiratory distress syndrome, chronic lung disease, and intraventricular hemorrhage related to courses of antenatal corticosteroids, and outcome was similar for infants delivered at 7-13 days compared with those delivered at 1-6 days after receiving antenatal corticosteroids. Compared with those who received a single course, neonates who received [greater than or equal to]2 courses had lower birth weights (-39 g, P = .02), and those receiving [greater than or equal to]3 courses had increased risk of death (adjusted odds ratio, 2.8; 95% confidence interval, 1.3-5.9; P = .01) and lower levels of plasma cortisol at age 2 hours. Conclusion: In this retrospective analysis multiple courses of antenatal corticosteroids did not improve outcome and were associated with increased mortality, decreased fetal growth, and prolonged adrenal suppression. (Am J Obstet Gynecol 1999;181:709-17.) Author Affiliation: Philadelphia, Pennsylvania, and San Francisco, California Article History: Received 13 October 1998; Revised 4 January 1999; Accepted 8 May 1999 Article Note: (footnote) [star] From the Departments of Pediatrics and Biostatistics, University of Pennsylvania School of Medicine, The Children's Hospital of Philadelphia,a the Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, The Hospital of the University of Pennsylvania,b and the Department of Obstetrics and Gynecology, University of California, San Francisco.c Members of the North American Thyrotropin-Releasing Hormone Study Group are listed at the end of the article., [star][star] Supported by grants RO1-HD29201, MO1-RR00040, MO1-RR0000425, MO1-RR01271 and P50-HL56401 from the National Institutes of Health and by Perinatal Associates, Inc, Hospital for Sick Children, Toronto, and the Children's Hospital of Eastern Ontario Research Institution., a Reprint requests: Roberta A. Ballard, MD, Department of Pediatrics, University of Pennsylvania School of Medicine, The Children's Hospital of Philadelphia, Division of Neonatology, 34th St and Civic Center Blvd, Philadelphia, PA 19104., aa 0002-9378/99 $8.00 + 0 6/1/99917

Byline: William A. Block, Michael L. Draper, James C. Rose, Jeffrey Schwartz Keywords: Fetal development; adrenal gland; steroidogenesis; ovine Abstract: Objective: Adrenal steroidogenesis is important for maturation of fetal organ systems and plays a role in triggering parturition in ovine pregnancies. Studies have suggested a differential increase in baseline cortisol between twin gestations near term. Our aim was to further delineate the mechanisms responsible for the differences between the hypothalamic-pituitary-adrenal axes of twin fetuses in vivo. Study Design: Surgery was performed on pregnant ewes (n = 6) with twin gestations to implant fetal vascular catheters. After recovery but while the subjects were resting, plasma cortisol concentrations were similar in both fetuses. Fetuses received, intravenously, boluses of adrenocorticotropic hormone at 2 doses, and plasma samples were obtained for analysis of the cortisol response. This stimulation by adrenocorticotropic hormone was then repeated in the same fetuses approximately 4 days later, after the increase of resting daily cortisol values in one but not the other fetus. Results: Cortisol responses to adrenocorticotropic hormone before changes in daily resting cortisol concentrations were indistinguishable between twins. However, after separation of daily resting cortisol values, fetuses in group A (elevated resting cortisol concentration) demonstrated a significantly increased response to stimulation by adrenocorticotropic hormone. Conclusion: These results suggest a differential development in response to stimulation by adrenocorticotropic hormone between twin fetuses in vivo as the mechanism responsible for the asynchronous elevation of one twin's resting plasma cortisol concentration. (Am J Obstet Gynecol 1999;181:498-502.) Article History: Received 10 December 1998; Revised 24 February 1999; Accepted 31 March 1999 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, the Department of Physiology and Pharmacology, and the Perinatal Research Laboratories, Wake Forest University School of Medicine., [star][star] Supported by National Institutes of Health grant HD11210-20., a Reprint requests: William A. Block, Jr, MD, Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, East Tennessee State University, Johnson City, TN 37614., aa 0002-9378/99 $8.00 + 0 6/1/98995

Byline: Stephen T. Vermillion, David E. Soper, Jennifer Chasedunn-Roark Keywords: Neonatal sepsis; preterm premature rupture of membranes; betamethasone Abstract: Objective: We sought to determine the effect of antenatal betamethasone exposure on the incidence of early onset neonatal sepsis in patients with preterm premature rupture of membranes. Study Design: We performed a nonconcurrent prospective analysis of infants delivered between 24 and 34 weeks' gestation after preterm premature rupture of membranes. Patients with preterm premature rupture of membranes were categorized into 3 groups on the basis of the following betamethasone exposures: (1) none (control subjects), (2) two 12-mg doses in a 24-hour interval on admission (single course), and (3) weekly administration after the initial single course (multiple courses). All included patients received prophylactic antibiotics for group B streptococci. Discrete data were tested for significance with the I.sup.2 test. Continuous data were tested for significance with an analysis of variance. Multiple logistic regression analysis was performed to determine the confounding effect of the multiple variables that were considered risk factors for early-onset neonatal sepsis. All P values of < .05 were considered significant. Results: Three hundred seventy-four patients with preterm premature rupture of membranes were included, 203 of whom were evaluated in the control group, 99 in the single-course group, and 72 in the group receiving multiple courses of betamethasone. Early-onset neonatal sepsis was significantly associated with multiple courses of corticosteroids (P < .001) and gestational age (P = .002). Multiple courses of antenatal betamethasone were significantly associated with chorioamnionitis (P = .004) and endometritis (P = .004). Single-course corticosteroid administration was not significantly associated with any maternal or neonatal infectious complications. Conclusions: Multiple courses of antenatal betamethasone administered to patients with preterm premature rupture of membranes is associated with an increased risk of early-onset neonatal sepsis development. (Am J Obstet Gynecol 1999;181:320-7.) Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, Medical University of South Carolina., [star][star] Reprint requests: Stephen T. Vermillion, MD, 96 Jonathan Lucas St, Suite 634, Charleston, SC 29425., a 0002-9378/99 $8.00 + 0 6/6/99901

Byline: Leslie Pratt, Ronald R. Magness, Terry Phernetton, Susan K. Hendricks, David H. Abbott, Ian M. Bird Keywords: Corticosteroids; fetal organ maturity; fetal rabbit; pulmonary; respiratory distress syndrome; surfactants Abstract: Objective: The aim of the study was to determine whether reduced birth weight, adrenal suppression, and lung maturation occur in parallel and are cumulative with increasing courses of betamethasone. Study Design: Time-bred rabbits were assigned to a control group or to receive saline solution or 1, 2, or 3 courses of betamethasone (early treatment, beginning day 19). Two additional groups (n = 5 per group) were given 1 or 2 late courses (late treatment). Birth weight, serum cortisol, adrenal 17[alpha]-hydroxylase (P450c17) messenger ribonucleic acid and fetal lung surfactant proteins A and B were quantified on day 27. Results: Fetal weight was inversely proportional to the number of courses, with late treatment having a greater effect. Maternal cortisol and P450c17 levels were progressively suppressed with each early course, but fetal cortisol and P450c17 levels were only suppressed after 3 courses. A single late treatment profoundly suppressed both maternal and fetal cortisol and P450c17 messenger ribonucleic acid levels. In contrast, fetal lung surfactant proteins A and B increased progressively with betamethasone courses, regardless of timing. Conclusions: Time from last injection to delivery determined adrenal suppression, whereas total betamethasone courses determined surfactant protein production. Lower birth weight was dependent on the number of courses and was greater with late treatment. (Am J Obstet Gynecol 1999;180:995-1005.) Author Affiliation: Madison, Wisconsin From the Perinatal Research Labs.sup.a and the Division of Maternal-Fetal Medicine,.sup.b Department of Obstetrics and Gynecology,.sup.c the Department of Meat and Animal Science,.sup.d and the Wisconsin Regional Primate Research Center,.sup.e University of Wisconsin-Madison Article History: Received 22 May 1998; Revised 9 November 1998; Accepted 23 November 1998 Article Note: (footnote) [star] Supported in part by The Wisconsin Perinatal Foundation, Madison, and by grant awards NIH HL49210, NIH HD33255, NIH HL57653, NIH HL56702, AHA(WI) 95-GB-41, and NIH RR00167., [star][star] Reprint requests: Ian M. Bird, PhD, 7E Meriter Hospital, 202 S Park St, Madison, WI 53715., a 0002-9378/99 $8.00 + 0 6/1/96053

Byline: Shelley J. Chapman, John C. Hauth, Sidney F. Bottoms, Jay D. Iams, Baha Sibai, Elizabeth Thom, Atef H. Moawad, Gary R. Thurnau Keywords: Amniotic rupture; corticosteroids; prematurity Abstract: Objective: The aim of the study was to determine the effects of antenatal maternal corticosteroid treatment on selected neonatal outcomes in infants weighing [less than or equal to]1000 g at birth after preterm rupture of membranes. Study Design: In a 1-year (1992-1993) prospective observational study, the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network collected outcome data for 766 infants who did not have a major fetal anomaly and who had a birth weight [less than or equal to]1000 g (378 were born after preterm rupture of membranes). Only fetuses deemed potentially viable by the obstetrician were included in our analysis. Selected neonatal outcomes were compared between mothers who did and did not receive antenatal corticosteroids. Logistic regression variables included birth weight, sex, race, amnionitis, tocolytic therapies, mode of delivery, and surfactant use. Results: Two hundred fourteen of the 378 infants whose mothers had preterm rupture of membranes were deemed potentially