Embed Size (px)
388 SPO Abstracts
514 URINARY EXCRETION (UE) OF IETA2 MICROGLOIULIN (12M) DURING PREGNANCY. sa Lew', P Tsung', 0 Drell",~, Depts Med & OB/GYN, Geo Washington U, Washington, DC, and Depts OB/GYN, Molecular Biology & Genetics, Hutzel Hosp/Wayne State Umv, Detroit, MI.
B2M, a protein non-covalently linked to cellular class major histocompatibility antigens, necessary for cell-cell recognition, is present on all nucleated cell membranes_ It has a molecular weight of 11 ,800 daltons. Non-cell associated B2M is freely filtered by the glomerulus, and reabsorbed by the proximal tubule. Normal UE 82M is <370 ~gl24 hr & serum B2M level is between 1 to 2 mglL. The aim of this study was to determine UE B2M (~gl24 hr by ELISA) & creatinine clearance (CrCI) (mllminll.73m2) in normal ambulatory pregnant females. Resu~s (mean.:t. SO):
1.40 of preg 4 5 6 7 8 9 n 3 2 3 3 5 7 CrCI 122.±12 104±16 141j:19 134t44 104t25 92t24 UE 82M 142t48 14Ot50 334t89 432t289 771t552 1146tl071 UE 82M/CrCI 1.2 1.4 2.4' 3.2' 7.4' 12.5' 'Signijicant increase (t test, p<O.OI)
No patient had abnormal urinary protein excretion. Serum B2M measured In 9 SUbjects was normal to slightly elevated. FI~ered load of B2M rose throughout the course of pregnancy in association with Increased UE B2M beginning in the 6th month. These data suggest increased fetal and/or maternal B2M production dUring pregnancy. Increased UE B2M tends to preserve Circulating values near the normal range. The proximal tubule may play an important role in modulating renal B2M handling and thereby maintaining serum B2M levels in near normal range during pregnancy.
515 ARTERIAL ffiESSURE RESroNSE 'IO MAXIMAL ISCJo!EI'RIC EXERCISE rn PREX:;NANI' ~.
Fred K. IptgerinqX, Akkeliene van den 13er1j', Piet C. StnIykx , Henk C.S. Wallenburg. Dept. Ob/Gyn, Erasmus university School of Medicine am Health Sciences, Rotterdam, '!he Netherlarrls
We studied the arterial pressure response to maximal leg exercise in 15 healthy volunteers at 29 am 35 weeks' pregnancy, am 8 weeks postpartum. Restim arterial pressure at 35 weeks' gestation was silllilar to the postpartum control value of 88. 2±2. 2 IIIlI Hg, rut it was reduced by 7% at 29 weeks' gestation. Voluntary rnaxilnal effort averaged 2381±139 N in the postpartum period, was silllilar at 29 weeks', am was reduced by 10% at 35 weeks' gestation. Mean arterial pressure sha.red a linear increase with force to an average rnaxintum value of 128.9±4.0 IIIlI Hg, or 46% above the restim value in the postpartum period. '!he pressure response was unaffected by gestation, despite the pregnancy-associated reduction in blood pressure am vascular resistance at rest. It seems likely that local denmx:l or lt1.lSCle ischerni.a governs the exercise pressor reflex also durim· pregnancy.
Januar) 199 1 Am J Ob"Cl Gynecol
516 THE INFLUENCE OF MATERNAL WEIGHT GAIN ON TWIN BIRTHIIEIGHT Zoe A. Tllton,MD, MS. MPH', Cathryn M. Dee', Sally A. Ledennanx, PhD'. Department of Obstetrics & Gynecology, Sloane Hospital for Women, the Institute of Human Nutrition and the School of PubliC Health, Col umbi a Presbyteri an Medi ca 1 Center, New York, NY
The Importance of maternal factors to birthwelght has been well-documented in Singleton pregnancies, With prenatal welght gain haVing the largest Single impact. Much less IS known about determinants of birthwelght in tWins . The effect of prenatal weight gain and other maternal factors on tWln blrthwelght was studied by a 5-year retrospectIVe chart review of 360 tWin deliveries between January, 1985, and December, 1989. Patients were di vi ded 1 nto outcome groups as follows: Group 1: deli very at ! 37 weeks and blrthwel ght of both twi ns ! 2500 grams, and Group 2: dell very at < 37 weeks or blrthwel ght < 2500 grams for at least one twin. Our results showed that the mean weight gain per week over the durat i on of pregnancy was SI gni fi cant 1 y hi gher for Group 1 (1.15 lb/wk) vs. Group 2 (0.86 lb/wk, p<0.05). There was no dl fference in hel ght or prepregnant wei ght between the two groups. The study population was 34% White, 27% Black, and 35% HispaniC. Only 33% of Black mothers were In Group I, compared to 50% of both Whi tes and HI spani cs. By chi -square anal ys 1 s, there were Sl gni fi cantl y fewer prlmi parous women, smokers and drug users in Group 1 as compared to Group 2 (p<0 . 05). Comparing only those dellveries occurring at ~ 37 weeks, mean total pregnancy weight gain was significantly higher for mothers whose neonates both weighed at least 2500 grams, as compared to mothers who had one or more neonates wei ghi ng < 2500 grams (45 1 b vs. 36 1 b; p<0 . 05). lie conclude that prenatal weight gain IS a Significant factor Influencing birthwelght in tWins. Maternal factors Including ethnicity, parity, and substance abuse had a smaller but important influence on twin blrthweight.
517 MIDPREGNANCY SERUM THROMBOXANE B2 LEVELS AND SUBSEQUENT PREECLAMPSIA IN NULLIPARAS. JC Hauth, RL Copperx, M Dubardx , RL Goldenberg, CR Parker Jrx_ Division of Maternal-Fetal Med_, University of Alabama at Birmingham, Alabama
A predominance of thrornboxane B2 (TBX 2 )
compared to 6-ketoprostaglandin F ~a. has been found in the plasma of women with preeclampsia_ Moreover, the daily prophylactic treatment of nulliparous women with 60 mg of acetylsalicylate has significantly decreased plasma levels of the vasoconstrictor metabolite TBX2 as compared to the vasodilator metabolite 6-keto PGF ~a. and significantly decreased the incidence of preeclampsia_ However, the relationship of midpregnancy levels of these vasoactive prostanoids and the subsequent development of preecla~psia is not known. We measured serum TBX 2 levels at midpregnancy in 100 healthy nulliparous women. Six of 56 women with a TBX 2 level ~ 6400 pg/ml subsequently developed preeclampsia (2 severe, 4 mild). None of the 41 women with a TBX 2 level < 6400 pg/ ml developed preeclampsla (p=_032) . Other outcomes in these 100 women were similar: gestational age at delivery (39 weeks), median birthweight (3195 vs. 3220 gm) and the incidence of pre term delivery (10% vs _ 12%), Our data provides further confirmation regarding the role of the vasoconstrictor thrornboxane A2 in the pathophysiology of preeclampsia.