Correspondence
Blood Glucose Monitoring in Gestational Diabetes Mellitus
N Engl J Med 1996; 334:598-599February 29, 1996
- Article
To the Editor:
Careful medical management has improved perinatal outcomes among women with diabetes that antedates pregnancy, but the benefits of diagnosing and regulating glucose intolerance that develops during pregnancy are less clear. The study by de Veciana and colleagues (Nov. 9 issue)1 has not persuaded us that tight glucose control affects outcomes of clinical importance in unselected women with gestational diabetes. For example, there was no difference in the overall rates of cesarean delivery in the postprandial- as compared with the preprandial-monitoring group.
Furthermore, the women in this study had unusually high mean plasma glucose values while fasting and after glucose loading at the time of diagnosis (141 and 215 mg per deciliter, respectively), and the majority had elevated glycosylated hemoglobin values. In contrast, most women with gestational diabetes have fasting blood glucose concentrations below 105 mg per deciliter and normal glycosylated hemoglobin values at the time of diagnosis.2,3 Also, gestational diabetes was diagnosed earlier in pregnancy (mean, 22 weeks of gestation) than is usual. Together, these observations suggest either that the women studied had particularly severe gestational diabetes or that a high proportion of them had previously undiagnosed nongestational diabetes. In line with this latter possibility (recognized by the authors themselves), it would have been helpful to know how many of the women continued to have glucose intolerance after delivery.
Against any potential benefit of screening for and treating gestational diabetes must be weighed the expense, inconvenience (as many as seven daily finger-sticks and multiple insulin injections), anxiety, and potential complications associated with the treatment regimen. Until an effect on an outcome of clinical importance is proved, we agree with a recent meta-analysis of treatment trials that concludes, “There is nothing . . . to substantiate the wide recommendation that all pregnant women should be screened for `gestational diabetes,' let alone that they should be treated with insulin.”4
4 ReferencesRaj K. Bansal, M.D.
Jeffrey L. Ecker, M.D.
Russell K. Laros, Jr., M.D.
University of California, San Francisco, San Francisco, CA 941431
de Veciana M ,Major CA ,Morgan MA , et al. Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy. N Engl J Med 1995;333:1237-1241
Full Text | Web of Science | Medline2
Sacks DA ,Greenspoon JS ,Fotheringham N . Could the fasting plasma glucose assay be used to screen for gestational diabetes? J Reprod Med 1992;37:907-909
Web of Science | Medline3
Shah BD ,Cohen AW ,May C ,Gabbe SG . Comparison of glycohemoglobin determination and the one-hour oral glucose screen in the identification of gestational diabetes. Am J Obstet Gynecol 1982;144:774-777
Web of Science | Medline4
Walkinshaw SA. Diet + insulin vs diet alone for `gestational diabetes.' In: Enkin MW, Keirse MJNC, Renfrew MJ, Neilson JP, eds. Pregnancy and childbirth module. Cochrane database of systematic reviews. April 20, 1993. (Review no. 06650.)
To the Editor:
de Veciana et al. found that in women with gestational diabetes who were treated with insulin, glycemic control was superior when they were treated according to the results of postprandial blood glucose monitoring, as compared with preprandial monitoring. There was less fetal macrosomia, a reduced need for cesarean section, and less neonatal hypoglycemia.
We wonder whether these results were due to some intrinsic superiority of postprandial glucose monitoring or whether they might instead relate to the glycemic goals in the two study groups. Maintaining blood glucose values below 140 mg per deciliter one hour postprandially represents a more rigorous standard than maintaining preprandial values in the range of 60 to 105 mg per deciliter. The results support this view, in that the glycosylated hemoglobin values were lower in the postprandial-monitoring group. Since there is a strong correlation between a postprandial blood glucose value and a subsequent preprandial value,1,2 it may be that postprandial glucose values below 140 mg per deciliter equate with preprandial glucose values of, for example, less than 85 mg per deciliter. Had such a goal been chosen for the patients in the preprandial-monitoring group, it seems likely that those women would have required more insulin and had lower glycosylated hemoglobin values and improved fetal outcomes. Preprandial blood glucose values of less than 85 mg per deciliter are not an unrealistic goal for women with gestational diabetes and are much closer to preprandial values in nondiabetic pregnant women3 than the range chosen for preprandial monitoring in this study.
If the above interpretation is correct, one would expect the women in the postprandial-monitoring group to have had lower preprandial and bedtime blood glucose values than the women in the preprandial-monitoring group. Conversely, higher postprandial values would be expected in the preprandial-monitoring group. Do the authors have any data on this issue? Information on bedtime glucose values would be especially helpful, because higher glucose concentrations at this time may last into the night and have a major impact on overall glycemic control.
3 ReferencesJ.M. Miles, M.D.
St. Luke's Hospital, Kansas City, MO 64111S.W. Coppack, F.R.C.P.
