1400-P: Adverse Perinatal and Long-Term Outcomes Differ among Physiologic Subtypes of Gestational Glucose Intolerance
Background: Gestational diabetes mellitus (GDM) is associated with adverse perinatal and long-term outcomes; it is unclear if these outcomes are equally distributed among all affected women. We aimed to define physiologic subtypes of gestational glucose intolerance using beta-cell (BC) function and...
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Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2019-06, Vol.68 (Supplement_1) |
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Zusammenfassung: | Background: Gestational diabetes mellitus (GDM) is associated with adverse perinatal and long-term outcomes; it is unclear if these outcomes are equally distributed among all affected women. We aimed to define physiologic subtypes of gestational glucose intolerance using beta-cell (BC) function and insulin sensitivity (IS) parameters and characterize adverse outcomes associated with each subtype.
Methods: We used homeostasis model assessment to estimate BC function and IS from fasting glucose and insulin levels at 16-20 weeks gestation. We defined BC and IS defects using the 50th percentile in 1369 women with normal subsequent 50g glucose load tests (GLTs, performed at 24-30 weeks gestation). We categorized 158 women whose GLTs were abnormal (1-hour glucose ≥130 mg/dl) according to the predominant physiologic defect. We compared hyperglycemia-associated adverse outcomes across physiologic subtypes. We used logistic regression to adjust for potential confounders.
Results: Among 158 women, 59 (37%) had BC defects, 83 (53%) had IS defects, 10 (6%) had both, 6 (4%) had neither. Women with IS defects (vs. those with BC defects) were more likely develop GDM (13% vs. 2% by Carpenter-Coustan criteria, P=0.03), while women with BC defects were more likely to develop pregnancy-associated hypertension (20% vs. 7%, P=0.02). Women with IS defects (vs. women with BC defects) were more likely to develop postpartum glucose intolerance (prediabetes/type 2 diabetes) (29% vs. 3%, P |
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ISSN: | 0012-1797 1939-327X |
DOI: | 10.2337/db19-1400-P |