437 GLYCEMIC CONTROL AND BIRTH PERCENTILE: TARGETED THRESHOLDS THATMINIMIZE SHOULDER DYSTOCIA IN DIABETES IN PREGNANCY ODED LANGER1,BARAK ROSENN2, LOIS BRUSTMAN3, 1St. Luke’s Roosevelt Hospital Center,Obstetrics and Gynecology, New York, New York, 2St. Luke’s RooseveltHospital Center, Obstetrics & MFM, New York, New York, 3St. Luke’sRoosevelt Hospital Center, Obstetrics & Gynecology, New York, New York

OBJECTIVE: If the factors contributing to shoulder dystocia could bemodified, it could result in decreased rate and prevention. We sought toinvestigate the relationship between levels of glycemia, birth percentiles andthe occurrence of shoulder dystocia.

STUDY DESIGN: Diabetic subjects using memory-based self monitoringblood glucose were treated with diet or insulin. The rate of SHD in each meanblood glucose and birth percentile categories was calculated. Mean bloodglucose categories: low-90, 91-100, 101-110, 111-high mg/dl; birth percentiles:low-49, 50-69, 70-89, 90-high. Variables identified in the univariant analysis asbeing significant or borderline significant were included in multiple variablelogistic regression analysis.

RESULTS: The overall incidence of SD was 6.7% in the GDM group(82/1215) and PGDM 6.0% (35/545). For GDM subjects: (1.) a continuousincrease in the rate of SHD for the first 3 categories of mean blood glucose(1.9, 4.7, 7.8 percent, p=0.05) and similar rate between the third and fourthglucose categories (7.8 vs. 8.7%) (2.) SHD in the low-49 birth percentile was0.5%; 50-69, 70-89 and 90-high categories was 1.3, 3.9 and 14%, respectively,p=0.0000). In PGDM: (1.) a 4-fold higher rate of SHD was found above thefirst 2 glucose categories (3.0 vs. 12%). (2.) No SHD in the low-49 birthpercentile; in the 50-69, 1.7% and in the 70-89, 8.7%, and in the 90-high,18.2%, p=0.0000). For GDM and PGDM, logistic regression with adjustmentfor confounding effects found mean blood glucose, parity, birth percentile andinstrumental delivery significant contributors to SHD. Obesity, previousGDM, previous macrosomia, weight at delivery and ethnicity were non-contributing variables.

CONCLUSION: When mean blood glucose levels are targeted to !90mg/dland the estimated birth percentile O70 is included in determining method ofdelivery, it may be possible to decrease the rate of SHD in diabetic patients.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2006.10.476

438 WEIGHT GAIN IN GDM: WHEN MET, UNMET AND UNDER-MET NEEDS DETERMINETHE RATE OF LGA ODED LANGER1, ORLI MOST2, 1St. Luke’s Roosevelt HospitalCenter, Obstetrics and Gynecology, New York, New York, 2New YorkUniversity, Obstetrics and Gynecology, New York, New York

OBJECTIVE: The role of weight gain on fetal size in GDM remainsindecisive. We sought to determine the impact of weight gain on LGA/SGArelative to other variables.

STUDY DESIGN: 2454 GDM women were evaluated. Weight gain wasstratified into categories by 5 lb increments. Obesity (BMI O29); glycemiccontrol (good ! 100mg/dl); maternal age; parity. LGA and SGA O90th or!10th percentile. Analysis; univariant and logistic regression.

RESULTS: The table displays the rate (%) of LGA stratification by weightgain categories, level of glycemic control and treatment modalities. (1.) theincidence of SGA was similar in all weight gain categories, treatmentmodalities and level of glycemic control (range 5-10%); (2.) logistic regressionwhen the dependent variable was LGA revealed that treatment modality(p=0.00005), level of glycemic control (p=0.00000), previous macrosomia(p=0.00000), parity (p=0.00000), weight gain in pregnancy (p=0.00000) andobesity (p=0.003) had significant net contributing effects. Ethnicity anddisease severity were non-significant.

CONCLUSION: Well-controlled insulin-treated GDM patients gaining !30pounds will improve LGA rates. The challenge of growth diversity is toaddress the multi-factorial variables that can be met (glucose control, treat-ment modality) to improve outcome rather than unmet variables (unmodifi-able, i.e., parity, maternal age, obesity). By further addressing under-metfactors (i.e., glycemic control and weight gain) will minimize growth diversity.