Whittington Hospital, London N19 3UA, United Kingdom1
Holman RR ,Turner RC . The basal plasma glucose: a simple relevant index of maturity-onset diabetes. Clin Endocrinol (Oxf) 1981;14:279-286
CrossRef | Web of Science | Medline2
Golay A ,Swislocki AL ,Chen YD ,Jaspan JB ,Reaven GM . Effect of obesity on ambient plasma glucose, free fatty acid, insulin, growth hormone, and glucagon concentrations. J Clin Endocrinol Metab 1986;63:481-484
CrossRef | Web of Science | Medline3
Lind T. A prospective multicentre study to determine the influence of pregnancy upon the 75g oral glucose tolerance test: the Diabetic Pregnancy Study Group of the European Association for the Study of Diabetes. In: Sutherland HW, Stowers JM, Pearson DWM, eds. Carbohydrate metabolism in pregnancy and the newborn IV. London: Springer-Verlag, 1989:209-26.
To the Editor:
The exclusive focus by most investigators, including de Veciana et al., on maternal blood glucose concentrations in the management of gestational diabetes neglects important biologic variability in the fetal response to maternal diabetes. We have reported that fetal ultrasonography early in the third trimester can identify the majority of fetuses not at excess risk for macrosomia,1 thus allowing insulin treatment to be directed specifically at the minority of women whose fetuses are responding to mild gestational diabetes in a way that places them at risk for macrosomia. This approach allows the fetal response to maternal diabetes to be considered in selecting the most appropriate therapy for the mother. We applaud de Veciana et al. for demonstrating that postprandial blood glucose monitoring is useful for the management of maternal hyperglycemia, but we encourage them and other investigators to consider not only maternal blood glucose concentrations but also patterns of fetal growth and development when designing treatment regimens for women with gestational diabetes.
1 ReferencesThomas A. Buchanan, M.D.
Siri L. Kjos, M.D.
Martin N. Montoro, M.D.
University of Southern California School of Medicine, Los Angeles, CA 900331
Buchanan TA ,Kjos SL ,Montoro MN , et al. Use of fetal ultrasound to select metabolic therapy for pregnancies complicated by mild gestational diabetes. Diabetes Care 1994;17:275-283
CrossRef | Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: Bansal and colleagues suggest that our findings may be related to the presence of severe (insulin-requiring) gestational diabetes or undiagnosed pregestational diabetes in a large proportion of the women. We agree and believe that it is particularly in this group of women that aggressive glycemic control is warranted. The women who had cesarean sections for cephalopelvic disproportion all had a trial of labor. A similar number of women whose fetuses were suspected of having macrosomia on the basis of ultrasonographic evidence had elective cesarean sections (five in the preprandial-monitoring group and three in the postprandial-monitoring group) and were not included in the analysis of data on cephalopelvic disproportion. The unusually high mean plasma glucose values measured during fasting and after glucose loading were expected, since we excluded women with gestational diabetes controlled by diet at <30 weeks' gestation. Undoubtedly, the benefits of screening for and treating gestational diabetes must be weighed against the expense, inconvenience to patients, and complication of treatment; however, we believe that a subgroup of women with more severe glucose intolerance (perhaps those with fasting hyperglycemia at diagnosis) is likely to benefit from aggressive intervention.
We acknowledge Miles and Coppack's comment regarding the possibility that differences in the goals for glycemic control in the groups, rather than an intrinsic superiority of postprandial monitoring, may explain the findings. The goals for glycemic control were chosen because they are commonly accepted in obstetrical practice in the United States. Women with glucose intolerance that is exacerbated during pregnancy tend to have hyperinsulinemia and insulin resistance after meals, and they therefore often have postprandial hyperglycemia before preprandial hyperglycemia. In such women, fetal macrosomia has been correlated with postprandial glucose control.1 Moreover, gestational diabetes is diagnosed by the identification of hyperglycemia after glucose loading. Thus, although different goals for glycemic control, with more stringent goals for preprandial glucose concentrations, might have made the outcomes more similar, we believe that this would not have been the case for the reason given above. The bedtime glucose values were similar in the two groups.
We agree with Buchanan and colleagues that biologic variability in the fetal response to maternal diabetes may have an important role in the pathophysiology of fetal macrosomia and that the maintenance of glycemic control is not itself the only answer. Clearly, ultrasonographic identification of fetuses not at excess risk for macrosomia is helpful; however, targeting only pregnancies with identifiable macrosomia in the third trimester may result in the initiation of insulin therapy late in pregnancy, when the benefits of maintenance of euglycemia may be smaller than when therapy is initiated earlier.
1 ReferencesMargarita de Veciana, M.D.
Eastern Virginia Medical School, Norfolk, VA 23507Mark A. Morgan, M.D.
University of Pennsylvania, Philadelphia, PA 19104Carol A. Major, M.D.
University of California, Irvine, Orange, CA 926681
Combs CA ,Gunderson E ,Kitzmiller JL ,Gavin LA ,Main EK . Relationship of fetal macrosomia to maternal postprandial glucose control during pregnancy. Diabetes Care 1992;15:1251-1257
CrossRef | Web of Science | Medline
- Citing Articles (1)
Citing Articles
1
G. Leguizamón, H. Krupitzki, D. Glujovsky, M. Olivera Ravasi, E. A. Reece. (2002) Blood glucose monitoring in gestational diabetes mellitus: 1- versus 2-h blood glucose determinations. Journal of Maternal-Fetal and Neonatal Medicine 12:6, 384-388
CrossRef
