Disease relevance of Fetal Macrosomia

• Several maternal plasma fuel abnormalities have been described in gestational diabetes mellitus (GDM), and all may contribute to the development of fetal macrosomia, generally because of the surfeit of calories they provide [1].
• To study the role of enteroinsular hormones in fetal macrosomia and neonatal hypoglycemia in infants of diabetic mothers, we measured plasma concentrations of free and total immunoreactive insulin, C-peptide, pancreatic glucagon, enteroglucagon, and gastric inhibitory polypeptide at birth in 35 IDMs and 35 infants of normal mothers [2].
• OBJECTIVE: To determine the possible relation between maternal serum insulin-like growth factor I and II (IGF-I and IGF-II) in women with insulin-dependent diabetes mellitus and fetal macrosomia [3].
• If maternal hyperglycemia is not well controlled, excess glucose is transmitted to the fetus, which can lead to fetal macrosomia and maternal and fetal complications [4].
• We conclude that patients with resolving polyhydramnios have a significantly higher prevalence of glucose intolerance and fetal macrosomia than patients with normal pregnancies [5].

High impact information on Fetal Macrosomia

• Fetal macrosomia occurs despite nearly normal maternal blood glucose levels in women with diabetes treated with insulin [6].
• Treatment regimens designed to lower verified ambulatory blood glucose measurements may help reduce fetal macrosomia in women with milder forms of gestational diabetes or in women with relative glucose intolerance without a substantial increase in severe hypoglycemia [7].
• Maternal fasting serum triglyceride levels in midpregnancy might be an independent predictor of fetal macrosomia in those women [8].
• OBJECTIVES: We sought to reanalyze the concept of fetal macrosomia with regard to the ponderal index and to investigate the role of insulin, insulinlike growth factor I, leptin, and maternal factors on birth size in a population of infants with nondiabetic mothers [9].
• CONCLUSION: These data suggest that the modulation of placental transport of L-arginine by glucose and insulin could contribute to the fetal macrosomia observed in diabetic mothers [10].

Chemical compound and disease context of Fetal Macrosomia

• In particular we noted an increased rate of fetal macrosomia in the glibenclamide treated group, which in theory could have been drug mediated [11].

Biological context of Fetal Macrosomia

• RESULTS: At entry, neither the hourly oGTT values, HbA1c, nor the entry glucose profile differed significantly between pregnancies with and without fetal macrosomia [12].

Gene context of Fetal Macrosomia

• The lack of change in number or binding affinity of placental trophoblastic receptors for insulin, IGF-I and IGF-II tends to exclude a significant regulatory role of these receptors in the production of fetal macrosomia [13].
• On the association between maternal phosphoglucomutase 1 (PGM1) and fetal macrosomia in diabetic pregnancy [14].
• Erb/Duchenne's palsy: a consequence of fetal macrosomia and method of delivery [15].
• 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) [12].
• CONCLUSIONS: We conclude that the SCT/FL ratio is a poor sonographic predictor of fetal macrosomia in the non-diabetic pregnancy and does not improve fetal weight estimations by conventional sonographic parameters [16].

Analytical, diagnostic and therapeutic context of Fetal Macrosomia

• This study was undertaken to determine if intensive dietary therapy, home blood glucose monitoring, and the selective use of insulin can be effective in preventing fetal macrosomia [17].

References