Related Experiment Videos
Biphasic intrauterine growth in insulin-dependent diabetic pregnancies
T A Siddiqi1, M Miodovnik, F Mimouni
1Department of Obstetrics and Gynecology, University of Cincinnati, College of Medicine, Ohio 45267.
Insights
In insulin-dependent diabetic pregnancies, fetuses experience early growth delay followed by accelerated growth, potentially linked to glucose toxicity and later hyperinsulinism. This biphasic pattern contrasts with normal fetal development.
Area of Science:
- Maternal-Fetal Medicine
- Endocrinology
- Developmental Biology
Background:
- Early fetal growth delay (7-14 weeks) is observed in insulin-dependent diabetic (IDD) pregnancies.
- Macrosomia is a known complication in infants of mothers with IDD.
- A biphasic pattern of fetal growth in IDD pregnancies is hypothesized.
Purpose of the Study:
- To compare fetal growth patterns in IDD pregnancies versus normal pregnancies.
- To investigate the biphasic growth hypothesis in IDD pregnancies.
Main Methods:
- Sonographic measurements of biparietal diameter (BPD) and abdominal circumference (AC) were compared between 106 IDD pregnancies and 117 controls.
- Strict glycemic control targets were maintained for diabetic patients (fasting ≤ 100 mg/dl, postprandial < 140 mg/dl).
- Gestational age was determined by last menstrual period and confirmed by Ballard score at birth.
Main Results:
- A biphasic BPD growth pattern was identified in IDD pregnancies (cubic equation, R²=0.935), absent in controls (quadratic equation, R²=0.917).
- Early fetal growth delay was more pronounced in fetuses that subsequently developed macrosomia (p<0.01).
- Similar biphasic growth patterns were observed for AC measurements.
Conclusions:
- Fetal growth in IDD pregnancies exhibits a biphasic pattern: initial delay followed by accelerated growth.
- Early growth delay may result from glucose toxicity or other metabolites.
- Subsequent accelerated growth is potentially driven by fetal hyperinsulinism (15-20 weeks gestation).
Abstract:
Early fetal growth delay (7-14 weeks of gestation) has been reported in insulin-dependent diabetic (IDD) pregnancies and in several animal models. Macrosomia is a classic feature of the infant of the IDD mother. We hypothesized therefore that a biphasic pattern of fetal growth exists in IDD pregnancies. We compared fetal growth measurements [biparietal diameter (BPD) and abdominal circumference (AC)] obtained sonographically from 106 IDD pregnancies (Class B-RT) to similar data obtained from 117 normal, nondiabetic patients. The goals for diabetic glycemic control were: fasting blood sugar less than or equal to 100 mg/dl and postprandial blood sugar less than 140 mg/dl. From one to five ultrasonographic measurements were performed at varying gestational ages in all study patients. For data analysis, one examination from each pregnancy was randomly selected by computer. Gestational age (GA) was calculated from last menstrual period and corroborated by infant physical examination (Ballard score) at birth. BPD growth pattern was biphasic in the diabetic group, described by a cubic equation: BPD = 4.99 - 0.567GA + 0.037(GA)2 - 0.0005(GA)3, R2 = 0.935. Such a biphasic pattern did not exist in the control population [BPD = -3.0323 + 0.473(gestation) - (-0.0040)(gestation)2, R2 = 0.9173]. Early growth delay was greater in fetuses that subsequently developed macrosomia (p less than 0.01). Similar results were found for AC measurements. We conclude that fetal growth delay occurs in the first half of the IDD pregnancy, followed by a phase of increased growth. The mechanism of the early growth delay is unclear. We speculate that early growth delay may be due to a "toxic" effect of glucose or other metabolite; and subsequent increased growth relates to fetal hyperinsulinism which develops from weeks 15 to 20 of gestation.