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SPO Abstracts
January 1992 Am J Ohstet Gynecol
THE PRODUCTION OF INSULIN-LIKE GROWTH FACTORS (IGF) I AND II IN HUMAN PREGNANCY. !!........Ji... WinnE M.D., W.H. Daughaday, M.D. X (*), B. X Travedi, M.S. (*). Div. of Maternal-Fetal Medicine, St. Louis U. and Div. of Metabolism (*), washington U., st. Louis, MO. While it well-established that the insulin-like growth factors play an important role in post~atal growth, the impact of these substances on fetal growth remains to be determined. In this study, we measured the concentrations of the Pro-IGF-II E 1-21, IGFII, and IGF-I in the maternal serum (MS), the umbilical cord serum (CS) and the amniotic fluid (AF) during the third trimester of pregnancy. The IGFs and Pro-IGF-II E 1-21 were measured using the radioimmunoassay (RIA) after acid-acetone extraction. PRO-IGF-II IGF-II IGF-I (Mean ± SD) (Mean ± SD) (Mean ± SD) MS 120 ± 38 824 ± 550 560 ± 171 CS 232 ± 48 292 ± 46 126 + 31 AF 933 ± 67 1280 ± 290 78 ~ 16 Conclusions: 1) The AF concentrations of both Pro-IGF-II and IGF-II are significantly higher than the paired CS concentrations; 2) The concentrations of both Pro-IGF-II and IGF-II are significantly higher than those of IGF-I in both es and AF; 3) There is no correlation between maternal levels of IGFs and those in the AF or es. Speculations: 1) The production of IGFs in the fetal compartments does not appear to depend on maternal IGFs; 2) IGF-II may play a more important role than IGF-I in modulating fetal growth.
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ELEVATED LEVELS OF MSAFP & cICAM·l IN AMNIOTIC FLUID AT 16 WEEKS MAY MARK EARLY INTRAUTERINE INFLAMMATION. CM Salaliax, CAVogel X ,JP ezzu!!o', M LentnerX E Maino~ix, JPBurnsx, EPhillipsonx,RRothlein X G Foye, L Silberman x DeptLab Med+ ObiGyn Danbury Hosp~al CT, Boehringer·lngleheim Corp CT, Dept OblGynHartford Hospital CT, TAC, Rhode Island Hosp~al, RI. Elevated MSAFP concentrations ([eMSAFP]) in mid trimester are associated with increased risk of poor outcome for the structura!!y normal fetus. We previously identified an increased incidence of chronic placental inflammation (vi!!itis) in cases of growth retardation associated with midtrimester [eMSAFP). The hypothesis that chronic intrauterine inflammation is also present in the midtrimester was tested by assaying amniotic fluid (AF) for the circulating form of interce!!ular adhesion molecule·l (c!CAM·l), a marker of inflammatory responses demonstrated in increased serum levels in the presence of hepatic and cardiac a!!ograft rejection. 40 patients had amniocentesis at IS-17 weeks for maternal age/anxiety with normal [MSAFP). 20 patients had amniocentesis at IS-17 weeks for evaluation of [eMSAFP) (>2.0 corrected MOM). cICAM-l assays were performed by ELISA. Nonparametric testing of data gave the fo!!owing results (mean +/- SE). AF.[cICAM·l1, normal [MSAFPl = 36.8 pg/ml +/·8.0. AF.cICAM·l),[eMSAFP) =132.6 pg/ml +/. 33 (p
355
RELATIONSHIP OF AMNIOTIC FLUID C·PEPTIDE LEVELS TO NEONATAL BODY COMPOSITION M.A..~, P.M. Catalano, R.J.Kehl, A.ThomasX, MetroHeakh Medical
Center, Case Western Reserve University. Cleveland, Ohio. Amniolic fluid C-peptide levels have been previously shown to correlate with birth weighl in diabelic pregnancies. It has been suggested Ihat insulin acts as a felal growth hormone and Ihat amniotic fluid C-peplide levels correlate with felal insulin production. The purpose of this study was 10 examine whether amniotic fluid C-peptide levels have a stronger correlalion with neonatal body composition as compared with 10lal birthweighl. We hypothesized Ihal felal insulin production as reflected by amniotic fluid C-peplide would more dosely correlate with felal fal depOSition. In order 10 obtain a sample with a wide range of felal fat mass 13 women with singleton pregnancies consisting of 9 diabetics (Class A1·2, A2·5, B·l, 0·1) and 4 women with normal glucose screening underwent amniocentesis after an overnight fast within one week of delivery. Gestational age range was 37-40 weeks. 3 infants were LGA, 10 AGA, and 1 SGA by normative birthweight data for our institution. C·peptide was measured by RIA. Neonatal body composition was analyzed within 24 hours of delivery with anthropometric measurements. For the total group there was a significant correlation between C·peptide and fat mass (r=.58, p=.038) and % fat mass (r= .59, p=.035) but not with total weight (r=.30) or lean mass (r= .11). The SGA infant (from an AI) had the lowest % fat mass and was clinica!!y growth retarded. Removing it from the analysis strengthened the correlation of C·peptide with fat mass (r= .68, p=.014) and % fat mass (r=.69, p=.014) but not with total weight or lean mass. These data suggest that the level of fetal insulin production affects fetal growth primarily through body fat when adequate substrate is available and that continuation of this study is warranted to determine if this relationship holds for subgroups based on diabetic status and weight for gestational age. Supported by NIH RR·00210 and 22965
CALCIUM METABOLISM IN PREGNANTWOMEN RECEMNG
CHRONIC MAGNESIUM THERAPY FOR PRETERM LABOR. L G Smijh Jr R J. SchanillfX. P. Bumsx, USOAIARS Children's Nutr. Res. Qr. and Dept. QhlGyn. Baylor Coil. Med .• Houston. lX. Because short·term MgS04 affects calcium metabolism in pregnant women , we hypothesized that Iong·term use of MgS04 would affect mineral homeostasis and bone mineralization adversely. We studied 22 women receiving long-term MgS04 (duration 8 to 66 d. average daily dose 52 ± 10 g1d. mean ± SO) as therapy for preterm labor. A control population (1I-31) also requiring a similar degree and duration of strict bedrest for obstetrical indications were enrolled and matched for age (30 ± 3 wk) and delivery (33 ± 4 wk). Weekly serum and urine measurements were obtained for 4 wi\. The groups had similar serum concentrations of albumin. osteoca!cin. and v~amin 0 metabolHes and urinary excretion of creatinine. phosphorus. and zinc. The following indices differed from the baseline (in the MgS04 group). did not fluctuate during the study interval. and remained signifICantly different between the two groups:
&li[agg llilu.
Serum Mg(mgldl} Serum Ca (mgidl) Serum PTH (pmoIII) Urine Mg (mgl24-h) Urine Ca (mg/24-h)
J.tgSQJ 5.2 ± 1.1 7.0±0.5 SO± 16 245±96 844 ± 313
~ 1.8 ± 0.2 8.3 ± 0.4 48±S 94±S7 342 ± 145
R
«l.001 «l.001 .0.001 «l.001 «l.001
There were no differences in bone mineral content at delivery. Our data suggest that perturbations in calcium metabolism do not adapt to long-term MgS04 therapy and that large urinary losses 01 Ca are a concern.