viable; 62 of these mothers received antenatal steroids and 152 did not. Groups were similar with respect to gestational age, birth weight, race, amnionitis, and delivery mode. Women who received antenatal steroids were more likely to have received tocolysis (P < .001). Univariate and regression analyses controlling for multiple confounders confirmed no neonatal benefits of maternal corticosteroid use. Conclusions: Corticosteroid treatment in women with preterm rupture of membranes was of no apparent benefit to neonates weighing [less than or equal to]1000 g. (Am J Obstet Gynecol 1999;180:677-82.) Author Affiliation: Birmingham, Alabama From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Alabama at Birmingham,.sup.a and the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network..sup.b A complete list of members of the Network and their institutional affiliations appears at the end of the article Article History: Received 22 April 1998; Revised 14 July 1998; Accepted 22 September 1998 Article Note: (footnote) [star] Supported by the National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network grants HD27869 (University of Alabama at Birmingham), HD27917 (Wayne State University, Detroit), HD27915 (The Ohio State University, Columbus), HD21414 (University of Tennessee, Memphis), HD19897 (The Biostatistics Coordinating Center, George Washington University, Washington, D.C.), HD27861 (University of Chicago), HD27883 (Medical University of South Carolina, Charleston), HD27860 (Bowman Gray School of Medicine, Winston-Salem), HD21434 (University of Southern California, Los Angeles), HD21410 (Magee Women's Hospital, Pittsburgh), HD27889 (University of Oklahoma, Oklahoma City), and HD27905 (University of Cincinnati)., [star][star] Reprint requests: Shelley J. Chapman, MD, University of Alabama at Birmingham, Department of Obstetrics and Gynecology, 618 S 20th St, Room OHB 451, Birmingham, AL 35233-7333., a a Deceased. , aa 6/1/94598

Byline: Bo Hyun Yoon, Roberto Romero, Jong Kwan Jun, Eli Maymon, Ricardo Gomez, Moshe Mazor, Joong Shin Park Keywords: Parturition; cortisol; dehydroepiandrosterone sulfate; interleukin-6; premature rupture of the membranes; prematurity; chorioamnionitis; preterm labor Abstract: Objective: The role of steroid hormones in the control of human parturition has been a subject of debate. Activation of the fetal hypothalamic-pituitary-adrenal axis leading to an increase in plasma cortisol is followed by the onset of parturition in sheep. In contrast, androgens, specifically, dehydroepiandrosterone sulfate, have been implicated in the control of parturition in nonhuman primates. The purpose of this study was to determine the relationship between human fetal plasma cortisol and dehydroepiandrosterone sulfate and the onset of preterm labor in patients with preterm premature rupture of the membranes. Study Design: Fetal blood sampling was performed in 51 patients with preterm premature rupture of membranes who were not in labor on admission. Amniotic fluid was cultured for aerobic and anaerobic bacteria and mycoplasmas. Corticosteroids had not been administered before fetal blood sampling. Cortisol and dehydroepiandrosterone sulfate were measured with sensitive and specific immunoassays. Analysis was conducted with nonparametric statistics and survival analysis. Results: (1) Patients who went into spontaneous labor and delivered within 7 days of cordocentesis had a significantly higher median level of fetal plasma cortisol but not of dehydroepiandrosterone sulfate than those delivered after 7 days (for fetal plasma cortisol: median 8.35 [4.7 to 12.4] [mu]g/dL vs median 4.75 [3.0 to 10.4] [mu]g/dL, P < .0001; for fetal plasma dehydroepiandrosterone sulfate: median 154.4 [8.6 to 333.8] [mu]g/dL vs median 194.6 [96.7 to 402.5] [mu]g/dL, P = .09). (2) The cordocentesis-to-delivery interval was significantly shorter in patients with a fetal plasma cortisol value of [greater than or equal to]7 [mu]g/dL (derived by receiver-operating characteristic curve analysis) than in those with fetal cortisol Author Affiliation: Seoul, Korea Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, College of Medicine, Seoul National University., [star][star] Supported by grant No. 97-04-03-08-01-3 from the Korea Science and Engineering Foundation (KOSEF)., a Drs Romero, Maymon, Gomez, and Mazor have participated as private citizens, not as agents of the US government or any of the universities to which they hold appointments., aa Reprint requests: Bo Hyun Yoon, MD, PhD, Department of Obstetrics and Gynecology, Seoul National University Hospital, Seoul, 110-744, Korea., acents 0002-9378/98 $5.00 + 0 6/6/92970

