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Response to Comment on: Hernandez et al. Patterns of Glycemia in Normal Pregnancy: Should the Current Therapeutic Targets Be Challenged? Diabetes Care 2011;34:1660–1668

  1. Teri L. Hernandez, PHD, RN1,2
  1. Jacob E. Friedman, PHD3
  1. Rachael E. Van Pelt, PHD4
  1. Linda A. Barbour, MD, MSPH1,5
  1. From the 1Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado; the
  2. 2Division of Women, Children, and Family Health, College of Nursing, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado; the
  3. 3Department of Pediatrics, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado; the
  4. 4Division of Geriatric Medicine, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado; and the
  5. 5Division of Obstetrics and Gynecology, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado
  1. Corresponding author: Teri L. Hernandez, teri.hernandez{at}ucdenver.edu.
Diabetes Care 2011 Nov; 34(11): e175-e175. https://doi.org/10.2337/dc11-1542
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We appreciate Ryan's (1) thoughtful comments. The intent of our pooled analysis was to describe a normal pattern of glycemia in nonobese pregnant women according to the published data (2). We demonstrated that, similar to the Hyperglycemia and Adverse Pregnancy Outcomes (HAPO) study (3), glucose concentrations in normal pregnancy are lower than were previously appreciated. If the treatment goal for pregnancies affected by diabetes is to mimic patterns of glycemia in normal pregnancy, then a contemporary understanding of normo- or euglycemia is warranted. On the basis of our review, we suggested that prospective trials test whether 1- and 2-h postprandial (PP) targets of <122 and <110 mg/dL can attenuate incidence of fetal macrosomia and large-for-gestational-age (LGA) infants.

Ryan's concern that fasting blood glucose (FBG) was 10 mg/dL lower in our pooled analysis compared with the HAPO trial (70.9 ± 7.8 vs. 80.9 ± 6.9 mg/dL) (2,3) is well-taken. It is possible that the FBG was higher in HAPO because the women were overweight (mean BMI 27.7 ± 5 kg/m2) in comparison with a mostly normal-weight population in our pooled analysis. Our own recent data (4) showed a mean plasma FBG at 28 weeks gestation of 76 ± 3 mg/dL in normal-weight women. However, the pooled data are simply descriptive means. We do not suggest that the lower FBG target ± 1 SD be tested in an interventional trial because HAPO has already determined, based on outcome data, that a mean FBG ≥92 mg/dL confers a 1.75-fold increased risk of LGA. Because we do not have such powerful outcome data for 1- and 2-h PP therapeutic targets, we recommend that PP targets be prospectively tested.

Ryan argued against testing lower PP targets because the Maternal-Fetal Medicine Units Network trial (5) already demonstrated that adopting conventional targets to treat gestational diabetes resulted in a low frequency (7.1%) of LGA. However, it is important to recall that that trial excluded women with fasting hyperglycemia (≥95 mg/dL), a strong predictor of LGA. Further, the majority of women (426/462) attained a median 2-h PP glucose in the range of 97.3–107.8 mg/dL across meals, which met our suggested lower target of <110 mg/dL, potentially accounting for the low frequency of LGA.

We acknowledge the concern for an increased risk of small-for-gestational-age (SGA) if lower PP targets are adopted. However, in the context of obesity and gestational diabetes, SGA is less likely to occur when compared with lean women with type 1 diabetes who are at higher risk for placental insufficiency. The data of Langer and Mazze (6) suggested that mean 24-h glucose between 87–104 mg/dL minimizes SGA and LGA incidence. Our pooled mean 24-h glucose + 1 SD of 98 mg/dL supports this range.

We acknowledge that adopting lower therapeutic glucose targets will not guarantee lower macrosomia/LGA rates and that other nutrients, such as maternal triglycerides, likely contribute to excess fetal fat accretion, as supported by our data (4). To be clear, we do not suggest that lower PP targets be adopted based on our review. However, we do suggest that lower targets be prospectively tested to appropriately determine whether they might decrease the rate of LGA infants and, more importantly, excess neonatal adiposity—an even stronger predictor of childhood obesity.

Acknowledgments

No potential conflicts of interest relevant to this article were reported.

  • © 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

References

  1. 1.↵
    Ryan EA. Comment on: Hernandez et al. Patterns of glycemia in normal pregnancy: should the current therapeutic targets be challenged? Diabetes Care 2011;34:1660–1668 (Letter). Diabetes Care 2011;34:e174. DOI: 10.2337/dc11-1359.
  2. 2.↵
    1. Hernandez TL,
    2. Friedman JE,
    3. Van Pelt RE,
    4. Barbour LA
    . Patterns of glycemia in normal pregnancy: should the current therapeutic targets be challenged? Diabetes Care 2011;34:1660–1668
    OpenUrlFREE Full Text
  3. 3.↵
    1. Metzger BE,
    2. Lowe LP,
    3. Dyer AR,
    4. et al.
    ; HAPO Study Cooperative Research Group. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med 2008;358:1991–2002
    OpenUrlCrossRefPubMedWeb of Science
  4. 4.↵
    1. Harmon KA,
    2. Gerard L,
    3. Jensen DR,
    4. et al
    . Continuous glucose profiles in obese and normal-weight pregnant women on a controlled diet: metabolic determinants of fetal growth. Diabetes Care 2011;34:2198–2204
  5. 5.↵
    1. Landon MB,
    2. Spong CY,
    3. Thom E,
    4. et al.
    ; Eunice Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. A multicenter, randomized trial of treatment for mild gestational diabetes. N Engl J Med 2009;361:1339–1348
    OpenUrlCrossRefPubMedWeb of Science
  6. 6.↵
    1. Langer O,
    2. Mazze R
    . The relationship between large-for-gestational-age infants and glycemic control in women with gestational diabetes. Am J Obstet Gynecol 1988;159:1478–1483
    OpenUrlCrossRefPubMedWeb of Science
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Response to Comment on: Hernandez et al. Patterns of Glycemia in Normal Pregnancy: Should the Current Therapeutic Targets Be Challenged? Diabetes Care 2011;34:1660–1668
Teri L. Hernandez, Jacob E. Friedman, Rachael E. Van Pelt, Linda A. Barbour
Diabetes Care Nov 2011, 34 (11) e175; DOI: 10.2337/dc11-1542

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Response to Comment on: Hernandez et al. Patterns of Glycemia in Normal Pregnancy: Should the Current Therapeutic Targets Be Challenged? Diabetes Care 2011;34:1660–1668
Teri L. Hernandez, Jacob E. Friedman, Rachael E. Van Pelt, Linda A. Barbour
Diabetes Care Nov 2011, 34 (11) e175; DOI: 10.2337/dc11-1542
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