An abnormal screening glucose challenge test in pregnancy predicts postpartum metabolic dysfunction, even when the antepartum oral glucose tolerance test is normal.
OBJECTIVE
In pregnancy, a normal result on the oral glucose tolerance test (OGTT) that follows an abnormal screening glucose challenge test (GCT) is considered a reassuring finding, requiring no further intervention. The obstetrical and metabolic implications of this presentation, however, have not been well studied. Thus, we sought to characterize the obstetrical and postpartum metabolic significance of an abnormal GCT in women with normal glucose tolerance (NGT) on antepartum OGTT.


METHODS
A total of 259 women with NGT on antepartum OGTT (166 with an abnormal GCT and 93 with a normal GCT) underwent (i) metabolic evaluation in pregnancy, (ii) assessment of obstetrical outcome at delivery and (iii) repeat metabolic characterization by OGTT at 3 months postpartum.


RESULTS
Neither infant birthweight nor Caesarean section rate differed between the abnormal GCT and normal GCT groups. At 3 months postpartum, however, compared to the normal GCT group, the abnormal GCT group exhibited greater glycaemia (mean area under the glucose curve (AUC(gluc)) 19.6 vs. 18.3, P = 0.0021), lower insulin sensitivity (median insulin sensitivity index (IS(OGTT)) 9.5 vs. 11.3, P = 0.0243) and poorer beta-cell function (median insulinogenic index/Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) 9.8 vs. 14.1, P = 0.0013). On multiple linear regression analyses, an abnormal GCT emerged as (i) the strongest independent predictor of postpartum AUC(gluc) (t = 2.77, P = 0.006) and (ii) the strongest independent negative predictor of log insulinogenic index/HOMA-IR (t = -2.36, P = 0.0191). Furthermore, the GCT was the antepartum parameter that best predicted postpartum pre-diabetes (area under the receiver operating characteristic curve (AROC) = 0.754).


CONCLUSIONS
An abnormal antepartum GCT, even when followed by a normal OGTT, is associated with postpartum glycaemia and beta-cell dysfunction, factors that may portend an increased future risk of diabetes in this patient population.
Retnakaran
Ravi
R
Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Division of Endocrinology, University of Toronto, Toronto, Canada. rretnakaran@mtsinai.on.ca
Qi
Ying
Y
Sermer
Mathew
M
Connelly
Philip W
PW
Hanley
Anthony J G
AJ
Zinman
Bernard
B
D000328:Adult; D016640:Diabetes, Gestational / Q000175:diagnosis / Q000378:metabolism*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D049590:Postpartum Period / Q000378:metabolism*; D011236:Prediabetic State / Q000175:diagnosis* / Q000378:metabolism; D011247:Pregnancy; D012307:Risk Factors