Byline: Emanuela Marinoni, Claudia Korebrits, Romolo Di Iorio, Ermelando V. Cosmi, John R.G. Challis Keywords: Corticotropin-releasing hormone; pregnancy; placenta; betamethasone Abstract: OBJECTIVE: The objective was to determine the effects of in vivo administration of prenatal betamethasone in patients at 26 to 35 weeks' gestation on corticotropin-releasing hormone concentrations in maternal and fetal plasma and amniotic fluid, and on corticotropin-releasing hormone localization in placenta and fetal membranes. STUDY DESIGN: A total of 49 pregnant women at risk for preterm delivery between 26 and 35 weeks' gestation were studied. Twenty-six patients received betamethasone (12 mg intramuscularly) for stimulation of fetal lung maturity. Cord blood, amniotic fluid, placental tissue, and fetal membranes were obtained from 22 of these patients at delivery by elective cesarean section at 33.8 [+ or -] 2.4 weeks' gestation. In control patients (n = 23) at comparable gestational age, blood samples were taken for hormone analysis (n = 8), and cord blood, amniotic fluid, and tissues were collected at elective cesarean section at 34.1 [+ or -] 2.3 weeks' gestation. Concentrations of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol were determined by radioimmunoassay. Localization of tissue immunoreactive corticotropin-releasing hormone was assessed by immunohistochemistry. RESULTS: Betamethasone caused approximately 90% reduction in maternal cortisol and 50% reduction in maternal plasma adrenocorticotropic hormone. In patients at >30 weeks' gestation, there was a significant increase in maternal plasma corticotropin-releasing hormone concentrations after betamethasone; maternal corticotropin-releasing hormone was not altered significantly in untreated patients. Corticotropin-releasing hormone levels were raised in umbilical cord blood by 48 hours and in amniotic fluid 1 week after betamethasone administration. There was increased immunohistochemical staining for corticotropin-releasing hormone in placental syncytiotrophoblast and in fetal membranes of patients treated with betamethasone. CONCLUSIONS: These studies provide the first evidence for in vivo stimulation of plasma corticotropin-releasing hormone, likely of placental origin, by glucocorticoids in third trimester human pregnancy. The results suggest that increases in endogenous cortisol during normal gestation may contribute to placental corticotropin-releasing hormone output and to the rise in maternal plasma corticotropin-releasing hormone concentrations during late pregnancy. (Am J Obstet Gynecol 1998;178:770-8.) Author Affiliation: Rome, Italy, and Toronto, Ontario, Canada Article History: Received 23 June 1997; Revised 2 September 1997; Accepted 9 October 1997 Article Note: (footnote) [star] From the 2nd Department of Obstetrics and Gynecology, University 'La Sapienza,'a and Departments of Physiology and Obstetrics and Gynecology, University of Toronto.b , [star][star] Supported by the Italian National Council of Research (CNR) and The Medical Research Council of Canada., a Reprint requests: Dr. John R.G. Challis, Department of Physiology, Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8., aa 6/1/86762

Byline: Jeffrey D. Stewart, Christina L. Gonzalez, H.Dix Christensen, William F. Rayburn Keywords: Betamethasone; multidose; dose comparison; growth; development; mouse Abstract: Objective: Our purpose was to determine in a randomized, placebo-controlled manner whether multiple antenatal doses of betamethasone affect long-term growth and development of exposed mouse offspring. Study Design: Sixty pregnant CD-1 mice received either two, four, or eight antepartum doses of 0.1 mg betamethasone or placebo. Perinatal outcomes, growth, and development of the offspring were compared in a blinded manner. Variables were compared by analysis of variance or I.sup.2 testing. Results: Betamethasone-exposed subjects gained less weight during pregnancy and were delivered of fewer live pups, with fewer male survivors and lower birth weights. These trends were dose related. Growth measurements were similar after the neonatal period. No differences in functional development and physical maturation in the offspring were noted. The reproductive capability, perinatal outcomes, and growth and development of the second-generation offspring were unaffected by betamethasone exposure. Conclusion: Multiple antenatal dosings of betamethasone, reaching toxic levels, did not have an impact on the long-term growth and development of the surviving mouse offspring. Author Affiliation: Oklahoma City, Oklahoma Article Note: (footnote) [star] From the Section of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology,a and the Department of Pharmacology and Toxicology,b University of Oklahoma Health Sciences Center., [star][star] Supported by the J.W. Records Perinatal Research Fund., a Reprint requests: Jeffrey D. Stewart, MD, University of Oklahoma Health Science Center, Department of Obstetrics and Gynecology, Section of Maternal-Fetal Medicine, P.O. Box 26901, 4SP710, Oklahoma City, OK 73190., aa 0002-9378/97 $5.00 + 0 6/6/84564

