DOI: 10.2337/dc08-0126
Isolated Hyperglycemia at 1-Hour on Oral Glucose Tolerance Test in Pregnancy Resembles Gestational Diabetes in Predicting Postpartum Metabolic Dysfunction
1Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Canada rretnakaran{at}mtsinai.on.ca ABSTRACT Objective: Gestational impaired glucose tolerance (GIGT), defined by a single abnormal value on antepartum 3-hour OGTT, is a metabolically heterogeneous disorder. Indeed, the antepartum metabolic phenotype of women with a single abnormal value at 1-hour during the OGTT (1-hr GIGT) resembles that of women with gestational diabetes (GDM), whereas GIGT at 2- or 3-hours (2/3-hr GIGT) is similar to normal glucose tolerance (NGT). Thus, we hypothesized that 1-hr GIGT would be associated with the same adverse outcomes as GDM: (i) increased infant birthweight and (ii) postpartum metabolic dysfunction. Methods: 361 women underwent (i) antepartum glucose challenge test (GCT) and 3-hr OGTT, (ii) assessment of obstetrical outcome at delivery, and (iii) metabolic characterization by OGTT at 3-months postpartum. The antepartum GCT/OGTT identified 5 study groups: (i) GDM (n=97); (ii) 1-hr GIGT (n=28); (iii) 2/3-hr GIGT (n=34); (iv) abnormal GCT with NGT on OGTT (abnormal GCT NGT)(n=128); and (v) normal GCT with NGT on OGTT (normal GCT NGT)(n=74). Results: Caesarian-section rate was higher in women with 1-hr GIGT but birthweight did not differ significantly between the non-GDM groups (p=0.1978). At 3-months postpartum, glycemia (area-under-glucose-curve) progressively increased across the groups from normal GCT NGT to abnormal GCT NGT to 2/3-hr GIGT to 1-hr GIGT to GDM (p<0.0001), while both insulin sensitivity (ISOGTT) and beta-cell function (insulinogenic index/HOMA-IR) progressively decreased (p=0.002 and p<0.0001, respectively). The strongest independent negative predictors of insulinogenic index/HOMA-IR were GDM (t=-4.1,p<0.0001) and 1-hr GIGT (t=-3.8,p=0.0002). Conclusions: Like GDM, 1-hr GIGT is associated with postpartum glycemia, insulin resistance, and beta-cell dysfunction.
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