Weight Gain Diet Treated Insulin-Treated

Category(lbs) Poor Control Good Control Poor Control Good Control

Low-10 16.7 12.9 14.6 9.511-15 9.4 12.7 10.5 8.016-20 22.4 11.0 13.2 7.421-25 14.6 14.4 13.6 8.426-30 25.6 13.8 23.6 9.931-High 24.6 19.9 25.8 17.7

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2006.10.477

439 FIRST TRIMESTER FETAL CARDIAC FUNCTION-IS THERE A DIFFERENCE BETWEENTHE DIABETIC AND NON-DIABETIC POPULATION? NOREEN RUSSELL1,MICHAEL FOLEY2, FIONNUALA MCAULIFFE3, 1National Maternity Hospital,Dublin, Ireland, 2University College Dublin, Obstetrics & Gynaecology, Du-blin, Ireland, 3University College Dublin, Obstetrics & Gynecology, Dublin,Ireland

OBJECTIVE: Evidence of cardiomyopathy occurs in about 40% of infants ofdiabetic mothers and causes symptoms in 5% of these babies. Mechanisms forthis cardiomyopathy are unclear. It is possible that alterations in intracardiacblood flow early in pregnancy may result in later structural defects. The aim ofthis study is to determine if indices of fetal cardiac function differ between thenormal and diabetic pregnancies in early pregnancy.

STUDY DESIGN: This is a prospective observational study of first trimesterfetuses, 29 from type 1 diabetic (IDDM) pregnancy and 32 from normalpregnancy. All fetal echoes were performed transabdominally between 12 – 15weeks gestational age with institutional ethics approval and parental consent.Systolic and diastolic cardiac function parameters were measured (E/A ratio,IVRT, ICT, left and right sided TEI).

RESULTS: There were alterations in intracardiac flow patterns in fetuses ofIDDM mothers in both sides of the heart.

CONCLUSION: Even in early pregnancy differences are evident betweendiabetic and non diabetic pregnancy, suggesting impaired fetal cardiac con-tractility in diabetic pregnancy. Alternations in intracardiac blood flow maycause later cardiac structural changes such as thickening of the intraventricularseptum, a feature of cardiomyopathy. These findings serve to emphasise furtherthe importance of strict glycaemic control in the periconceptual period.

Indices of cardiac function in normal and diabetic pregnancy (IDDM),

mean G SD

Normal (n=32) IDDM (n=29) P-value

GA (weeks) 13.3G0.7 13.7G1.1 0.15CRL (mm) 79G7 78G11 0.62Left E/A 0.6G0.07 0.56G0.06 0.038*Left TVI 3.6G1.1 2.9G1 0.022*IVRT ms 41G6 45G9 0.032*ICT ms 36G/�9 37G/�12 0.791Left TEI 0.51G0.1 0.54G0.15 0.326Right E/A 0.61G0.06 0.62G0.07 0.753Right TVI 4.1G1.9 3.1G1.1 0.022*Right Tei 0.54G/�0.12 0.56G/�0.23 0.719

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2006.10.478

440 IGF-1 AND IGFBP3 LEVELS IN NORMAL AND DIABETIC PREGNANCYNOREEN RUSSELL1, DEREK BRAZIL2, MARY COFFEY2, MICHAEL FOLEY3,FIONNUALA MCAULIFFE4, 1National Maternity Hospital, Dublin, Ireland,2University College Dublin, Dublin, Ireland, 3University College Dublin,Obstetrics and Gynaecology, Dublin, Ireland, 4University College Dublin,Obstetrics & Gynecology, Dublin, Ireland

OBJECTIVE: Insulin growth factor (IGF1) is a 70 amino acid polypeptidehomologous to the insulin precursor pro-insulin. It has both in vivo and in-vitro insulin-like effects and also demonstrates growth-promoting effects.Insulin growth factor binding protein (IGFBP3) is the major IGF bindingprotein in human plasma. The aim of this study is to determine the differencesbetween IGF1 and IGFBP3 levels in maternal and fetal serum samples ininsulin dependant diabetic (IDDM) and non-diabetic pregnancy.

STUDY DESIGN: With institutional ethics approval and maternal writtenconsent serum samples from IDDM and non-diabetic patients were drawn inthe first trimester (13-14 weeks), n=15 and n=18 respectively, and thirdtrimester (33-36 weeks), n=16 and n=13 respectively. After delivery, cordbloods were taken from babies of IDDM (n=12) and non-diabetic mothers(n=13). The IGF1 and IGFBP3 levels were measured using enzyme-linkedimmunosorbent assay technique (ELISA).

RESULTS: Mean serum IGF 1 is lower in maternal serum in the diabeticpopulation when compared to the non-diabetic population in both the firstand third trimesters (p!0.05). There is no significant difference in cord bloodIGF1 level in babies born to diabetic mothers when compared to non-diabeticmothers. There is no significant difference between the cohorts in eithermaternal or cord blood IGFBP3 levels.

CONCLUSION: The decreased levels of IGF1 without a decrease in IGFBP3suggests that IGF1 is decreased in IDDM mothers. Previous studies haveshown that IGF1 levels are decreased in maternal serum of IUGR fetuses butfound no difference between diabetic and non-diabetic populations. Thefindings of this study suggest that there are alterations in the growth axis indiabetic pregnant women and that differences in growth factors may have arole in the ‘overgrowth’ seen in these infants.

0002-9378/$ - see front matterdoi:10.1016/j.ajog.2006.10.479

SMFM Abstracts S137