Byline: Michael G. Gravett, George J. Haluska, Michael J. Cooka, Miles J. Novy Keywords: Intrauterine infection; preterm parturition; fetal-placental estrogen biosynthesis Abstract: OBJECTIVE: Our purpose was to describe the temporal and quantitative relationships among intrauterine infection, fetal-placental steroid biosynthesis, and preterm labor in a nonhuman primate model. STUDY DESIGN: On approximately day 130 of gestation (term 167 days) chronically instrumented rhesus monkeys (Macaca mulatta) were infected with 10.sup.6 colony-forming units of group B streptococci either by intraamniotic (n = 4) or choriodecidual (n = 2) inoculation. As controls, four additional chronically instrumented noninfected monkeys were followed up to spontaneous parturition. Amniotic fluid and maternal and fetal arterial blood were serially sampled in all monkeys (both before and after infection) for progesterone, estrone, estradiol, dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, and cortisol by specific radioimmunoassays, and uterine activity was continuously recorded. RESULTS: Spontaneous parturition was preceded by gradual and significant increases in the plasma concentrations of fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione and fetal and maternal levels of estrone, estradiol, and progesterone but not by changes in cortisol. In contrast, infection-associated parturition (either intraamniotic or choriodecidual) was characterized by abrupt increases in fetal dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, progesterone, and cortisol but not by increases in maternal or fetal estrone or estradiol. Infection-associated steroid changes occurred concurrently with or after increases in uterine activity. CONCLUSION: Infection-associated preterm parturition is associated with dramatic increases in fetal adrenal steroid biosynthesis but not by corresponding increases in placental estrogen biosynthesis. This suggests that fetal stress is accompanied by placental dysfunction and that infection-associated parturition is not dependent on the increased estrogen biosynthesis observed in spontaneous parturition. (Am J Obstet Gynecol 1996;174:1725-33.) Author Affiliation: Beaverton and Portland, Oregon Article Note: (footnote) [star] From the Division of Reproductive Sciences, Oregon Regional Primate Research Center,a the Departments of Obstetrics and Gynecology, Legacy Emanuel Hospital and Health Center, b and the Department of Obstetrics and Gynecology, Oregon Health Sciences University. c , [star][star] Supported by National Institutes of Health grants No. RR00163, RR05412, HD-06159, and HD-18185., a Reprint requests: Michael G. Gravett, MD, Department of Obstetrics and Gynecology, Legacy Emanuel Hospital, 2801 N. Gantenbein Ave., Portland, OR 97227., aa 0002-9378/96 $5.00 + 0 6/6/72174

Byline: C.R. Parker, M.W. Atkinson, J. Owen, W.W. Andrews Keywords: Betamethasone; fetal adrenal; steroid; cortisol; dehydroepiandrosterone sulfate; cholesterol; apolipoprotein B; pregnancy; fetal lung maturation Abstract: OBJECTIVE: Prior studies suggest that fetal plasma cholesterol is regulated in part by the rate of uptake and utilization of low-density lipoprotein cholesterol by the fetal adrenals for use in steroid biosynthesis. Direct evidence for this phenomenon and the kinetics of this process is, however, virtually impossible to obtain in a controlled experiment in the developing human. In the current study we sought to take advantage of the anticipated transient inhibition of the hypothalamic-pituitary-adrenal axis that occurs after antenatal therapy with glucocorticosteroids, to evaluate the temporal relationship between fetal adrenal steroids and plasma lipoprotein cholesterol levels in umbilical cord blood at delivery. STUDY DESIGN: Umbilical cord serum was obtained at delivery from 136 infants (30.5 [+ or -] 2.7 weeks' gestation) who previously had been treated in utero with betamethasone, 12 mg per 12 or 24 hours for one or two doses and from 308 preterm infants (30.5 [+ or -] 2.1 weeks) who had not been exposed to such therapy. We quantified the concentrations of dehydroepiandrosterone sulfate and cortisol as representative fetal adrenal steroids and also measured the total cholesterol and apolipoprotein B; the relationship between the steroids and lipids as a function of the interval between initial treatment and delivery was analyzed. RESULTS: Umbilical cord levels of dehydroepiandrosterone sulfate and cortisol were significantly reduced within the first 24 hours after initial treatment and remained significantly lower than in control infants through 4 days after initial treatment. In contrast, serum levels of cholesterol were significantly increased 3 to 4 days after treatment but fell on day 5. Serum levels of apolipoprotein B generally followed the same pattern as cholesterol. Cholesterol levels also were higher than normal in infants delivered >1 week after initial betamethasone treatment. CONCLUSIONS: The results of this study are consistent with the view that the plasma cholesterol pool in the fetus is regulated, at least in part, by the rate of uptake of low-density lipoprotein cholesterol and utilization by the fetal adrenals as substrate for steroidogenesis. Betamethasone also may influence cholesterol and lipoprotein synthesis in the fetus. (AM J OBSTET GYNECOL 1996;174:562-5.) Author Affiliation: Birmingham, Alabama Article History: Received 3 March 1995; Revised 27 April 1995; Accepted 5 June 1995 Article Note: (footnote) [star] From the Department of Obstetrics and Gynecology, University of Alabama at Birmingham., [star][star] Supported by National Institutes of Health grant No. HD 22969., a Reprint requests: C. Richard Parker, Jr., PhD, Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35233-7333., aa 0002-9378/96 $5.00 + 0 6/1/66854

