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How Much Does Tight Glucose Control Diminish Fetal Macrosomia in Diabetes?
Abstract & Commentary
Synopsis: Fetal growth acceleration is identifiable by ultrasound at about 24 weeks. "Normal" parameters of glucose control during the first trimester and throughout pregnancy do not seem to be related to the growth potential of the LGA fetus of a diabetic mother. Fluctuations in glucose levels rather than basal levels are probably more determinant in fetal growth acceleration.
Source: Greco P, et al. Fetal Diagn Ther. 2003;18(6): 437-441.
The literature has been confusing regarding the relationship between glucose control in diabetes and fetal size. Fetal macrosomia is a complication worth averting, and it has been convenient to think that tight control of blood sugars would always do this.
Greco and colleagues from Italy set out to assess fetal growth in Type I diabetics who were in a highly regimented program of glucose monitoring from the first trimester of pregnancy (capillary glucose levels 7 times a day and glycosylated hemoglobin values once a month). The 98 women in the study all had ultrasound examinations in the first trimester, at 16-18 weeks and then every 3 weeks thereafter. The results were intriguing and, perhaps, discouraging on the surface. Greco et al found that mean glucose levels did not correlate statistically with fetal size, as reflected by the fetal abdominal circumference (AC) and birth weight. The same lack of relationship was found with glycosylated hemoglobin.
They did find that the AC of fetuses destined to be large for gestational age (LGA) infants were larger at 24 weeks than the appropriate for gestational age (AGA) babies in the study. This trend continued throughout pregnancy, as the LGA fetuses maintained growth profiles that were consistently different from AGA fetuses.
Comment by John C. Hobbins, MD
There is no doubt that fetal macrosomia is associated with out-of-control diabetes. There are some studies that show that bringing blood sugar levels into reasonable range might reduce the incidence of macrosomia, while other studies suggest that tight glucose control might not be the answer. The Italian study shows that mean blood sugars (representing short-term control) and glycosylated hemoglobin (representing long-term control) did not correlate with fetal size at birth. While this study was undertaken in a group of patients who were all very tightly monitored, it in no way implies that attempting to control blood sugars will be to no avail in all pregestational diabetics.
In fact, the full story on fetal macrosomia is not out yet. For example, the incidence of LGA (above the 90 percentile) in this study was almost doubled (17.3%) over the expected rate despite scrupulous glucose monitoring.
The seemingly simplistic idea that maternal/fetal hyperglycemia triggers release of fetal insulin—a stimulator of fetal growth—certainly should not be discarded, since the fetal pancreas may respond more to large swings in glucose levels that would not be reflected in the mean glucose levels analyzed in the Italian study. The fact that other agents (now being explored) might be working in tandem with fetal insulin could explain why the LGA fetuses in this study fell off the curve by the 24th week of gestation.
There is also good news here. I like the idea of assessing fetal growth with AC alone since infants of diabetics have large livers and an overabundance of triglycerides in the subcutaneous tissue, both of which would be reflected in a cross-sectional view of the upper fetal abdomen. The size of the head and limbs, included in all standard biometric assessments and incorporated into estimations of fetal weight, more often take into account genetic predispositions, rather than fetal corpulence. The above study suggests that if the AC is within normal limits by (let us say) 26 weeks, it is very unlikely that the fetus would be macrosomic at birth. In contrast, if the AC is ahead of dates at this point, then the likelihood of macrosomia at birth is substantial and would warrant a careful evaluation of fetal size and evidence of body-to-head disproportion before birth. This, in turn, could play a role in labor management.
In summary, the above study in no way suggests that diabetics need not have comprehensive glucose monitoring since failure to do so could undoubtedly result in a higher rate of macrosomia. However, the study shows that even tight control (by their regimen) will not completely prevent macrosomia, suggesting that there is more to macrosomia than hyperglycemia alone. Last, the macrosomic die seems to be cast by mid-pregnancy.
Dr. Hobbins is Professor and Chief of Obstetrics, University of Colorado Health Sciences Center, Denver
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