AIM: The current therapeutic strategies to reduce macrosomia rates in gestational diabetes (GDM) have focused on the normalizing of maternal glucose levels. The aim of our study was 1.) to compare maternal glycemic values with the presence of fetal macrosomia at different gestational ages (GA) and with LGA at birth in a cohort of women with glucose intolerance and standard diabetic therapy. METHODS: 306 women with GDM and 97 with impaired glucose tolerance underwent ultrasound examinations at entry and, after initiation of therapy, monthly in addition to standard diabetic therapy. Measurements from the entry diagnostic oGTT, glucose profile and HbA1c and from subsequent glucose profiles obtained within 3 days of the ultrasound at 5 categories of GA age (20-23, 24-27 etc) were retrospectively compared between pregnancies with and without fetal macrosomia, defined as an abdominal circumference (AC) > or = 90th percentile. Maternal prepregnancy BMI was adjusted for and BMI > or = 30 kg/m2 was defined as obesity. RESULTS: At entry, neither the hourly oGTT values, HbA1c, nor the entry glucose profile differed significantly between pregnancies with and without fetal macrosomia. In a total of 919 pairs of ultrasound/glucose profiles there was no significant difference in glucose levels at every GA category neither in lean nor in obese woman except for the fasting glucose of 32-35 GA. The fetal macrosomia rate in each GA category and the rate of LGA were significantly higher in obese women: e.g. 14.5 vs 28% at diagnosis, 15.7 vs 26.7% at 32-35 weeks, 15.5 vs 25.0% at birth (p < 0.05 for each comparison). CONCLUSION: The association of maternal glucose values and fetal macrosomia was limited to the fasting glucose values between 32-35 weeks while maternal obesity appeared to be a strong risk factor for macrosomia throughout pregnancies with GDM. In obese women the high fetal macrosomia rate did not appear be normalized by therapy based on maternal euglycemia.
AIM: The current therapeutic strategies to reduce macrosomia rates in gestational diabetes (GDM) have focused on the normalizing of maternal glucose levels. The aim of our study was 1.) to compare maternal glycemic values with the presence of fetal macrosomia at different gestational ages (GA) and with LGA at birth in a cohort of women with glucose intolerance and standard diabetic therapy. METHODS: 306 women with GDM and 97 with impaired glucose tolerance underwent ultrasound examinations at entry and, after initiation of therapy, monthly in addition to standard diabetic therapy. Measurements from the entry diagnostic oGTT, glucose profile and HbA1c and from subsequent glucose profiles obtained within 3 days of the ultrasound at 5 categories of GA age (20-23, 24-27 etc) were retrospectively compared between pregnancies with and without fetal macrosomia, defined as an abdominal circumference (AC) > or = 90th percentile. Maternal prepregnancy BMI was adjusted for and BMI > or = 30 kg/m2 was defined as obesity. RESULTS: At entry, neither the hourly oGTT values, HbA1c, nor the entry glucose profile differed significantly between pregnancies with and without fetal macrosomia. In a total of 919 pairs of ultrasound/glucose profiles there was no significant difference in glucose levels at every GA category neither in lean nor in obesewoman except for the fasting glucose of 32-35 GA. The fetal macrosomia rate in each GA category and the rate of LGA were significantly higher in obesewomen: e.g. 14.5 vs 28% at diagnosis, 15.7 vs 26.7% at 32-35 weeks, 15.5 vs 25.0% at birth (p < 0.05 for each comparison). CONCLUSION: The association of maternal glucose values and fetal macrosomia was limited to the fasting glucose values between 32-35 weeks while maternal obesity appeared to be a strong risk factor for macrosomia throughout pregnancies with GDM. In obesewomen the high fetal macrosomia rate did not appear be normalized by therapy based on maternal euglycemia.
Authors: Alison M Stuebe; Mark B Landon; Yinglei Lai; Catherine Y Spong; Marshall W Carpenter; Susan M Ramin; Brian Casey; Ronald J Wapner; Michael W Varner; Dwight J Rouse; Anthony Sciscione; Patrick Catalano; Margaret Harper; George Saade; Yoram Sorokin; Alan M Peaceman; Jorge E Tolosa Journal: Am J Obstet Gynecol Date: 2012-05-02 Impact factor: 8.661
Authors: W Ricart; J López; J Mozas; A Pericot; M A Sancho; N González; M Balsells; R Luna; A Cortázar; P Navarro; O Ramírez; B Flández; L F Pallardo; A Hernández-Mijas; J Ampudia; J M Fernández-Real; R Corcoy Journal: Diabetologia Date: 2005-07-29 Impact factor: 10.122
Authors: Ravi Retnakaran; Ying Qi; Mathew Sermer; Philip W Connelly; Anthony J G Hanley; Bernard Zinman Journal: J Clin Endocrinol Metab Date: 2008-12-09 Impact factor: 5.958