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2010.06.011 Byline: Alexandre Hertig (a)(d), Philippe Liere (e), Nathalie Chabbert-Buffet (c)(d), Julie Fort (g), Antoine Pianos (e), Bernard Eychenne (e), Annie Cambourg (e), Michael Schumacher (e), Nadia Berkane (c), Guillaume Lefevre (b), Serge Uzan (c)(d), Eric Rondeau (a)(d), Patrick Rozenberg (g), Marie-Edith Rafestin-Oblin (f) Keywords: aromatase; estradiol; preeclampsia; 2-methoxyoestradiol Abstract: Experimental data have revealed the critical role played by 2-methoxy-estradiol, a metabolite of 17[beta]-estradiol, in the pathophysiology of preeclampsia. We used gas chromatography/mass spectrometry to measure a whole panel of hormonal steroids in the plasma from women during the third trimester of their pregnancy. Author Affiliation: (a) APHP, Urgences Nephrologiques et Transplantation Renale and Inserm U702, HA[acute accent]pital Tenon, Paris, France (b) Service de Biochimie et Hormonologie, HA[acute accent]pital Tenon, Paris, France (c) Service d'Obstetrique et Gynecologie, HA[acute accent]pital Tenon, Paris, France (d) UPMC, Universite Paris 6, Paris, France (e) UMR788 Inserm-University Paris-Sud XI, Universite Paris XI, Paris, France (f) Inserm U773, Centre de Recherche Biomedicale Bichat-Beaujon, Paris, France (g) Service d'Obstetrique et Gynecologie, HA[acute accent]pital de Poissy, Poissy, France Article History: Received 3 December 2009; Revised 19 March 2010; Accepted 8 June 2010 Article Note: (footnote) Cite this article as: Hertig A, Liere P, Chabbert-Buffet N, et al. Steroid profiling in preeclamptic women: evidence for aromatase deficiency. Am J Obstet Gynecol 2010;203:477.e1-9. , This work was supported by INSERM and by the European Section of the Aldosterone Council (ESAC). Dr Rafestin-Oblin received an Interface INSERM AP-HP fellowship. Dr Hertig had full access to all data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis., Reprints not available from the authors., Drs Hertig and Liere contributed equally to this work.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2009.10.859 Byline: Jason N. Hashima (a), Yinglei Lai (b), Ronald J. Wapner (c), Yoram Sorokin (d), Donald J. Dudley (e), Alan Peaceman (f), Catherine Y. Spong (g), Jay D. Iams (h), Kenneth J. Leveno (i), Margaret Harper (j), Steve N. Caritis (k), Michael Varner (l), Menachem Miodovnik (m), Brian M. Mercer (n), John M. Thorp (o), Mary J. O'Sullivan (p), Susan M. Ramin (q), Marshall Carpenter (r), Dwight J. Rouse (s), Baha Sibai (t) Keywords: antenatal corticosteroids; BMI; neonatal morbidity; obesity; prematurity Abstract: The aim of this study was to determine the effect of maternal body mass index on the incidence of neonatal prematurity morbidities in those who receive corticosteroids. Author Affiliation: (a) Departments of Obstetrics and Gynecology, Oregon Health & Science University, Portland, OR (b) The George Washington University Biostatistics Center, Washington, DC (c) Drexel University, Philadelphia, PA (d) Wayne State University, Detroit, MI (e) University of Utah, Salt Lake City, UT (f) Northwestern University, Chicago, IL (g) Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD (h) Ohio State University, Columbus, OH (i) University of Texas Southwestern Medical Center, Dallas, TX (j) Wake Forest University Health Sciences, Winston-Salem, NC (k) University of Pittsburgh, Pittsburgh, PA (l) University of Utah, Salt Lake City, UT (m) Columbia University, New York, NY, and University of Cincinnati, Cincinnati, OH (n) Case Western Reserve University, Cleveland, OH (o) University of North Carolina at Chapel Hill, Chapel Hill, NC (p) University of Miami, Miami, FL (q) The University of Texas Health Science Center at Houston, Houston, TX (r) Brown University, Providence, RI (s) University of Alabama at Birmingham, Birmingham, AL (t) University of Tennessee, Memphis, TN Article History: Received 28 May 2009; Revised 24 July 2009; Accepted 16 October 2009 Article Note: (footnote) This study was supported by Grants (HD21410, HD21414, HD27869, HD27917, HD27905, HD27860, HD27861, HD27915, HD34122, HD34116, HD34208, HD34136, HD40500, HD40485, HD40544, HD40545, HD40560, HD40512, HD40485, HD36801) from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and Grant M01-RR-000080 from the National Center for Research Resources., Besides the authors, the following members contributed to the protocol development and coordination between clinical research centers (Michelle DiVito, RN; Francee Johnson, RN, BSN), protocol/data management and statistical analysis (Elizabeth Thom, PhD; Lisa Mele, ScM), and guidance and mentorship (Jorge Tolosa, MD, MCSE). Additional members of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network are listed at the end of this article., Cite this article as: Hashima JN, Lai Y, Wapner RJ, et al, for the Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. The effect of maternal body mass index on neonatal outcome in women receiving a single course of antenatal corticosteroids. Am J Obstet Gynecol 2010;202:263.e1-5.