American Diabetes Association
Andrews_et_al_-_Supplemental_Materials.pdf (283.18 kB)

Risk of neonatal hypoglycemia in infants of mothers with gestational glucose intolerance

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posted on 2024-05-24, 14:33 authored by Chloe Andrews, Jacqueline Maya, Carolin C.M. Schulte, Sarah Hsu, Tanayott Thaweethai, Kaitlyn E. James, Jose Halperin, Camille E. Powe, Sarbattama Sen

OBJECTIVE: To examine the relationship between gestational glucose intolerance (GGI) and neonatal hypoglycemia (NH).

RESEARCH DESIGN & METHODS: This was a secondary analysis of 8262 mother-infant dyads who delivered at two hospitals between 2014-2023. We categorized maternal glycemic status as normal glucose tolerance (NGT), GGI, and gestational diabetes (GDM). We defined NGT as a normal glucose load test (GLT), GGI as an abnormal GLT with 0 (GGI-0) or 1 (GGI-1) abnormal values on the 100-gram oral glucose tolerance test, and GDM as an abnormal GLT with ≥2 abnormal values on the glucose tolerance test. NH was defined as blood glucose <45 mg/dL or an International Classification of Disease (ICD) diagnosis of NH. We used logistic regression analysis to determine associations between maternal glucose tolerance category and NH and conducted a sensitivity analysis using delta-adjusted multiple imputation, assuming that unscreened infants had a rate of NH as high as 33%.

RESULTS: Twelve percent of infants had NH. In adjusted models, infants born to mothers with GGI-0 had 1.28 (95% confidence interval (CI) 1.12, 1.65), GGI-1 had 1.58 (95% CI 1.11, 2.25), and GDM had 4.90 times (95% CI 3.81, 6.29) higher odds of NH compared to infants born to mothers with NGT. Associations in sensitivity analyses were consistent with the primary analysis.

CONCLUSIONS: GGI is associated with increased risk of NH. Future research should examine these associations in a cohort with more complete neonatal blood glucose ascertainment and determine the clinical significance of these findings on long-term child health.


The GCD59 study was supported by NIH/NIDDK grant number R01 DK118528. The MHC study was supported by the MGH Claflin Distinguished Scholar Award and the MGH Physician Scientist Development Award. JM was supported by a T32 training grant for endocrinology (T32DK007028- 47S1).


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