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• W1997295587 abstract "ObjectiveThere is paucity of information if different BMI levels result in varying rates of LGA. We sought to determine how levels of maternal weight influence infant size.Study designWe evaluated 4632 gestational diabetic (2 or more abnormal values) and 1638 non-diabetic pregnant women (glucose values normal). BMI categories were defined based on pre-pregnancy weight. Birth weight was large (>90th) and small (<10th) percentile for a given gestational age. Fetal macrosomia was birth weight >4000 gm.ResultsGDM subjects were: underweight (BMI <20, n=129); normal weight (BMI 20-25, n=1087); overweight (BMI 26-29, n=1864); obese (BMI 30-35, n=905); morbidly obese (BMI 36-40, n=594) and extremely morbid obese (BMI >41, n=357)}. (1.) The rate of SGA was 2-fold higher in the underweight group (16%) compared to other categories (5-7%) regardless of glycemic control. (2.) Similar rates of LGA were found in the underweight and normal weight categories (9 and 12%, respectively). A significantly higher rate of LGA was found in each of the overweight and obese categories (17-20%). (3.) For patients achieving the targeted level of glycemic control (mean <100 mg/dl), there were comparable rates of LGA (11-13%) in all BMI categories. (4.) For patients failing to achieve targeted level of glycemic control (mean >100 mg/dl), the rate of LGA was 15% for the under and normal weight categories and 22-31% for all other categories. (5.) For non-diabetic patients in the under and normal weight categories, the rate of LGA was 6 and 12%, respectively with comparable rates of LGA for all other categories (16-19%). The SGA rate for this group was 10% in the underweight and similar in all other weight categories (6%).ConclusionGrowth diversity thresholds are maternal size dependent: underweight for SGA and overweight for LGA. In GDM women, improving glycemic control will significantly affect the rate of overgrowth. ObjectiveThere is paucity of information if different BMI levels result in varying rates of LGA. We sought to determine how levels of maternal weight influence infant size. There is paucity of information if different BMI levels result in varying rates of LGA. We sought to determine how levels of maternal weight influence infant size. Study designWe evaluated 4632 gestational diabetic (2 or more abnormal values) and 1638 non-diabetic pregnant women (glucose values normal). BMI categories were defined based on pre-pregnancy weight. Birth weight was large (>90th) and small (<10th) percentile for a given gestational age. Fetal macrosomia was birth weight >4000 gm. We evaluated 4632 gestational diabetic (2 or more abnormal values) and 1638 non-diabetic pregnant women (glucose values normal). BMI categories were defined based on pre-pregnancy weight. Birth weight was large (>90th) and small (<10th) percentile for a given gestational age. Fetal macrosomia was birth weight >4000 gm. ResultsGDM subjects were: underweight (BMI <20, n=129); normal weight (BMI 20-25, n=1087); overweight (BMI 26-29, n=1864); obese (BMI 30-35, n=905); morbidly obese (BMI 36-40, n=594) and extremely morbid obese (BMI >41, n=357)}. (1.) The rate of SGA was 2-fold higher in the underweight group (16%) compared to other categories (5-7%) regardless of glycemic control. (2.) Similar rates of LGA were found in the underweight and normal weight categories (9 and 12%, respectively). A significantly higher rate of LGA was found in each of the overweight and obese categories (17-20%). (3.) For patients achieving the targeted level of glycemic control (mean <100 mg/dl), there were comparable rates of LGA (11-13%) in all BMI categories. (4.) For patients failing to achieve targeted level of glycemic control (mean >100 mg/dl), the rate of LGA was 15% for the under and normal weight categories and 22-31% for all other categories. (5.) For non-diabetic patients in the under and normal weight categories, the rate of LGA was 6 and 12%, respectively with comparable rates of LGA for all other categories (16-19%). The SGA rate for this group was 10% in the underweight and similar in all other weight categories (6%). GDM subjects were: underweight (BMI <20, n=129); normal weight (BMI 20-25, n=1087); overweight (BMI 26-29, n=1864); obese (BMI 30-35, n=905); morbidly obese (BMI 36-40, n=594) and extremely morbid obese (BMI >41, n=357)}. (1.) The rate of SGA was 2-fold higher in the underweight group (16%) compared to other categories (5-7%) regardless of glycemic control. (2.) Similar rates of LGA were found in the underweight and normal weight categories (9 and 12%, respectively). A significantly higher rate of LGA was found in each of the overweight and obese categories (17-20%). (3.) For patients achieving the targeted level of glycemic control (mean <100 mg/dl), there were comparable rates of LGA (11-13%) in all BMI categories. (4.) For patients failing to achieve targeted level of glycemic control (mean >100 mg/dl), the rate of LGA was 15% for the under and normal weight categories and 22-31% for all other categories. (5.) For non-diabetic patients in the under and normal weight categories, the rate of LGA was 6 and 12%, respectively with comparable rates of LGA for all other categories (16-19%). The SGA rate for this group was 10% in the underweight and similar in all other weight categories (6%). ConclusionGrowth diversity thresholds are maternal size dependent: underweight for SGA and overweight for LGA. In GDM women, improving glycemic control will significantly affect the rate of overgrowth. Growth diversity thresholds are maternal size dependent: underweight for SGA and overweight for LGA. In GDM women, improving glycemic control will significantly affect the rate of overgrowth." @default.
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• W1997295587 date "2006-12-01" @default.
• W1997295587 modified "2023-09-23" @default.
• W1997295587 title "GDM and non-GDM: Do maternal levels of BMI indicate varying rates in growth diversity?" @default.
• W1997295587 doi "https://doi.org/10.1016/j.ajog.2006.10.473" @default.
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