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2009.09.033 Byline: Matthias Loehle (a), Matthias Schwab (a), Susan Kadner (b), Kristal M. Maner (c), Jeffrey S. Gilbert (d), J. Thomas Brenna (c), Stephen P. Ford (e), Peter W. Nathanielsz (d), Mark J. Nijland (d) Keywords: antenatal glucocorticoids; glucocorticoid formulation; lung maturation Abstract: Glucocorticoid administration to women in preterm labor improves neonatal mortality and morbidity. Fetal exposure to glucocorticoid levels higher than those appropriate to the current gestational stage has multiple organ system effects. Some, eg, fetal hypertension, are maximal at lower than the clinical dose. We hypothesized that the clinical dose has supramaximal lung maturational effects. Author Affiliation: (a) Department of Neurology, University of Jena, Jena, Germany (b) Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY (c) Division of Nutritional Sciences, Cornell University, Ithaca, NY (d) Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, TX (e) Department of Animal Science, University of Wyoming, Laramie, WY Article History: Received 14 January 2009; Revised 11 June 2009; Accepted 28 September 2009 Article Note: (footnote) This study was supported by Grant NIH Heart Lung Blood Institute 068649, NHLBI, NIH, HHS., Reprints not available from the authors., Cite this article as: Loehle M, Schwab M, Kadner S, et al. Dose-response effects of betamethasone on maturation of the fetal sheep lung. Am J Obstet Gynecol 2010;202:186.e1-7.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2008.02.047 Byline: Emanuela Marinoni (a), Claudio Letizia (c), Francesca Ciardo (b), Giovanna Corona (b), Massimo Moscarini (b), Romolo Di Iorio (b) Keywords: adiponectin; fetus; glucocorticoids; leptin; pregnancy Abstract: The aim of this study was to determine the effects of in vivo administration of prenatal betamethasone on leptin and adiponectin concentration in maternal and fetal circulation. Author Affiliation: (a) Centre for Scientific Research, San Pietro Hospital, Fatebenefratelli, Rome, Italy (b) Department of Gynecology, Perinatology, and Child Health, School of Medicine, University 'La Sapienza,' Rome, Italy (c) Department of Clinical Sciences, School of Medicine, University 'La Sapienza,' Rome, Italy. Article History: Received 5 June 2007; Revised 22 February 2008; Accepted 25 February 2008 Article Note: (footnote) Cite this article as: Marinoni E, Letizia C, Ciardo F, et al. Effects of prenatal betamethasone administration on leptin and adiponectin concentrations in maternal and fetal circulation. Am J Obstet Gynecol 2008;199:141.e1-141.e6.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2007.05.008 Byline: Jeremy McCallum (a), Norman Smith (b), James N. MacLachlan (a), Turhan Coksaygan (c), Matthias Schwab (d), Peter Nathanielsz (c), Bryan S. Richardson (a) Keywords: antenatal glucocorticoid; fetal cerebral protein synthesis Abstract: Although antenatal glucocorticoids have well-known benefits for infants who are born preterm by the enhancement of pulmonary maturation, adverse effects on brain growth and development have been reported in several animal-based studies. We have used the chronically catheterized ovine fetus to determine the effects of synthetic glucocorticoids that are administered at doses used clinically on cerebral protein synthesis during early brain development using [.sup.13C]-leucine tracer method. Author Affiliation: (a) Departments of Obstetrics and Gynecology and of Physiology and Pharmacology; Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada (b) Department of Biochemistry; Schulich School of Medicine & Dentistry, University of Western Ontario, London, ON, Canada (c) Center for Pregnancy and Newborn Research, University of Texas Health Science Center at San Antonio, San Antonio, TX (d) Department of Neurology, Friedrich Schiller University School of Medicine, Jena, Germany. Article History: Received 24 November 2006; Accepted 1 May 2007 Article Note: (footnote) Supported by grants from the Canadian Institutes of Health Research (B.S.R.), the Max Kade Foundation (M.S.), and National Heart, Lung, and Blood Institute grant HL 68649 (P.N.). Dr Richardson is a recipient of the Wyeth Clinical Research Chair for Women's Health in Perinatology. Cite this article as: McCallum J, Smith N, MacLachlan JN, et al. Effects of antenatal glucocorticoids on cerebral protein synthesis in the preterm ovine fetus. Am J Obstet Gynecol 2008;198:103.e1-103.e6.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2007.06.041 Byline: Joram Sawady (a), Brian M. Mercer (a), Ronald J. Wapner (b), Yuan Zhao (c), Yoram Sorokin (d), Francee Johnson (e), Donald J. Dudley (f), Catherine Y. Spong (g), Alan M. Peaceman (h), Kenneth J. Leveno (i), Margaret Harper (j), Steve N. Caritis (k), Menachem Miodovnik (l), John M. Thorp (m), Susan Ramin (n), Marshall W. Carpenter (o), Dwight J. Rouse (p) Keywords: antenatal corticosteroid; histopathologic finding; placenta; preterm birth Abstract: In utero exposure to repeated doses of antenatal corticosteroids (ACSs) has been shown to reduce fetal growth. Our goal was to evaluate whether weekly betamethasone (R-ACS) alters placental growth and histologic findings. Author Affiliation: (a) Departments of Pathology and Obstetrics and Gynecology, Metro Health Medical Center, Case Western Reserve University, Cleveland, OH (b) Department of Obstetrics and Gynecology, Drexel University College of Medicine, Philadelphia, PA (c) Biostatistics Center, George Washington University, Rockville, MD (d) Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI (e) Ohio State University, Columbus, OH (f) University of Utah, Salt Lake City, UT (g) National Institute of Child Health and Human Development, Bethesda, MD (h) Departments of Obstetrics and Gynecology, Northwestern University, Chicago, IL (i) University of Texas Southwestern Medical Center, Dallas, TX (j) Wake Forest University School of Medicine, Winston-Salem, NC (k) Magee Women's Hospital, Pittsburgh, PA (l) Columbia University, New York, NY (m) University of North Carolina Chapel Hill, Chapel Hill, NC (n) University of Texas Houston, Houston, TX (o) Brown University, Providence, RI (p) University of Alabama, Birmingham, AL. Article History: Received 12 March 2007; Revised 4 May 2007; Accepted 24 June 2007 Article Note: (footnote) Supported by grants from the National Institute of Child Health and Human Development (HD21410, HD21414, HD27869, HD27917,HD27905, HD27860, HD27861, HD27915, HD34122, HD34116, HD34208, HD34136, HD40500, HD40485, HD40544, HD40545, HD40560, HD40512, HD36801) and by grant M01 RR000080 from the National Center for Research Resources, a component of the National Institutes of Health. The contents of this article are solely the responsibility of the authors and do not necessarily represent the official view of National Center for Research Resources or National Institutes of Health. Reprints not available from the authors. Cite this article as: Sawady J, Mercer B, Wapner RJ, et al. The National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network BEARS study: impact of repeated doses of antenatal corticosteroids on placental growth and histologic condition. Am J Obstet Gynecol 2007;197:281.e1-281.e8.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ajog.2006.12.018 Byline: Allison M. Ring (1), Jeffery S. Garland (2), Brian R. Stafeil (1), Margaret H. Carr (3), Gail S. Peckman (3), Richard A. Pircon (3) Keywords: antenatal steroid; latency; neonatal morbidity; premature Abstract: This study was undertaken to determine whether the neonatal benefit of a single complete course of antenatal corticosteroids diminishes when delivery is remote from administration (>14 days). Author Affiliation: (1) Department of Obstetrics and Gynecology, Medical College of Wisconsin Affiliated Hospitals, St. Joseph Regional Medical Center, Milwaukee, WI (2) Department of Pediatrics, St. Joseph Regional Medical Center, Milwaukee, WI (3) Center for Obstetrical Research and Education, St. Joseph Regional Medical Center, Milwaukee, WI. Article Note: (footnote) Cite this article as: Ring AM, Garland JS, Stafeil BR, et al. The effect of a prolonged time interval between antenatal corticosteroid administration and delivery on outcomes in preterm neonates: a cohort study. Am J Obstet Gynecol 2007;196:457.e1-457.e6. Reprints not available from the authors.

Byline: Sarah L. Berga Keywords: Diabetes; insulin resistance; polycystic ovary syndrome Abstract: Women with polycystic ovary syndrome come to the gynecologist with a variety of symptoms, including menstrual irregularities, hirsutism, acne, weight gain, obesity, and infertility. An accurate diagnosis requires both confirmation of signs and symptoms of polycystic ovary syndrome and exclusion of other disorders. Once the diagnosis of polycystic ovary syndrome has been established, the presence of concomitant conditions, such as hypertension, dyslipidemia, and diabetes, must be assessed. Because the cause of polycystic ovary syndrome is not clear, treatment options have focused on symptom management. Such treatment options include oral contraceptives, gonadotropin-releasing hormone analogs with 'add-back' hormone regimens, antiandrogens, ovulation-inducing agents, electrolysis, nutritional and weight loss counseling, exercise, laparoscopic ovarian drilling, and glucocorticoids. Pathogenic considerations, risk factor assessments, and treatment objectives combine to determine the choice of therapies. It is not clear whether insulin resistance is clinically important or causal in polycystic ovary syndrome symptom complex in all affected women. Polycystic ovary syndrome may be the final common expression of a variety of metabolic or neuroendocrine perturbations. If insulin resistance is a universal feature, it would make sense to treat with an insulin-sensitizing agent in the expectation that symptoms would resolve or improve. If insulin resistance is not the main etiologic factor, however, then insulin-sensitizing agents would be useful as adjunctive agents only for women with clinically important insulin resistance (eg, patients with polycystic ovary syndrome in whom insulin resistance causes hyperglycemia). In such cases an insulin-sensitizing agent could be instituted along with a program of weight loss and exercise. (Am J Obstet Gynecol 1998;179:S109-13.) Author Affiliation: Division of Reproductive Endocrinology, Department of Obstetrics, Gynecology, and Reproductive Sciences, The University of Pittsburgh, Magee-Womens Hospital. Pittsburgh, Pennsylvania Article Note: (footnote) [star] Reprint requests: Sarah L. Berga, MD, The University of Pittsburgh School of Medicine, Magee-Womens Hospital, 300 Halket St, Pittsburgh, PA 15213., [star][star] 0002-9378/98 $5.00 + 0 6/0/94972